thiopental and Hypoxia

Topics: Animals; Body Temperature; Disease Models, Animal; Hypothermia, Induced; Hypoxia; Mice; Nitrous Oxide; Thiopental; Time Factors

Topics: Abdomen; Anesthesia, Conduction; Anesthetics; Animals; Blood Flow Velocity; Blood Glucose; Carbon Dioxide; Chloroform; Cyclopropanes; Ethyl Ethers; Halothane; Humans; Hypotension, Controlled; Hypoxia; Insulin; Liver Circulation; Neuroleptanalgesia; Nitrous Oxide; Oxygen; Pentobarbital; Preanesthetic Medication; Regional Blood Flow; Shock; Sympathomimetics; Thiopental

Topics: Anesthetics; Arrhythmias, Cardiac; Catecholamines; Digitalis Glycosides; Electroshock; Heart Diseases; Humans; Hypercapnia; Hypertension; Hypothermia, Induced; Hypoxia; Intubation; Neostigmine; Potassium; Scopolamine; Succinylcholine; Surgical Procedures, Operative; Thiopental

(1) To investigate changes in arterial oxygen saturation via pulse oximeter (SpO2) during apnea and after reinstitution of manual ventilation at SpO2 of 95% or 90% following rapid sequence induction of anesthesia in children after 2-minute preoxygenation; (2) to determine whether the setting of a safe threshold of apneic period to an SpO2 of 95% is appropriate in children during anesthetic induction; and (3) to evaluate the influences of age, body weight, and height on the time from the start of apnea to SpO2 of 95%.. A clinical study of random design and comparison among groups.. Operating room of a plastic surgery hospital of the Chinese Academy of Medical Sciences and Peking Union Medical College.. 152 infants and children, ASA physical status 1, aged 3 months to 12 years, scheduled for elective plastic surgery.. Patients were divided into three age groups: Group 1-infants 3 months to 1 year (n = 39); Group 2 children 1 to 3 years (n = 41); and Group 3-children 3 to 12 years (n = 72). Patients in each age group were randomly allocated again to Subgroups A and B. After a 2-minute preoxygenation, anesthesia was induced with thiopental 5 mg/kg, fentanyl 5 micrograms/kg and suxamethonium 1.5 mg/kg. Patients were manually ventilated when SpO2 decreased to 90% in Subgroups A and 95% in Subgroups B, respectively, during apnea.. SpO2 was measured continuously with a Datex pulse oximeter applied to the right index finger. During apnea, the times for SpO2 to decrease to 09% (T99) and 95% (T99) in all children, and 90% (T90) in Subgroups A were recorded. The time for SpO2 to decrease from 95% to 90% (T95-90) in Subgroups A was also measured. After reinstitution of manual ventilation, the time when SpO2 continued to decrease (T1) and the time from the end of apnea to recovery of SpO2 baseline (T2) were determined. In addition, the lowest value of SpO2 after apnea was also recorded. The results showed that younger children were more susceptible than older children to the risk of hypoxemia during apnea. There were significant differences in T99, T95, T90, and T95-90 between the three age groups T1 and T2 were significantly longer in Group 3 than in Groups 1 and 2. There were significant differences in the lowest values of SpO2 following apnea among the three Subgroups A and between Subgroups A and B of each age group. During apnea, heart rate decreased gradually as SpO2 decreased, showing a significant decrease at SpO2 of 95%. Bradycardia was found in three children in Subgroups A. The apnea time to SpO2 of 95% correlated well with age, weight, and height by linear regression analysis.. The safe threshold of an apneic period setting to an SpO2 of 95% was appropriate in children during anesthesia induction. Despite the same duration of preoxygenation, younger children were more susceptible than elder ones to the risk of hypoxemia during apnea. The apnea time to SpO2 of 95% correlated with age, body weight, and height using linear regression analysis.

Topics: Age Factors; Anesthesia, Intravenous; Anesthetics, Intravenous; Apnea; Body Height; Body Weight; Bradycardia; Child; Child, Preschool; Disease Susceptibility; Elective Surgical Procedures; Fentanyl; Heart Rate; Humans; Hypoxia; Infant; Linear Models; Neuromuscular Depolarizing Agents; Oximetry; Oxygen; Respiration, Artificial; Risk Factors; Safety; Succinylcholine; Surgery, Plastic; Thiopental; Time Factors

The incidence and degree of hypoxaemia during induction of balanced anaesthesia and endotracheal intubation were studied prospectively in 80 healthy adults undergoing elective surgery randomly divided into four equal groups of 20. Group 1 was preoxygenated for three minutes. The other three groups were not preoxygenated. Groups 1 and 2 were ventilated with 100% oxygen, while Groups 3 and 4 were ventilated with 50% and 33% oxygen respectively. Anaesthesia was induced with thiopentone 3-5 mg/kg and endotracheal intubation was done after ventilating for one minute with the chosen gas. Arterial desaturation was measured by pulse oximetry. In Groups 1-3 there was a significant increase and in Group 4 a significant decrease in saturation from the preinduction value. The arterial oxygen saturation was similar in Groups 1 and 2. Two patients in Group 3 and four in Group 4 had hypoxaemia. This incidence was not statistically significant. We conclude that ventilation with 100% oxygen for one minute prior to intubation and preoxygenation for three minutes are equally effective in preventing hypoxaemia during induction.

Topics: Adolescent; Adult; Aged; Anesthesia, General; Anesthesia, Inhalation; Anesthesia, Intravenous; Evaluation Studies as Topic; Female; Humans; Hypoxia; Incidence; Intubation, Intratracheal; Male; Middle Aged; Monitoring, Intraoperative; Nitrous Oxide; Oximetry; Oxygen; Oxygen Inhalation Therapy; Prospective Studies; Thiopental

Anaesthesia was induced by inhalation in 100 children using nitrous oxide in oxygen supplemented by either halothane or isoflurane, with or without rectal thiopentone premedication. Respiratory problems occurred more frequently in the unpremedicated isoflurane group, resulting in significant reductions in oxygen saturation. Premedication reduced the frequency of these complications, and oxygen saturation was usually maintained.

Topics: Administration, Rectal; Anesthesia, Inhalation; Child; Child, Preschool; Female; Halothane; Humans; Hypoxia; Infant; Isoflurane; Male; Oxygen; Preanesthetic Medication; Random Allocation; Thiopental

Topics: Acids; Adjuvants, Anesthesia; Blood Urea Nitrogen; Chlorides; Clinical Trials as Topic; Humans; Hydroxybutyrates; Hypnotics and Sedatives; Hypoglycemia; Hypokalemia; Hypoxia; Metabolism; Nitrogen; Oxygen; Potassium; Sodium; Thiopental

Thiopental sodium (TPTS) is a barbiturate general anesthetic, while its effects on hypoxia/reoxygenation (H/R)-induced injury are still unclear. This study aimed to investigate whether TPTS exerts protective effects against the H/R-induced osteoblast cell injury and explore the underlying mechanisms. Osteoblast cell injury model was induced by the H/R condition, which was treated with or without TPTS. Cell viability and lactate dehydrogenase (LDH) release were determined by the corresponding commercial kits. The levels of oxidative stress were determined in the experimental groups. Cell apoptosis and Caspase-3 activities were determined by propidium iodide staining and substrate-based assay, respectively. Western blotting and qRT-PCR were performed to measure the mRNA and protein levels, respectively. Treatment with TPTS was able to increase cell viability and reduce LDH release in H/R-induced osteoblasts. Additionally, TPTS regulated oxidative stress in H/R-induced osteoblasts by suppressing malondialdehyde (MDA) and reactive oxygen species (ROS) as well as boosting superoxide dismutase (SOD). TPTS was able to suppress cell apoptosis by suppressing Caspase-3 activity and cleavage. TPTS exerted protective effects against cell injury and apoptosis induced by the H/R conditions, which were associated with its regulation of Akt signaling. Moreover, TPTS induced osteoblast differentiation under the H/R condition. In summary, TPTS attenuates H/R-induced injury in osteoblasts by regulating AKT signaling.

Topics: Animals; Apoptosis; Caspase 3; Cell Hypoxia; Cell Line; Cell Survival; Hypoxia; Myocytes, Cardiac; Oxidative Stress; Proto-Oncogene Proteins c-akt; Thiopental

Although many in vitro studies demonstrated that thiopental sodium (TPS) is a promising neuroprotective agent, clinical attempts to use TPS showed mainly unsatisfactory results. We investigated the neuroprotective effects of TPS against hypoxic insults (HI), and the responses of the neurons to l-glutamate and acetylcholine application. Neurons prepared from E17 Wistar rats were used after 2weeks in culture. The neurons were exposed to 12-h HI with or without TPS. HI-induced neurotoxicity was evaluated morphologically. Moreover, we investigated the dynamics of the free intracellular calcium ([Ca(2+)]i) in the surviving neurons after HI with or without TPS pretreatment following the application of neurotransmitters. TPS was neuroprotective against HI according to the morphological examinations (0.73±0.06 vs. 0.52±0.07, P=0.04). While the response to l-glutamate was maintained (0.89±0.08 vs. 1.02±0.09, P=0.60), the [Ca(2+)]i response to acetylcholine was notably impaired (0.59±0.02 vs. 0.94±0.04, P<0.01). Though TPS to cortical cultures was neuroprotective against HI morphologically, the [Ca(2+)]i response not to l-glutamate but to acetylcholine was impaired. This may partially explain the inconsistent results regarding the neuroprotective effects of TPS between experimental studies and clinical settings.

Topics: Acetylcholine; Animals; Anticonvulsants; Calcium; Cell Survival; Cells, Cultured; Cerebral Cortex; Dose-Response Relationship, Drug; Embryo, Mammalian; Female; Glutamic Acid; Hypoxia; Neurons; Potassium Chloride; Pregnancy; Rats; Rats, Wistar; Statistics, Nonparametric; Thiopental

People travelling to high altitude for occupational, recreational or religious purposes are mostly healthy and fit but sometimes they use drugs for common ailments like influenza, acute mountain sickness or chronic disease like diabetes. Limitation of oxygen at high altitude may compromise metabolism of drugs. Hence, we undertook this study to assess the effect of hypobaric hypoxia on some commonly used drugs in rats and rabbits.. Effect of intermittent hypobaric hypoxia on phenotypic expression of anesthetic drugs pentabarbitone, thiopentone and zoxazolamine (sleeping time) was assessed in rats exposed to 282.4 mm Hg equivalent to 25000 feet in a decompression chamber. Plasma clearance of some commonly used drugs was investigated in rabbits exposed to 429 mm Hg equivalent to 15000 feet. Pharmacokinetic parameters were computed by plotting drug concentration versus time curve on semi log scale.. A significant delay in regaining rightening reflex was observed in rats exposed to intermittent hypobaric hypoxia in response to zoxazolamine, pentobarbitone and thiopentone sodium. Pharmacokinetics of acetyl salicylic acid, gentamicin, phenobarbitone and acetazolamide showed increase in plasma half life (t 1/2), decrease in elimination rate constant (k el) and hence prolonged residence of these drugs in hypoxic animals.. This experimental study showed that hypoxia altered therapeutic effectiveness and clearance of several drugs, in rats and rabbits exposed to intermittent hypobaric hypoxia. s0 uch studies need to be done in human volunteers to see the effect of hypoxia on pharmacokinetics of some common drugs.

Topics: Animals; Humans; Hypoxia; Male; Oxygen; Rabbits; Rats; Rats, Wistar; Thiopental; Zoxazolamine

General anesthetics reduce neuron loss following focal cerebral ischemia in rodents. The relative efficacy of this action among different anesthetics clinically used for neuroprotection is uncertain. In addition, it remains unclear how anesthetics compare to neuroprotection afforded by mild hypothermia. This study was performed to evaluate the comparative effects of isoflurane, sodium pentothal, and mild hypothermia in a hippocampal slice model of cerebral ischemia and to determine if the mechanism of neuroprotection of isoflurane involves inhibition of glutamate excitotoxicity.. Survival and morphology of CA1, CA3, and dentate gyrus neurons in rat hippocampal slices were examined after 10 or 20 min of combined oxygen-glucose deprivation (in vitro ischemia) followed by a 5-h recovery period.. 10 or 20 min in vitro ischemia at 37 degrees C killed 35-40% of neurons in CA1 (P < 0.001), 6% in CA3 (not significant) and 18% in dentate (P < 0.05). Isoflurane (0.7 and 2.0%, approximately 0.45 and 1.5 minimum alveolar concentration), pentothal (50 microm, approximately 1 minimum alveolar concentration equivalent) and mild hypothermia (34 degrees C) all reduced CA1 cell loss and morphologic damage to similar degrees in 10- and 20-min periods of ischemia (P < 0.001). The noncompetitive N-methyl-D-aspartate antagonist MK-801 prevented cell damage, showing that N-methyl-D-aspartate receptor activation is an important mechanism of injury in this model. Glutamate (1 mm) produced cell loss similar to in vitro ischemia. Isoflurane (2%) prevented cell damage from glutamate exposure.. In hippocampal slices, neuron death from simulated ischemia was predominately due to activation of glutamate receptors. Isoflurane, sodium pentothal, an N-methyl-D-aspartate receptor antagonist, and mild hypothermia prevented cell death to similar degrees. For isoflurane, the mechanism appears to involve attenuation of glutamate excitotoxicity.

Topics: Anesthetics; Animals; Brain Ischemia; Cell Death; Hippocampus; Hypothermia; Hypoxia; Isoflurane; Neurons; Rats; Rats, Sprague-Dawley; Receptors, Glutamate; Thiopental

Although pulmonary function is minimally changed by neuraxial blockade in most cases, ventilatory arrest may ensue in rare cases. The authors examined the mechanism of apnea in a rabbit model of sudden ventilatory arrest during the combination of epidural anesthesia and hypoxia.. Rabbits were studied during alpha-chloralose sedation and spontaneous ventilation through a tracheostomy tube. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Respiratory rate and tidal volume were measured by pneumotachograph. Responses were recorded during administration of oxygen at inspired oxygen concentrations of 11% for 2.5 min and 0% for 40 s, before and after either thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or intramuscular lidocaine (15 mg/kg). In a third group of animals, epinephrine was given intravenously during epidural blockade to return mean arterial pressure to baseline values before hypoxia. In a fourth group of animals, which did not get lidocaine, sympathetic blockade and hypotension were produced with intravenously administered trimethaphan rather than epidural blockade.. Thoracolumbar epidural anesthesia decreased mean arterial pressure from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during hypoxia occurred in 90% of these animals (nine of ten) but in only 11% of animals (one of nine) after intramuscularly administered lidocaine (P < 0.01). Treatment of epidural hypotension with epinephrine prevented apnea (zero of nine animals). Apnea during hypoxia occurred in 50% (three of six) of animals given trimethaphan. Apnea in all groups was sudden in onset, with no preceding decreases in respiratory rate or tidal volume.. Epidural anesthesia results in a narrowed margin of safety for oxygen delivery to the brain and predisposes subjects to ventilatory arrest during hypoxia. This results from the combined effects of decreased blood oxygen content, which is due to decreased inspired oxygen concentration superimposed on circulatory depression due to neural blockade.

Topics: Anesthesia, Epidural; Anesthetics, Local; Animals; Apnea; Atropine; Blood Pressure; Epinephrine; Ganglionic Blockers; Heart Rate; Hypoxia; Lidocaine; Male; Rabbits; Thiopental; Trimethaphan

Previous studies in dogs and humans suggest that the carotid body chemoreceptor response to hypoxia is selectively impaired by halothane. The present studies in an open-loop canine preparation were performed to better delineate the effects of anesthetic concentrations of halothane on the carotid body chemoreceptor-mediated phrenic nerve response to an acute hypoxic stimulus.. Three protocols were performed to study the effects of halothane anesthesia on the phrenic nerve response to 1 min of isocapnic hypoxia (partial pressure of oxygen [PaO2] at peak hypoxia, 35-38 mmHg) in unpremedicated, anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. In protocol 1, the dose-dependent effects of halothane from 0.5-2.0 minimum alveolar concentration (MAC) on the hypoxic response during moderate hypercapnia (partial pressure of carbon dioxide [PaCO2], 60-65 mmHg) were studied in 10 animals. In protocol 2, the hypoxic responses at 1 MAC halothane near normocapnia (PaCO2, 40-45 mmHg) and during moderate hypercapnia were compared in an additional four animals. In protocol 3, the hypoxic response of 4 of 10 dogs from protocol 1 was also studied under sodium thiopental (STP) anesthesia after they completed protocol 1.. Protocol 1: Peak phrenic nerve activity (PPA) increased significantly during the hypoxic runs compared with the isocapnic hyperoxic controls at all halothane doses. The phrenic nerve response to the hypoxic stimulus was present even at the 2 MAC dose. Protocol 2: The net hypoxic responses for the two carbon dioxide background levels at 1 MAC were not significantly different. Protocol 3: The net hypoxic response of PPA for the STP anesthetic was not significantly different from the 1 MAC halothane dose. Bilateral carotid sinus denervation abolished the PPA response to hypoxia.. The phrenic nerve response to an acute, moderately severe isocapnic hypoxic stimulus is dose-dependently depressed but not abolished by surgical doses of halothane. This analysis does not suggest a selective depression of the carotid body chemoreceptor response by halothane. The observed hypoxic phrenic response was mediated by the carotid body chemoreceptors in vagotomized dogs because bilateral carotid sinus denervation abolished all increases in PPA.

Topics: Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Carbon Dioxide; Carotid Body; Dogs; Dose-Response Relationship, Drug; Halothane; Hypercapnia; Hypoxia; Phrenic Nerve; Respiration; Thiopental; Vagotomy

Topics: Anesthesia, Obstetrical; Cesarean Section; Female; History, 20th Century; Humans; Hypoxia; Neuromuscular Agents; Pregnancy; Thiopental

Extracellular accumulation of the excitatory neurotransmitter L-glutamate during cerebral hypoxia or ischemia contributes to neuronal death. Anesthetics inhibit release of synaptic neurotransmitters but it is unknown if they alter net extrasynaptic glutamate release, which accounts for most of the glutamate released during hypoxia or ischemia. The purpose of this study was to determine if different types of anesthetics decrease hypoxia-induced glutamate release from rat brain slices.. Glutamate released from cortical brain slices was measured fluorometrically with the glutamate dehydrogenase catalyzed formation of the reduced form of nicotinamide adenine dinucleotide phosphate. Glutamate release was measured in oxygenated (PO2 = 400 mmHg), hypoxic ((PO2 = 20 mmHg), and anoxic ((PO2 = 20 mmHg plus 100 microM NaCN) solutions and with clinical concentrations of anesthetics (halothane 325 microM, enflurane 680 microM, propofol 200 microM, sodium thiopental 50 microM). The source of glutamate released during these stresses was defined with toxins inhibiting N and P type voltage-gated calcium channels, and with calcium-free medium.. Glutamate released during hypoxia or anoxia was 1.5 and 5.3 times greater, respectively, than that evoked by depolarization with 30 mM KCl. Hypoxia/anoxia-induced glutamate release was not mediated by synaptic voltage-gated calcium channels, but probably by the reversal of normal uptake mechanisms. Halothane, enflurane, and sodium thiopental, but not propofol, decreased hypoxia-evoked glutamate release by 50-70% (P < 0.05). None of the anesthetics alter basal glutamate release.. The authors conclude that halothane, enflurane, and sodium thiopental but not propofol, at clinical concentrations, decrease extrasynaptic release of L-glutamate during hypoxic stress.

Topics: Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Cerebral Cortex; Enflurane; Glutamic Acid; Halothane; Hypoxia; In Vitro Techniques; Propofol; Rats; Rats, Sprague-Dawley; Thiopental

The purpose of this study was to determine the cumulative effects of brief intervals of hypoxia and hypercapnia on the pulsatile characteristics of the pulmonary arterial circulation of 48-h-old compared with 2-wk-old open-chest Yorkshire pigs while using two different anesthetic regimens: 1) azaperone and ketamine (4 and 12 mg/kg im, respectively) and 2) thiopental sodium (25 mg/kg i.v.). Animals 48 h old were randomly allocated to undergo mild hypoxia (inspired O2 fraction = 0.15), severe hypoxia (inspired O2 fraction = 0.05), or hypercapnia (inspired CO2 fraction = 0.20), whereas animals 2 wk old underwent severe hypoxia or hypercapnia. With use of Fourier analysis, characteristic impedance (Zo), mean input impedance (Zm), impedance moduli, and phase angles were determined. In 48-h-old pigs anesthetized with azaperone-ketamine, neither mild nor severe hypoxia altered Zo, Zm, or pulmonary vascular resistance (PVR), whereas hypercapnia increased Zo by 22% (P < 0.001), which persisted despite a return to normocapnia. In 48-h-old animals anesthetized with thiopental, baseline control Zo and Zm were lower than those in same-age pigs anesthetized with azaperone-ketamine. In thiopental-anesthetized 48-h-old pigs, both severe hypoxia and hypercapnia increased Zm and PVR but Zo was unaltered. In 2-wk-old pigs anesthetized with thiopental, severe hypoxia but not hypercapnia elevated Zm and PVR, whereas Zo was not changed with either stress. Results indicate age- and anesthetic-dependent responses of Zo, Zm, and PVR to severe hypoxia and hypercapnia. The persistent elevation in Zo caused by hypercapnia indicates a prolonged decrease in arterial compliance or a reduction in effective proximal pulmonary arterial radius.

Topics: Airway Resistance; Animals; Animals, Newborn; Azaperone; Blood Gas Analysis; Energy Metabolism; Female; Hemodynamics; Hypercapnia; Hypoxia; Ketamine; Lung; Male; Pulmonary Alveoli; Pulmonary Circulation; Swine; Thiopental; Transducers, Pressure; Vascular Resistance

Contradictory results have been reported in previous studies investigating the effect of isoflurane on hypoxic pulmonary vasoconstriction by indirect approaches. The current study measured the effects of one-lung ventilation (1LV) and isoflurane 1.5% by direct visual observation of the pulmonary microcirculation.. Ten New Zealand White rabbits were anesthetized with intravenous thiopental, alpha-chloralose, and piritramid. Arterial, central venous, pulmonary arterial, left atrial, and airway pressures and cardiac output were recorded continuously. 1LV was facilitated by a bronchial blocker in the right main bronchus. A transparent window was implanted into the right thoracic wall for videofluorescence microscopy of the subpleural pulmonary microcirculation. After intravenous injection of fluorescein isothiocyanate-labeled red blood cells, vessel diameters, red blood cell flux, red blood cell velocity, and dynamic microhematocrit were measured in pulmonary arterioles and venules during two-lung ventilation and 1LV during baseline anesthesia and with supplementary isoflurane 1.5%.. During intravenous anesthesia, 1LV caused significant reduction of vessel diameters and red cell flux and velocity and an increase in microvascular hematocrit in pulmonary arterioles and venules. The decreases in arteriolar diameters and red blood cell flux and velocity induced by 1LV were significantly attenuated by isoflurane as compared with those measured during baseline anesthesia (P = 0.010, P = 0.029 and P = 0.047). Accordingly, 1LV-induced reduction of venular red cell flux (P = 0.023) and velocity (P = 0.036) were less pronounced during isoflurane. Isoflurane caused a significant decrease in arterial pressure. Venous admixture increased and arterial oxygen tension decreased significantly during 1LV; the changes were more pronounced during 1LV with isoflurane 1.5% than during 1LV with baseline anesthesia.. 1LV leads to a marked reduction of microvascular diameters and blood flow in the hypoxic lung. Isoflurane 1.5% inhibits hypoxic pulmonary vasoconstriction in pulmonary arterioles and increases regional blood flow in the hypoxic lung.

Topics: Anesthesia, Intravenous; Animals; Hemodynamics; Hypoxia; Isoflurane; Lung; Microscopy, Fluorescence; Pulmonary Circulation; Pulmonary Gas Exchange; Rabbits; Thiopental; Vasoconstriction

Sedation using combined intravenous midazolam and fentanyl is a popular technique for minor gynaecological procedures. However, it is fraught with inconsistency in efficacy and has a greater tendency to perioperative oxygen desaturation. Fifty female ASA I patients scheduled for minor gynaecological procedures were given intravenous midazolam and fentanyl before surgery started. Intraoperative excessive movement that interfered with surgery and failure to maintain a patient airway were noted. Perioperative oxygen saturation was monitored with the pulse oximeter. In another group of 50 female ASA I patients, intravenous thiopentone was given and anaesthesia maintained with 67% nitrous oxide in 33% oxygen and 0.5% of isoflurane via a face mask. Results showed that 10% of the sedated patients had excessive movements that interfered with surgery, of which 6% needed a general anaesthetic. Twenty-two percent of the sedated patients needed maintenance of airway perioperatively. Perioperative oxygen desaturation was profound in incidence and degree in the sedated patients whereas no patient who received general anaesthesia desaturated. The perioperative incidence of desaturation in the sedated patients was 46%. Intraoperatively, 28% (p < 0.001) of the sedated patients had oxygen saturation in the range of 85 to 90% and 18% of them (p < 0.01) had oxygen saturation of less than 85%. Postoperatively 8% of the sedated patients had oxygen saturation of 85 to 90%. We conclude that general anaesthesia is more efficacious and safer than sedation in patients scheduled for minor gynaecological procedures. The same minimum standard of monitoring applied to general anaesthesia should be used for sedated patients.

Topics: Adolescent; Adult; Anesthesia, General; Conscious Sedation; Female; Fentanyl; Genitalia, Female; Humans; Hypoxia; Isoflurane; Midazolam; Middle Aged; Minor Surgical Procedures; Movement; Nitrous Oxide; Oximetry; Oxygen; Oxygen Inhalation Therapy; Thiopental

The effect of propofol and thiopentone on cerebral (CBF), myocardial (MBF), muscular, and arterial hepatic blood flow was assessed with radiolabelled microspheres in 12 chronically instrumented dogs, six given propofol and six thiopentone. Tissue blood flows were measured in the awake animal, after 30 min of normoxic anaesthesia (room air), and after 30 min of hypoxic anaesthesia using a mixture of 10% O2 and 3% CO2 in nitrogen. The decrease in CBF from awake to normoxic anaesthesia was similar with propofol and thiopentone (propofol: 77 +/- 8 to 38 +/- 3 ml min-1 100 g-1, P < 0.01; thiopentone: 66 +/- 3 to 33 +/- 2 ml min-1 100 g-1, P < 0.01). During hypoxia, CBF rose moderately in the two groups (respectively +19% and +28%, P < 0.05). The MBF increased in propofol and thiopentone groups after 30 min of anaesthesia with air (propofol: 97 +/- 23 to 137 +/- 15 ml min-1 100 g-1; thiopentone: 82 +/- 7 to 141 +/- 10 ml min-1 100 g-1) and increased still more during hypoxia. The increase in MBF was related to an increase in heart rate and blood pressure. The quadriceps blood flow decreased during anaesthesia in normoxia and in hypoxia. The diaphragmatic blood flow increased with thiopentone under hypoxia. The hepatic arterial blood flow was unchanged. It is concluded that the effects of propofol on regional blood flows are very similar to those of thiopentone.

Topics: Anaerobiosis; Animals; Blood Gas Analysis; Cardiac Output; Cerebrovascular Circulation; Coronary Circulation; Dogs; Heart Rate; Hepatic Artery; Hypoxia; Liver Circulation; Microspheres; Muscles; Propofol; Regional Blood Flow; Thiopental

Topics: Anesthesia, General; Animals; Brain; Brain Injuries; Cerebral Cortex; Fentanyl; Hypoxia; Isoflurane; Lung Diseases; Oxygen; Partial Pressure; Rabbits; Regional Blood Flow; Thiopental

Obese patients have a decreased functional residual capacity and, hence, a reduced oxygen supply during periods of apnea. To determine whether obese patients are at greater risk of developing hypoxemia during induction of anesthesia than patients of normal weight, 24 patients undergoing elective surgical procedures were studied. Group 1 (normal) were within 20% of their ideal body weight. Group 2 (obese) were more than 20% but less than 45.5 kg over ideal body weight. Group 3 (morbidly obese) were more than 45.5 kg over ideal body weight. Patients were preoxygenated for 5 min or until expired nitrogen was less than 5%. After induction of anesthesia and muscle relaxation the patients were allowed to remain apneic until arterial saturation as measured by pulse oximetry reached 90%. The time taken for oxygen saturation to decrease to 90% was 364 +/- 24 s in group 1, 247 +/- 21 s in group 2, and 163 +/- 15 s in group 3; these times are significantly different at P less than 0.05 between groups. Regression analysis of the data demonstrated a significant negative linear correlation (r = -0.83) between time to desaturation and increasing obesity. These results show that obese patients are at an increased risk of developing hypoxemia when apneic.

Topics: Adult; Anesthesia; Apnea; Humans; Hypoxia; Middle Aged; Obesity; Obesity, Morbid; Risk; Thiopental

The effects of intravenous almitrine under normoxic, hyperoxic, and hypoxic conditions were studied in 5 male beagle dogs (mean weight 15.2 +/- 5 kg) anaesthetized with thiopentone. Plasma concentrations of thiopentone were maintained constant at 27-29 mg.1(-1). Each animal underwent twice the three different experiments, with a lapse of a fortnight between each experiment: a) breathing room air, with intravenous administration of 1 mg.kg-1 almitrine over 30 s, b) breathing room air, then pure oxygen for 15 min, followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing pure oxygen, and c) breathing room air, then progressively less oxygen (FIO2 0.18, 0.16, 0.14, 0.12 for 5 min each), followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing a mixture with 12% oxygen. Tidal volume, respiratory rate, minute ventilation, inspiratory and expiratory duration, arterial pH, PaO2 and PaCO2 were measured respectively in room air, after 100% oxygen, in hypoxia (FIO2 = 0.12), before, 5 and 10 min after the injection of almitrine. Hyperoxia depressed ventilation (-21%), whilst hypoxia stimulated it (+126%), although significantly less than in the awake animal. Almitrine restored the respiratory response to hypoxia, but hyperoxia did not suppress respiratory stimulation due to the drug. It would therefore seem likely that almitrine acts on peripheral arterial chemoreceptors, but also on other structures. The results of this study suggest that almitrine may be useful in restoring the respiratory response to hypoxia during recovery from anaesthesia.

Topics: Almitrine; Anesthesia, General; Animals; Carbon Dioxide; Chemoreceptor Cells; Disease Models, Animal; Dogs; Hypoxia; Male; Oxygen; Oxygen Inhalation Therapy; Respiration; Thiopental

Cromolyn sodium has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV) in dogs and sheep, presumably by stabilizing mast cell membranes and thereby preventing the release of mediators such as leukotrienes. Because the effects of leukotriene synthesis and receptor blockers on HPV have been variable across studies, we studied the effect of cromolyn on HPV in the halothane-anesthetized sheep, a model in which we have found leukotriene synthesis and receptor blockers to be ineffective. In control animals, hypoxia (FIO2 = 0.13) increased pulmonary artery pressure (Ppa) 67% and pulmonary vascular resistance 85%, and these responses were reproducible with a second episode of hypoxia. In a second group of sheep, hypoxia (FIO2 = 0.13) during cromolyn administration (6 mg.kg-1.min-1) for 30 min increased (Ppa) 104% and increased pulmonary vascular resistance 124%. In a third group of sheep, cromolyn sodium (6 mg.kg-1.min-1) without hypoxia did not significantly affect pulmonary hemodynamics. We conclude that cromolyn sodium does not inhibit HPV in halothane-anesthetized sheep. In experimental designs in which cromolyn does alter HPV, the effect is more likely due to altered release of modulators of HPV rather than to decreased release of obligatory mediator of HPV.

Topics: Animals; Cromolyn Sodium; Halothane; Hemodynamics; Hypoxia; Infusions, Intravenous; Male; Pulmonary Artery; Sheep; Thiopental; Vasoconstriction

Five patients requiring general anesthesia but presenting with compromised airways were successfully intubated by blind awake intubation with the aid of regional anesthesia and the use of appropriate sedation. Arterial blood gases were collected at three intervals: presedation, postsedation, and postintubation. Analysis of the blood gases revealed varying degrees of hypoxemia, hypercarbia, and acidosis following deep sedation before intubation. A decrease in oxygen saturation was also observed. Supplemental oxygen is suggested to avoid the effects of arterial desaturation during the sedation process. If oxygen is not administered, the risk of moderate hypoxia associated with blind awake intubation must be considered along with alternative problems including loss of protective reflexes or the inability to ventilate during induction and intubation via a direct technique.

Topics: Adult; Anesthesia, General; Blood Gas Monitoring, Transcutaneous; Carbon Dioxide; Droperidol; Female; Fentanyl; Humans; Hypoxia; Intubation, Intratracheal; Male; Middle Aged; Partial Pressure; Thiopental; Wakefulness

Topics: Animals; Drug Interactions; Hypoxia; Mice; Nitrous Oxide; Reproducibility of Results; Thiopental

Etomidate was compared with thiopental with respect to preventing loss of brain high energy metabolites and accumulation of lactate during 20 min of hypoxemia (Pa2 of 16-19 mmHg) in rats with unilateral carotid artery ligation. Male Sprague-Dawley rats, anesthetized with halothane and nitrous oxide (N2O) in oxygen were randomly assigned to one of six groups. A normoxic control group which received 70% N2O in oxygen, a hypoxia group received no iv drug treatment (hypoxia-N2O), and four iv drug treatment groups (N2O was replaced by 70% nitrogen at the start of drug administration). The iv drug groups were treated as follows: hypoxia-etomidate low dose (1 mg.kg-1 iv followed by an infusion at 0.35 mg.kg-1.min-1); hypoxia-etomidate high dose (1 mg.kg-1 then 1.3 mg.kg-1.min-1); hypoxia-thiopental low dose (15 mg.kg-1, then 1.5 mg.kg-1.min-1); and hypoxia-thiopental high dose (15 mg.kg-1, then 5 mg.kg-1.min-1). After hypoxia or a corresponding period in the normoxic group, the brains were frozen in situ for later biochemical analysis. Blood was obtained prior to and at the end of hypoxia and analyzed for glucose. Brain metabolite concentrations on the side ipsilateral to the ligated carotid artery in the normoxia-N2O group were adenosine triphosphate (ATP), 2.76 +/- 0.1, phosphocreatione (PCr) 3.88 +/- 0.12, lactate 2.34 +/- 0.16, and glucose 3.56 +/- 0.28 (mumole.g-1 wet weight, mean +/- SE). There was no significant decrease in ATP in any of the hypoxia groups. PCr decreased by 45% (compared to normoxia-N2O) in the hypoxia-N2O group.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Brain; Brain Chemistry; Dose-Response Relationship, Drug; Energy Metabolism; Etomidate; Glucose; Halothane; Hypoxia; Lactates; Lactic Acid; Male; Nitrous Oxide; Random Allocation; Rats; Rats, Inbred Strains; Thiopental

The clinical course and the intracranial pressure (ICP) changes in 66 severe head injury patients presenting bulk enlargement of one cerebral hemisphere within a few hours of trauma have been analyzed. These patients represent 11% of a series of 589 severe head injury cases studied with computerized tomography (CT). Cerebral hemisphere swelling, which was associated with an ipsilateral subdural haematoma of variable extent in 58 patients (88%), or a large epidural haematoma in 5 patients (7%), and occurred as an isolated lesion in 3 patients (4%), carried the highest incidence of uncontrollable intracranial hypertension, the highest mortality rate and the shortest survival period after trauma in the authors' severe head injury series. The high incidence of arterial hypotension and/or hypoxaemia at admission (48% of cases), and the severity of clinical presentation (82%) of patients scored 5 patients or less in the Glasgow Coma Scale, 77% had uni- or bilateral mydriasis and 82% initial ICP above normal limits) correlated with the very poor final outcome (85% mortality). Only one of the 12 patients with normal initial ICP continued to have low pressure throughout the course. High dose thiopental failed to control severe intracranial hypertension in 29 patients (44%) who had a fulminant, malignant course. A transient decrease in ICP elevation was achieved in 17 patients (26%) and a definitive control in 12 patients (18%), among them the 10 survivors in this series. In the authors experience once ICP is controlled, and unless haemodynamic instability compells action to the contrary, barbiturate should not be discontinued until a control CT scan shows complete disappearance of the mass effect.

Topics: Adolescent; Adult; Aged; Brain Edema; Brain Injuries; Child; Child, Preschool; Humans; Hypertension; Hypoxia; Infant; Intracranial Pressure; Male; Middle Aged; Thiopental; Tomography, X-Ray Computed

The hypoxic mouse model, in which mice are subjected to an atmosphere of 5% O2 in nitrogen, has been used to screen anesthetics for possible cerebral protection by measuring their ability to prolong survival in mice exposed to hypoxia. Although prolonged survival time in this model is primarily due to a decreased cerebral metabolic rate produced by a specific anesthetic, results can also be influenced by body temperature, dose of anesthetic, and ventilatory or circulatory depression produced by the anesthetic. Using the hypoxic mouse model, the effects of thiopental in conjunction with changes in ambient temperature, changes in thiopental dose, and the presence or absence of nitrous oxide (N2O) were examined. Survival times were measured in eight groups of animals, either untreated animals or animals pretreated with 100 mg/kg thiopental intraperitoneally; exposed to hypoxia in the presence or absence of N2O; at ambient temperatures of either 25 degrees C or 35.5 degrees C. Survival times of seven additional groups of mice, either untreated or treated with doses of 50, 60, 70, 80, 90 or 120 mg/kg thiopental intraperitoneally, exposed to hypoxia in an ambient temperature of 35.5 degrees C were measured to determine a dose-response curve. At an ambient temperature of 35.5 degrees C in which the rectal temperature of both untreated and thiopental-treated animals was maintained near 36 degrees C, thiopental-treated animals did not survive any longer than the untreated animals. Exposure to N2O shortened survival times of both groups by approximately 20%.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Anesthetics; Animals; Body Temperature; Brain; Drug Evaluation; Hypoxia; Mice; Models, Biological; Nitrous Oxide; Oxygen Consumption; Thiopental; Ventilation-Perfusion Ratio

Topics: Anesthesia; Humans; Hypoxia; Intraoperative Complications; Oxygen; Oxygen Inhalation Therapy; Succinylcholine; Thiopental; Time Factors

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.

Topics: Animals; Blood Gas Monitoring, Transcutaneous; Dogs; Electroconvulsive Therapy; Hypercapnia; Hypoxia; Male; Respiration, Artificial; Seizures; Thiopental; Time Factors

A study was made of the effects of isothiobarbamine and guthimine (10 and 50 mg/kg, respectively) on the content of cAMP and cGMP in the brain cortex (BC) and hippocamp under normal conditions and hypoxia. Isothiobarbamine did not change the content of both cyclic nucleotides under normoxia, whereas under hypoxia it reduced the level of the cyclic nucleotides in the BC and raised it in the hippocamp. Guthimine increased their content in the BC and did not change it in the hippocamp under normoxia, whereas under hypoxia it increased the cAMP content in the hippocamp and did not change it in the BC. The cGMP content descended in both the structures under study.

Topics: Animals; Brain; Cerebral Cortex; Cyclic AMP; Cyclic GMP; Drug Evaluation, Preclinical; Guanylthiourea; Hippocampus; Hypoxia; Male; Rats; Rats, Inbred Strains; Thiopental; Thiourea

The influence of time on the pulmonary vasoconstrictor response to hypoxia was studied in six subjects during general anaesthesia and artificial ventilation prior to elective surgery. The lungs were intubated separately with a double-lumen bronchial catheter. After preoxygenation of both lungs for 30 min, the test lung was rendered hypoxic for 60 min by ventilation with 5% O2 in N2, with the control lung still being ventilated with 100% O2. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The fractional perfusion of the test lung decreased from 53% to 25% of cardiac output within the first 15 min of unilateral hypoxia. The pulmonary artery mean pressure increased by 14% and the pulmonary vascular resistance (PVR) of the test lung increased by 54%. Venous admixture increased from 21% to 39% of cardiac output, while the "true" shunt was maintained at about 15%. Arterial oxygen tension (Pao2) fell from 45 kPa to 12 kPa. Prolonging the unilateral hypoxic challenge caused no further change in the redistribution of the pulmonary blood flow, but cardiac output and pulmonary artery mean pressure continued to increase to 40%-50% above control values after 1 h of hypoxia. The PVR of the test lung remained unchanged. The findings suggest that there is an immediate vasoconstrictor response to hypoxia in the human lung and that there is no further potentiation or diminution, of the response during a 60-min period of hypoxia.

Topics: Adult; Anesthesia, Intravenous; Blood Pressure; Cardiac Output; Female; Humans; Hypoxia; Male; Middle Aged; Oxygen; Pulmonary Artery; Pulmonary Circulation; Pulmonary Gas Exchange; Thiopental; Vascular Resistance; Vasoconstriction

The effect of thiopental (100 mg X 1(-1] during total ischemia, low-flow ischemia, and severe hypoxia with maintained flow was investigated in the isolated perfused rat heart. During total ischemia the rate of decline of tissue creatine phosphate and adenosine triphosphate was no different in thiopental-treated and untreated hearts. The development of ultrastructural damage during total ischemia, the release of creatine kinase on reperfusion, and the exacerbation of ultrastructural damage after reperfusion were unaffected by thiopental. When thiopental was added to the perfusate during hypoxia and during low-flow ischemia at a normal pH(7.4), creatine kinase release during reoxygenation and during reperfusion was significantly less (P less than 0.005 and P less than 0.05, respectively) than in the untreated groups. After low-flow ischemia at a low pH (6.5), creatine kinase release was no different in thiopental-treated and untreated hearts. Thus, thiopental afforded protection of the myocardium in hypoxia and low-flow ischemia at pH 7.4 but not in total ischemia and low-flow ischemia at pH 6.5. The data are consistent with the hypothesis that during total ischemia and low-flow ischemia at pH 6.5, acidosis favors the entry of thiopental into the cell, causing inhibition of mitochondrial function and reduction of ATP production. During hypoxic perfusion and low-flow ischemia at pH 7.4, when the decrease in pH is less, the cardiodepressant effect of thiopental may offset any deleterious effect of the drug on intracellular organelles such as mitochondria.

Topics: Adenosine Triphosphate; Animals; Coronary Circulation; Coronary Disease; Creatine Kinase; Hydrogen-Ion Concentration; Hypoxia; In Vitro Techniques; Mitochondria, Heart; Myocardium; Perfusion; Phosphocreatine; Rats; Rats, Inbred Strains; Thiopental

Three groups of 12 rabbits each, anesthetized with ketamine (30 mg/kg, intramuscularly) and spontaneously breathing N2O-O2, were given intravenous injections of either placebo (group 1), thiopental (TP) (40 mg/kg, intravenously; group 2), or phenytoin (PNT) (15 mg/kg, intravenously; group 3). Four minutes later, succinylcholine was given and, while ventilation was controlled with N2O alone, changes in systolic blood pressure (SBP) and heart rate (HR) were measured. Tachycardia (greater than 210 beats/min) occurred in groups 1, 2, and 3-111, 107, and 151 sec later, respectively. SBP decreased below 100 torr at 189, 192, and 362 sec, respectively, and below 30 torr 245, 216, and 433 sec after the onset of hypoxia (P less than 0.05), respectively. Bradycardia (less than 30 beats/min) appeared 248, 219, and 439 sec (P less than 0.05), respectively. The onset of severe bradycardia and hypotension was significantly (P less than 0.05) delayed by PNT but not by TP. All rabbits in the placebo group died, while 3 and 8 of the animals given TP and PNT, respectively, survived; survival rate was significantly (P less than 0.05) increased by PNT but not by TP. Phenytoin appears to sustain cardiovascular function during hypoxia better than thiopental does, but phenytoin may not be more effective than thiopental in increasing survival.

Topics: Anesthesia, General; Animals; Blood Pressure; Heart Rate; Hemodynamics; Hypoxia; Ketamine; Phenytoin; Rabbits; Thiopental

Anesthetic hepatotoxicity was tested under various conditions of hypoxia in rats pretreated with phenobarbital. Administration of 0.3 MAC halothane or fentanyl in 9% oxygen (fractional concentration of inspired oxygen = 0.09) for 46 min produced centrilobular hepatic injury in all rats (P less than 0.001 vs all other groups). Isoflurane, nitrous oxide, and thiopental at 0.3 MAC did not produce hepatic injury greater than that produced in control rats given 9% oxygen, nor was significant injury produced in control phenobarbital-pretreated rats who breathed 6 or 7.5% oxygen for 46 min. With an inspired oxygen concentration of 7.5%, hepatic injury occurred after exposure to 92.5% nitrous oxide (P less than 0.05), but not after enflurane, isoflurane, or thiopental. When hypoxia associated with 9% oxygen was extended to 2 hr, 91% nitrous oxide produced significant injury (P less than 0.001 compared with the controls), while enflurane, isoflurane, and thiopental did not. These and previous results suggest that all anesthetics can produce liver injury in the hypoxic rat model and that the ranking of hepatotoxicity (most to least) may be halothane, fentanyl, nitrous oxide, enflurane = isoflurane = thiopental.

Topics: Animals; Fentanyl; Halothane; Hypoxia; Isoflurane; Liver; Male; Nitrous Oxide; Rats; Rats, Inbred Strains; Thiopental

Topics: Animals; Atmospheric Pressure; Cyanides; Etomidate; Hypoxia; Imidazoles; Male; Methohexital; Mice; Rats; Thiopental

Topics: Animals; Creatine Kinase; Heart; Hypoxia; In Vitro Techniques; Perfusion; Rats; Thiopental

Other investigators have demonstrated halothane-induced hepatic injury in rats anesthetized in hypoxic environments. The authors examined this phenomenon in mice and investigated plasma fluoride levels in mice and rats anesthetized with halothane in 40, 21 and 7 per cent oxygen with or without pretreatment with phenobarbital or carbon tetrachloride. They found no hepatic necrosis in mice. Mice produced less fluoride than rats. This difference in halothane metabolism between Sprague-Dawley rats and Swiss-Webster mice may explain the failure to observe hepatic necrosis in mice.

Topics: Animals; Biotransformation; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Fluorides; Halothane; Hypoxia; Male; Mice; Oxygen; Phenobarbital; Rats; Species Specificity; Thiopental

Topics: Adolescent; Adult; Anesthesia, General; Carbon Dioxide; Chemoreceptor Cells; Depression, Chemical; Halothane; Humans; Hypoxia; Reflex; Respiration; Thiopental; Tidal Volume

Oxygen uptake fell by 40% in rat adaptation to the periodic action of hypoxia under conditions of pressure chamber. This phenomenon did not disappear in animals in the state of profound anesthesia, and, consequently, was independent of adaptation changes of the cortical regulation of the animal motor activity. A cut of oxygen uptake by half persisted with the action of cold, noradrenaline, and 2,4-dinitrophenol, uncoupling oxidation and phosphorylation, on the organism. Thus, economic expenditure of oxygen in hypoxia adaptation could not be fully explained by increase of oxydation and phosphorylation conjugation.

Topics: Adaptation, Physiological; Anesthesia, General; Animals; Basal Metabolism; Cold Temperature; Dinitrophenols; Female; Hypoxia; Norepinephrine; Oxygen Consumption; Rats; Thiopental

We have assessed the impact of thiopentone on the hypoxic ventilatory reflex, and on the responses to carbon dioxide and doxapram. Thiopentone sedation did not detectably alter any of these aspects of ventilatory control. Thiopentone anaesthesia reduced ventilation and the ventilatory responses to hypoxia, carbon dioxide and doxapram, all approximately in paralle. We conclude that, in contrast to halothane, thiopentone does not selectively reduce the ventilatory response to hypoxia. During light thiopentone anaesthesia, a reasonably brisk hypoxic response is present.

Topics: Adolescent; Adult; Anesthesia; Female; Humans; Hypercapnia; Hypnotics and Sedatives; Hypoxia; Male; Respiration; Thiopental

Investigations during the last two decades have revealed a tendency to inpaired pulmonary gas exchange in patients during general anesthesia. In the awake state, arterial hypoxemia is counteracted by a mechanism which tends to normalize the ventilation/perfusion ratio of the lungs by way of a hypoxia-induced vasoconstriction in poorly ventilated areas. This results in a redistribution of perfusion to more adequately ventilated lung regions. Recent observations suggest, however, that this beneficial mechanism is blunted by some commonly used inhalation anesthetics. In the present study the effect of inhalation anesthetics and injectable anesthetics on the vasoconstrictor response to acute alveolar hypoxia have been compared in isolated blood-perfused rat lungs. The experiments showed that the response was unaffected by N2O and injectable anesthetics, while a reversible, dose-dependent damping effect was demonstrated for the volatile inhalation anesthetics, ether, halothane and methoxyflurance. The effect could be demonstrated at blood concentrations comparable to those used in clinical anesthesia, and it was not due to a general paralysis of the vascular smooth muscle. The findings might, at least in part, explain the occurrence of arterial hypoxemia during general inhalation anesthesia.

Topics: Anesthesia, Inhalation; Anesthesia, Intravenous; Anesthetics; Animals; Diazepam; Dose-Response Relationship, Drug; Droperidol; Ether; Fentanyl; Halothane; Hexobarbital; Hypoxia; Ketamine; Methoxyflurane; Nitrous Oxide; Partial Pressure; Pentazocine; Pentobarbital; Rats; Thiopental; Vasomotor System; Ventilation-Perfusion Ratio

Topics: Adolescent; Adult; Alfaxalone Alfadolone Mixture; Anesthesia, General; Brain Edema; Craniocerebral Trauma; Humans; Hypoxia; Intracranial Pressure; Intubation, Intratracheal; Male; Oxygen; Positive-Pressure Respiration; Postoperative Care; Respiration, Artificial; Thiopental

Under normal conditions the rate of the 32P-orthophosphate incorporation into the polyphosphoinositides was 30--40 times greater than into the other phospholipid fraction of the normal rat liver. There was a rapid postmortem alteration of the polyphosphoinositide content in the liver. Under conditions studied the changes in the phospholipid content were revealed in the polyphosphoinositide fractions only. The changes in the content and in the metabolic intensity of rat polyphosphoinositide in the liver were in many respects similar to those in the brain. Polyphosphoinositide fractions were found to be the most labile of all the phospholipid fractions in the rat liver.

Topics: Amphetamine; Animals; Electric Stimulation; Hypoglycemia; Hypoxia; Liver; Male; Phosphates; Phosphatidylinositols; Rats; Thiopental

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in seven chronically tracheostomized dogs awake and during anesthesia with pentobarbital (30 mg/kg, iv), ketamine, or thiopental (10 and 15 mg/kg, respectively, followed by infusion). Isocapnic hypoxic ventilatory drive (HVD) was expressed as the parameter A such that the higher the A, the greater the hypoxic drive. HVD(A) was significantly reduced from 259 +/- 28 (mean +/- SEM) in awake dogs, to 96 +/- 14 after pentobarbital, 161 +/- 27 after thiopental, and 213 +/- 23 after ketamine. Hypercapnic ventilatory drive (HCVD) as measured by S (slope of the VE-PACO2 response curve) was significantly reduced from 1.3 +/- .32 in awake dogs to 0.4 +/- .13 after pentobarbital, 0.5 +/- .12 after thiopental, and 0.6 +/- .11 after ketamine. In addition, hypercapnia-induced augmentation of hypoxic drive was markedly diminished by the two barbiturates but was unaffected by ketamine. Therefore, ketamine at this dose level afforded greater protection during exposure to hypoxia than did barbiturates. (Key words: Ventilation, hypoxic response; Hypoxia, ventilation; Oxygen, ventilatory response; Carbon dioxide, ventilatory response; Anesthetics, intravenous, ketamine; Anesthetics, intravenous, thiopental; Hypnotics, barbiturates, pentobarbital.)

Topics: Anesthesia, Intravenous; Animals; Carbon Dioxide; Dogs; Female; Hypercapnia; Hypoxia; Ketamine; Male; Oxygen Consumption; Pentobarbital; Respiration; Thiopental

Topics: Anesthesia, Intravenous; Angiotensin II; Animals; Blood; Blood Pressure; Brain; Brain Injuries; Carbon Dioxide; Cardiac Output; Cerebrospinal Fluid; Cerebrovascular Circulation; Dogs; Hemoglobinometry; Hydrogen-Ion Concentration; Hypoxia; Ketamine; Oxygen; Oxygen Consumption; Partial Pressure; Pressure; Regional Blood Flow; Respiration, Artificial; Respiratory Dead Space; Spirometry; Thiopental

Topics: Acid-Base Equilibrium; Anesthesia, General; Anesthesia, Obstetrical; Cesarean Section; Female; Fetal Diseases; Fetus; Humans; Hypoxia; Infant, Newborn; Lactates; Nitrous Oxide; Pregnancy; Pyruvates; Succinylcholine; Thiopental

Topics: Anesthesia, Inhalation; Child; Cyclopropanes; Cystoscopy; Halothane; Humans; Hypoxia; Nitrous Oxide; Oxygen; Thiopental; Ventilators, Mechanical

Topics: Adenosine Triphosphate; Anesthesia, General; Animals; Brain; Cerebral Arteries; Dogs; Electroencephalography; Glucose; Halothane; Hypoxia; Lactates; Oxidative Phosphorylation; Oxygen Consumption; Phosphocreatine; Pyruvates; Thiopental; Vascular Resistance

Topics: Adenosine Triphosphate; Anesthesia, Inhalation; Animals; Arteries; Brain; Dogs; Electroencephalography; Hypotension; Hypoxia; Lactates; Nitrous Oxide; Oxygen; Partial Pressure; Preanesthetic Medication; Shock, Hemorrhagic; Thiopental; Time Factors

Topics: Aminobutyrates; Analgesics; Animals; Barbiturates; Cats; Cerebral Cortex; Drug Synergism; Hexobarbital; Hypoxia; Lethal Dose 50; Mice; Morphine; Piperidines; Rabbits; Rats; Seizures; Thiopental; Thiosemicarbazones; Visual Cortex

Topics: Anesthetics; Animals; Autoradiography; Body Temperature; Depression, Chemical; Ethyl Ethers; Female; Hypoxia; In Vitro Techniques; Leucine; Methohexital; Nitrous Oxide; Pancreas; Pentobarbital; Protein Biosynthesis; Rats; Thiopental; Trichloroethylene; Urethane

Topics: Adult; Aged; Anesthesia; Arteries; Carbon Dioxide; Female; Gastrectomy; Humans; Hypoxia; Male; Middle Aged; Nitrous Oxide; Oxygen; Pentobarbital; Postoperative Complications; Preanesthetic Medication; Pylorus; Scopolamine; Thiopental; Time Factors; Tubocurarine

Topics: Air; Airway Resistance; Anesthesia; Animals; Arteries; Autonomic Nerve Block; Blood Gas Analysis; Blood Pressure; Dogs; Hypoxia; Lung Compliance; Muscle Contraction; Oxygen; Oxygen Inhalation Therapy; Postoperative Complications; Respiration; Respiratory Dead Space; Respiratory Insufficiency; Respiratory Tract Diseases; Thiopental; Tibia; Tubocurarine

Topics: Acid-Base Equilibrium; Acidosis; Adenosine Triphosphate; Adult; Aged; Anesthesia, General; Blood Glucose; Carbohydrate Metabolism; Ethyl Ethers; Female; Glycolysis; Halothane; Humans; Hypoxia; Lactates; Male; Metabolism; Middle Aged; Pyruvates; Shock, Hemorrhagic; Surgical Procedures, Operative; Thiopental

Topics: Anesthesia, Obstetrical; Anesthetics; Cesarean Section; Female; Humans; Hypoxia; Infant, Newborn; Pregnancy; Respiratory Function Tests; Tachycardia; Thiopental

Topics: Animals; Blood Gas Analysis; Carbon Dioxide; Chemoreceptor Cells; Denervation; Electric Stimulation; Femoral Artery; Hypoxia; Male; Manometry; Oxygen; Oxygen Consumption; Partial Pressure; Polarography; Rabbits; Regional Blood Flow; Thalamus; Thiopental

Topics: Animals; Blood Pressure; Body Temperature Regulation; Chloralose; Dogs; Forelimb; Ganglionic Blockers; Hindlimb; Hypotension; Hypoxia; Muscle Contraction; Neural Conduction; Pentobarbital; Pentolinium Tartrate; Perfusion; Phenoxybenzamine; Saphenous Vein; Sympathectomy; Sympathetic Nervous System; Temperature; Thiopental; Veins

Topics: Anesthesia, General; Anesthetics; Animals; Chloroform; Dogs; Ethyl Ethers; Halothane; Hypercapnia; Hypoxia; Methoxyflurane; Statistics as Topic; Thiopental; Trichloroethylene

Topics: Adjuvants, Anesthesia; Adult; Aged; Anesthesia, Endotracheal; Apnea; Carbon Dioxide; Female; Humans; Hypoxia; Injections, Intravenous; Male; Middle Aged; Oxygen; Preanesthetic Medication; Succinylcholine; Thiopental

Topics: Amines; Animals; Bretylium Compounds; Cardiac Glycosides; Epinephrine; Ethanol; Heart Atria; Heart Rate; Hypoxia; In Vitro Techniques; Isoproterenol; Pulse; Rabbits; Reserpine; Thiopental; Tyramine

Topics: Age Factors; Anesthesia, General; Blood Pressure; Body Temperature; Brain; Carbohydrate Metabolism; Carbon Dioxide; Cerebrovascular Circulation; Cyclopropanes; Glucose; Halothane; Humans; Hypoxia; Nitrous Oxide; Oxygen; Oxygen Consumption; Thiopental

Topics: Animals; Brain; Carbon Dioxide; Halothane; Hypoxia; Mice; Thiopental

Topics: Anesthesia; Anesthetics; Animals; Benperidol; Chloroform; Cyclopropanes; Dogs; Epinephrine; Ethers; Ethyl Ethers; Fentanyl; Halothane; Histamine; Hypoxia; Methoxyflurane; Norepinephrine; Respiration; Serotonin; Thiopental; Trichloroethylene

Topics: Anesthetics; Animals; Barbiturates; Brain; Carbon Dioxide; Cerebrovascular Circulation; Halothane; Hypoxia; Mice; Oxygen; Oxygen Consumption; Pregnanediones; Thiopental; Vasodilator Agents

Topics: Abdomen; Adult; Aged; Aminobutyrates; Anesthesia, General; Animals; Arousal; Bemegride; Benzamides; Carbon Dioxide; Central Nervous System Stimulants; Dextroamphetamine; Dogs; Doxapram; Humans; Hydrogen-Ion Concentration; Hypoxia; Methoxyflurane; Methylphenidate; Middle Aged; Nikethamide; Nitrous Oxide; Oxygen; Pentylenetetrazole; Picrotoxin; Thiopental

Topics: Adult; Brain; Central Nervous System Stimulants; Doxapram; Electroencephalography; Epilepsy; Female; Humans; Hydrochloric Acid; Hypertension; Hypoxia; Injections, Intravenous; Male; Middle Aged; Morpholines; Pyrrolidinones; Thiopental

Topics: Atropine; Humans; Hypoxia; Male; Middle Aged; Neostigmine; Polycythemia; Thiopental; Tubocurarine

Topics: Acetylcholine; Animals; Barbiturates; Body Temperature; Cerebral Cortex; Circadian Rhythm; Dogs; Electroconvulsive Therapy; Filariasis; Filarioidea; Humans; Hypoxia; India; Methamphetamine; Oximetry; Oxygen; Physical Exertion; Serotonin; Thiopental; Wuchereria

Topics: Amobarbital; Animals; Barbiturates; Brain; Carbon Dioxide; Hexobarbital; Hypoxia; Mice; Oxygen Consumption; Phenobarbital; Thiopental

Topics: Anesthetics; Animals; Halothane; Hypoxia; Mice; Pharmacology; Pregnanediones; Research; Thiopental; Urethane

Topics: Anesthetics; Chloroform; Cyclopropanes; Ether; Ethers; Halothane; Hypoxia; Methoxyflurane; Mice; Nitrous Oxide; Pharmacology; Research; Thiopental; Trichloroethylene

Topics: Alveolectomy; Anesthesia, Dental; Anesthesia, General; Barbiturates; Blood; Blood Pressure; Electrocardiography; Electroencephalography; Heart Rate; Humans; Hypoxia; Methohexital; Nitrous Oxide; Oxygen; Pulse; Thiopental; Tooth Extraction

Topics: Anesthesia, General; Atropine; Blood Gas Analysis; Carbon Dioxide; Halothane; Humans; Hypoxia; Oximetry; Papaverine; Postoperative Complications; Preanesthetic Medication; Respiratory Insufficiency; Thiopental

Topics: Aged; Dilatation; Electrocardiography; Heart; Humans; Hypoxia; Lidocaine; Phonocardiography; Shock; Shock, Hemorrhagic; Thiopental

Topics: Abortion, Therapeutic; Anesthesia; Anesthesia, Endotracheal; Curare; Female; Genital Neoplasms, Female; Geriatrics; Gynecology; Heart Failure; Humans; Hypoxia; Hysterectomy; Iatrogenic Disease; Mortality; Postoperative Complications; Preanesthetic Medication; Pregnancy; Pregnancy, Tubal; Preoperative Care; Pulmonary Edema; Statistics as Topic; Succinylcholine; Surgical Procedures, Operative; Switzerland; Thiopental; Toxicology

Topics: Anesthesia; Anesthesia, General; Atropine; Blood Gas Analysis; Carbon Dioxide; Carotid Arteries; Cerebral Angiography; Halothane; Humans; Hypoxia; Nitrous Oxide; Oximetry; Papaverine; Pharmacology; Preanesthetic Medication; Scopolamine; Surgical Procedures, Operative; Thiopental

Topics: Cyanides; Hippocampus; Hypoxia; Hypoxia, Brain; Neurons; Nitrogen; Nitrous Oxide; Pathology; Research; Thiopental; Toxicology

Topics: Animals; Asphyxia; Carbon Dioxide; Collapse Therapy; Epinephrine; Ganglia; Ganglia, Spinal; Hyperventilation; Hypoxia; Medulla Oblongata; Nitrogen; Pharmacology; Physiology; Pons; Rabbits; Research; Respiration; Respiration, Artificial; Sympathetic Nervous System; Thiopental; Vagotomy

Topics: Anesthesia; Anesthesiology; Disease Management; Hypoxia; Oxygen; Thiopental

Topics: Barbital; Barbiturates; Hypoxia; Oxygen; Sodium; Thiopental