thiopental and Hypothermia

In this study, we examined the cerebral oxygenation effects of two methods of pharmacologic burst suppression during cardiopulmonary bypass (CPB) in valvular heart surgery patients. Patients were randomly entered into one of three groups: control (n = 13, fentanyl and midazolam), control plus burst suppression doses of thiopental (n = 15), or control plus burst suppression doses of isoflurane (n = 16). Burst suppression (80% suppression) was accomplished in the thiopental and isoflurane groups 15 min before aortic cannulation and was maintained through aortic decannulation. Cerebral physiologic measurements were made during hypothermia (27-28 degrees C) and on rewarming to 36 degrees C. During hypothermia, burst suppression produced significant (P < 0.005) differences with regard to cerebral vascular resistance (P = 0.003), cerebral arterial venous oxygen difference [C(a-v)O2] (P = 0.032), cerebral blood flow (CBF) (P = 0.009), and cerebral oxygen delivery (P = 0.027). There was a similar pattern on rewarming, with groups differing significantly (P < 0.05) with respect to CBF (P = 0.016), cerebral vascular resistance (P = 0.008), oxygen delivery (P = 0.004), C(a-v)O2 (P = 0.043), and cerebral oxygen extraction (P = 0.046). Rewarming rates were similar among groups. There was no difference in neurologic outcome or requirement for inotropic support among groups. The time to awakening was increased (P = 0.0005) in the thiopental group. The thiopental group had lower cerebral oxygen delivery, but not lower cerebral metabolic rate of oxygen consumption, compared with the control group, resulting in widening C(a-v)O2 during CPB. This lack of coupling of oxygen delivery and consumption suggests that pharmacologic neuroprotective mechanisms are complex and involve more than an improvement in the ratio of global cerebral oxygen supply to demand.. This study demonstrates that the balance of cerebral oxygen delivery to consumption during cardiopulmonary bypass is altered differently by thiopental and isoflurane. As others have noted, it seems that cerebral protection is more complex than a simple improvement in the balance of oxygen delivery and consumption.

Topics: Adult; Aged; Brain; Cardiopulmonary Bypass; Cerebrovascular Circulation; Electroencephalography; Female; Heart Valves; Humans; Hypothermia; Isoflurane; Male; Middle Aged; Oxygen Consumption; Thiopental

Under modeling of thiopental coma influence of sodium succinate and (or) external warming for the support of normal body temperature (isothermal regimen) on the gas exchange, blood gas content, acid-base status and survival rate was studied in rats. In the absence of therapy hypothermia was developed (-9.4 degrees C), O(2) consumption decreased by a factor 5, oxygenation of arterial blood (pO(2)) did not change while that of venous blood increased, where with arteriovenous oxygen tension gradient decreased by half. Blood tension of carbon dioxide (pCO(2)) increased twice, respiratory and metabolic acidosis was developed. Survival rate under absence of a therapy was 42%, with isolated use of isothermal regimen or succinate therapy alike-50%; with their use in combination drastically increased up to 92%. Succinate increased arteriovenous gradient of pO(2), decreased deficit of buffer bases, increased bicarbonate concentration. At isothermal regimen accumulation of CO(2) in the blood was diminished, its excretion was increased, pH of blood approached normal values. Combined use of both therapy agents increased O(2) consumption and potentiated their positive influence on acid-base status. The implication is that hypothermia restrains effect of succinate in barbiturate coma; prevention of hypothermia in combination with succinate administration is highly effective method of experimental therapy of barbiturate intoxication.

Topics: Anesthetics, Intravenous; Animals; Blood Gas Analysis; Body Temperature; Carbon Dioxide; Coma; Female; Hypothermia; Lethal Dose 50; Oxygen; Oxygen Consumption; Rats; Succinic Acid; Thiopental; Time Factors

Rats poisoned with one LD50 of thiopental or amytal are shown to increase oxygen consumption when intraperitoneally given sucinate, malate, citrate, alpha-ketoglutarate, dimethylsuccinate or glutamate (the Krebs cycle intermediates or their precursors) but not when given glucose, pyruvate, acetate, benzoate or nicotinate (energy substrates of other metabolic stages etc). Survival was increased with succinate or malate from control groups, which ranged from 30-83% to 87-100%. These effects were unrelated to respiratory depression or hypoxia as judged by little or no effect of succinate on ventilation indices and by the lack of effect of oxygen administration. Body cooling of comatose rats at ambient temperature approximately 19 degrees C became slower with succinate, the rate of cooling correlated well with oxygen consumption decrease. Succinate had no potency to modify oxygen consumption and body temperature in intact rats. A condition for antidote effect of the Krebs intermediate was sufficiently high dosage (5 mmol/kg), further dose increase made no odds. Repeated dosing of succinate had more marked protective effect, than a single one, to oxygen consumption and tended to promote the attenuation of lethal effect of barbiturates. These data suggest that suppression of whole body oxygen consumption with barbiturate overdose could be an important contributor to both body cooling and mortality. Intermediates of Krebs cycle, not only succinate, may have a pronounced therapeutic effect under the proper treatment regimen. Availability of Krebs cycle intermediates may be a limiting factor for the whole body oxygen consumption in barbiturate coma, its role in brain needs further elucidation.

Topics: Amobarbital; Animals; Antidotes; Body Temperature; Citric Acid Cycle; Coma; Female; Hypnotics and Sedatives; Hypothermia; Injections, Intraperitoneal; Oxygen Consumption; Poisoning; Rats; Succinic Acid; Thiobarbiturates; Thiopental

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

Clinical studies have implicated surgery in promoting infections and compromising immune functions, including natural killer cell activity. Animal studies indicate that surgery-induced suppression of natural killer cell activity also promotes tumor metastasis. Hypothermia, a common surgical complication, has been suggested to underlie some of the deleterious consequences of surgery. This study evaluated the effect of hypothermia on the activity and number of blood natural killer cells and on host susceptibility to metastasis. The involvement of adrenergic mechanisms was also considered.. Fischer-344 rats remained awake in their cages (control group) or were anesthetized with 70 mg/kg thiopental and maintained for 2.5 h at core body temperatures of 30-32 degrees C (hypothermia group) or 38 degrees C (normothermia group). Thereafter, at several time points, blood was drawn so natural killer cell activity could be assessed, or rats were injected with syngeneic MADB106 tumor cells that metastasize only to the lungs. Lungs were removed 9 h later for assessment of lung tumor retention, or 4 weeks later for counting of metastases.. Normothermic anesthesia reduced natural killer cell activity (lytic units at 30% specific killing, mean +/- SEM) to 39+/-6.2% of control levels and hypothermia further reduced it to 15+/-6.6%. These changes were not accompanied by alterations in the numbers of circulating natural killer cells. Hypothermia increased tumor retention to 250% of control levels, and the number of metastases increased from 1.1+/-0.4 to 4.7+/-1.2. Normothermia had no significant effects on this index. Nadolol (0.4 mg/kg), a beta-adrenergic antagonist, significantly attenuated the effect of hypothermia on tumor retention.. Hypothermia under thiopental anesthesia suppresses natural killer cell activity and compromises host resistance to metastatic formation, possibly via adrenergic mechanisms. Such suppression may place patients with metastasizing tumors or dormant viral infections at greater risk for complications after intraoperative hypothermia.

Topics: Adrenergic beta-Antagonists; Anesthesia; Anesthetics, Intravenous; Animals; Hypothermia; Killer Cells, Natural; Lung Neoplasms; Male; Rats; Rats, Wistar; Receptors, Adrenergic; Thiopental

The role of body and hindlimb temperature in the control of blood flow in nerve and muscle was assessed by laser Doppler flowmetry. Following surgical exposure of nerve, initial measurements were taken for 5 min at hindlimb temperatures of 30-31 degrees C. A second set of identical measurements was then made either with or without warming to 37 degrees C. Without warming, nerve laser Doppler flow (NLDF) increased by 14.5+/-3.2% (mean+/-SEM) but, with warming, decreased by 40.9+/-8.2%. In contrast, adduccamerontor magnus muscle laser Doppler flow (MLDF) decreased without warming (14.7+/-1.0%) and increased with warming (20.4+/-12.8%). Because blood pressure was not significantly altered by changes in hindlimb temperature, the patterns of changes in vascular conductance (laser Doppler flow/blood pressure) were not significantly different from that seen with NLDF and MLDF. Thus, warming to physiological temperatures was associated with decreased NLDF and vascular conductance and increased MLDF and vascular conductance. These data may have implications for the interpretation of nerve blood flow data obtained at different hindlimb temperatures.

Topics: Adjuvants, Anesthesia; Animals; Body Temperature; Female; Hindlimb; Hypothermia; Laser-Doppler Flowmetry; Muscle, Skeletal; Neural Conduction; Pentobarbital; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Sciatic Nerve; Thiopental

In an earlier study on the effect of mild hypothermia (34 degrees C) on the cerebral metabolic rate for oxygen (CMRO2) in rats, we used norepinephrine (NE) to support arterial blood pressure while inducing isoelectricity on the electroencephalogram (EEG) with thiopental (TP). Even with administration of sufficient TP to reduce a fully active EEG to an isoelectric EEG, CMRO2 was often unchanged. Based on this observation, we hypothesized that NE had activated CMRO2 despite thiopental coma. Therefore, we studied the effect of NE compared with donor blood (DB) infusion to maintain arterial blood pressure during TP-induced isoelectric EEG on whole-brain CBF (H2 clearance) and CMRO2 during normothermia (38 degrees C) and mild hypothermia (34 degrees C) in rats during 70% N2O/30% O2 analgesia. Cerebral blood flow (CBF) and CMRO2 were measured in four groups of rats at 38 degrees C followed by measurements at either 38 degrees C (two groups) or 34 degrees C (two groups) and during TP-induced EEG isoelectricity. Within each of the two groups at 38 degrees C and 34 degrees C, arterial pressure was sustained by either DB (n = 10) or NE (n = 9) infusion. At 38 degrees C, CMRO2 in the DB and NE groups was 7.92 +/- 1.05 and 6.4 +/- 0.80 mL x 100 g-1.min-1 and decreased to 50% of normal (3.95 +/- 0.70 and 3.32 +/- 0.40 mL x 100 g-1.min-1, respectively) during TP isoelectricity for a functional:basal CMRO2 distribution of 50% +/- 4% and 50% +/- 4%. At 34 degrees C, CMRO2 values in the DB and NE groups were 6.31 +/- 1.41 and 5.41 +/- 2.02 mL x 100 g-1.min-1, respectively. During TP-induced isoelectricity, CMRO2 values in both groups were reduced to 2.37 +/- 0.43 and 3.55 +/- 1.27 mL x 100g-1.min-1, respectively, resulting in a functional:basal CMRO2 distribution of 61%:38% in the DB group and the reverse, or 27%:73%, in the Ne group. Basal CMRO2 was significantly (P < 0.05) larger in the NE-infused rats. These results suggest that NE infusion, by increasing CMRO2 during mild hypothermia, could nullify its protective effects in the ischemic brain.

Topics: Adrenergic alpha-Agonists; Analgesics; Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Blood Pressure; Blood Transfusion; Body Temperature; Brain; Brain Ischemia; Cerebrovascular Circulation; Coma; Electroencephalography; Hypothermia; Hypothermia, Induced; Male; Neuroprotective Agents; Nitrous Oxide; Norepinephrine; Oxygen Consumption; Rats; Rats, Wistar; Thiopental

Topics: Animals; Barbiturates; Brain; Brain Ischemia; Coronary Circulation; Cryotherapy; Disease Models, Animal; Evaluation Studies as Topic; Hypothermia; Male; Norepinephrine; Oxygen Consumption; Rats; Rats, Wistar; Thiopental

The purpose of this study was to determine the extent to which localized hypothermia of a monitored extremity alters the assessment of recovery from vecuronium-induced neuromuscular blockade. Bilateral integrated evoked electromyographic (IEMG) responses were measured in the ulner distribution of 14 anaesthetized patients who had differing upper extremity temperatures as measured at the adductor pollicis to determine whether localized hypothermia alters the clinical assessment of spontaneous recovery from vecuronium-induced neuromuscular blockade. All patients received general anaesthesia with thiopentone, N2O/O2 and opioid; 11/14 patients received isoflurane for blood pressure control. Bilateral adductor pollicis, oesophageal and ambient temperatures, and IEMG evoked response (t1) expressed as percent unparalyzed control were recorded during the anaesthetic. The difference in evoked response between the warmer and the colder upper extremity was calculated at 25%, 50% and 75% spontaneous recovery from neuromuscular blockade in the warm extremity. Differences in temperature between extremities ranged from 0.2-11 degrees C. The difference in IEMG-evoked response between extremities was proportional to the difference in temperature, and there was a direct correlation (r = 0.78) between IEMG response and extremity temperature; IEMG response was absent when extremity temperature was less than 25 degrees C. We concluded that localized hypothermia in the monitored extremity decreases the IEMG-evoked response to vecuronium neuromuscular blockade; the greater the temperature decrease, the less the evoked response.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Anesthesia Recovery Period; Anesthesia, General; Arm; Body Temperature; Electromyography; Esophagus; Evoked Potentials; Humans; Hypothermia; Isoflurane; Middle Aged; Muscle, Skeletal; Narcotics; Neuromuscular Junction; Nitrous Oxide; Temperature; Thiopental; Ulnar Nerve; Vecuronium Bromide

Temperature and volatile anesthetic agents influence neuromuscular transmission. Because mild hypothermia is common during general anesthesia, the authors sought to determine the relationship between the core temperature, adductor pollicis muscle temperature, and the twitch response of the adductor pollicis muscle, during isoflurane anesthesia in 15 patients undergoing elective surgery in which muscle relaxants were not required. Five patients were allowed to cool spontaneously, five were cooled actively, and normothermia was maintained actively in the remaining five. In the normothermic patients (core greater than 36.5 degrees C, muscle greater than 35.7 degrees C), the twitch response of the muscle remained unchanged from control values. In the patients who were cooled passively or actively, a muscle temperature threshold was observed (35.2 degrees C), below which twitch response of the muscle diminished by 10-15%/degrees C decrease in muscle temperature. To ensure that the adductor pollicis muscle temperature remained above 35.2 degrees C, the core temperature had to be maintained above 36 degrees C. A significant linear relationship (P less than 0.05) was found between the adductor pollicis muscle temperature and twitch tension below the threshold for each individual patient in the cooled groups (correlation coefficient range, 0.80-0.99). Thus, there is a temperature-related decrease in adductor pollicis twitch response during isoflurane anesthesia, and the temperature of this muscle should be maintained above 35-35.5 degrees C during studies of neuromuscular transmission. This can be achieved by maintaining core temperature above 36 degrees C.

Topics: Anesthesia, Inhalation; Body Temperature; Electric Stimulation; Humans; Hypothermia; Hypothermia, Induced; Isoflurane; Muscle Contraction; Muscles; Nitrous Oxide; Skin Temperature; Thiopental; Thumb; Time Factors

The Portex blood warming coil (200/700/000) and water bath (500/111/010) were tested by comparing the body temperatures of two groups of patients undergoing similar operations, but having transfusions of different rate and quantity. The skin and oesophageal temperatures in the massively transfused patients (5-31 units) did not differ significantly from those having minor transfusions (1-5 units). The temperatures were well maintained in both groups. The lowest mean oesophageal temperatures, during the transfusions, were 35.2 +/- 0.2 in the massively transfused patients and 35.4 +/- 0.1 (SEM) in the control group. The warming capacity of the Portex blood warmer was therefore sufficient for our patients. If, however, transfusion rates, higher than those in this study (maximum 96 ml min-1 during the rapid transfusion phase) are needed, a more effective blood warmer may be beneficial.

Topics: Anesthesia, General; Blood Preservation; Blood Transfusion; Cold Temperature; Enflurane; Fentanyl; Humans; Hypothermia; Nitrous Oxide; Thiopental; Transfusion Reaction

The effect of temperature (37 degrees C, 28 degrees C, and 18 degrees C), 160 mg/kg lidocaine, and 40 mg/kg thiopental on the efflux of cellular potassium in the cerebral cortex during complete global ischemia was examined. Cerebral ischemia was induced in dogs on cardiopulmonary bypass circulation by stopping the pump. Potassium concentration was measured on the brain surface by a valino-mycine-membrane electrode, which in its response corresponded well to an inserted microelectrode. Hypothermia reduced the ischemic potassium efflux rate to about 50 per cent at 28 degrees C, and about 25 per cent at 18 degrees C. At all temperature levels lidocaine caused an additional reduction in the potassium efflux rate of about 50 per cent, probably by reducing membrane ion permeability in accordance with its local anesthetic action. Thiopental had no effect on the potassium efflux during ischemia. This study opens the possibility that lidocaine, like hypothermia, may provide protection of the ischemic brain.

Topics: Animals; Brain; Brain Ischemia; Cardiopulmonary Bypass; Cell Membrane Permeability; Dogs; Hypothermia; Lidocaine; Potassium; Thiopental

The rectal temperature of 15 cats and 18 dogs was recoded during anaesthesia and surgery. There was a mean decrease of 3-4 degrees C in animals weighing less than 10kg and of 1-5 degrees C in animals weighing on average 30-2kg. In four dogs which were protected from accidental hypothermia by the use of a circulating warm water blanket, the mean decrease in rectal temperature was 0-5 degrees C.

Topics: Alfaxalone Alfadolone Mixture; Anesthesia; Anesthesia, Inhalation; Anesthesia, Intravenous; Animals; Body Temperature; Cat Diseases; Cats; Dog Diseases; Dogs; Female; Halothane; Hypothermia; Ketamine; Male; Methoxyflurane; Nitrous Oxide; Rectum; Shivering; Thiopental

Topics: Animals; Dose-Response Relationship, Drug; Drug Synergism; Hypothermia; Mesylates; Mice; Motor Activity; Piperazines; Rats; Sleep; Thiopental; Tranquilizing Agents

Topics: Anesthesia; Blood Transfusion; Brain; Carotid Arteries; Carotid Artery Thrombosis; Electroencephalography; Endarterectomy; Endarterectomy, Carotid; Heart, Artificial; Humans; Hypothermia; Hypothermia, Induced; Mortality; Perfusion; Succinylcholine; Thiopental; Vascular Surgical Procedures

Topics: Acidosis; Blood Gas Analysis; Carbon Dioxide; Cardiac Surgical Procedures; Heart; Heart Septal Defects; Heart Septal Defects, Atrial; Heart, Artificial; Hypercapnia; Hypothermia; Hypothermia, Induced; Metabolism; Preanesthetic Medication; Succinylcholine; Thiopental; Thoracic Surgery

Topics: Adolescent; Cardiac Surgical Procedures; Curare; Humans; Hypothermia; Hypothermia, Induced; Iran; Meperidine; Preanesthetic Medication; Promethazine; Pulmonary Valve Stenosis; Thiopental; Thoracic Surgery

Topics: Anesthesia; Blood Proteins; Blood Viscosity; Cyclopropanes; Equipment and Supplies; Erythrocytes; Halothane; Hematocrit; Heparin; Humans; Hypothermia; Norepinephrine; Pharmacology; Plasma; Thiopental

Topics: Dogs; Erythrocyte Aggregation; Heart; Heart, Artificial; Heparin; Hypothermia; Hypothermia, Induced; Perfusion; Pharmacology; Protamines; Research; Thiopental

Topics: Amitriptyline; Antidepressive Agents; Antipsychotic Agents; Chlorpromazine; Chlorprothixene; Hypothermia; Hypothermia, Induced; Imipramine; Mice; Research; Reserpine; Thiopental

Topics: Anesthesia; Anesthesia, Inhalation; Atmosphere; Bis-Trimethylammonium Compounds; Blood Flow Velocity; Blood Gas Analysis; Cerebral Infarction; Cerebrovascular Circulation; Cerebrovascular Disorders; Dogs; Halothane; Hyperbaric Oxygenation; Hypothermia; Hypothermia, Induced; Infarction; Neurosurgery; Oxygen; Research; Thiopental

Topics: Body Temperature; Dogs; Electrocardiography; Epinephrine; Hot Temperature; Hypothermia; Hypothermia, Induced; Isoproterenol; Metabolism; Norepinephrine; Pharmacology; Research; Sympathomimetics; Thiopental; Tubocurarine

Topics: Acetylcholine; Aminobutyrates; Amphetamine; Amphetamines; Atropine; Chlordiazepoxide; Chlorpromazine; Cocaine; Convulsive Therapy; Electroconvulsive Therapy; Fever; Hexobarbital; Histamine; Hypothermia; Hypothermia, Induced; Lidocaine; Lobeline; Morphine; Papaverine; Phenobarbital; Promethazine; Thiopental

Topics: Blood Vessels; Heart; Humans; Hypothermia; Thiopental

Topics: Animals; Body Temperature; Electroencephalography; Electrophysiologic Techniques, Cardiac; Hypothermia; Ice; Rats; Thiobarbiturates; Thiopental