thiopental and Ischemic-Attack--Transient

This review has indicated that barbiturates are useful in controlling ICP during anaesthesia in patients with intracranial hypertension. While laboratory data indicate that intraoperative administration of barbiturates during episodes of transient cerebral ischaemia, associated with surgical revascularization procedures, should be efficacious, current intraoperative results claiming benefit are anecdotal. Continuous high-dose barbiturate therapy (induced barbiturate coma) for occlusive stroke and persistently increased intracranial pressure is currently undergoing clinical trials. While it is clear that this therapy can often reduce increased ICP in head injured patients, its influence on neurological outcome remains to be determined by a multicentre trial at present in progress. Despite evidence that high-dose barbiturate therapy can reduce the area of infarction in occlusive stroke in the laboratory, organized clinical trials have not yet commenced. Until more definitive knowledge is available concerning the influence of high-dose barbiturate therapy in treating different forms of cerebral ischaemia, its application should be viewed sceptically and limited to centres willing to create an organized data base for inter-institutional evaluation of this form of treatment. If barbiturate therapy proves successful and the mechanisms involved are better understood, drugs with fewer side-effects and risks may become available to combat cerebral ischaemia.

Topics: Animals; Barbiturates; Brain Ischemia; Cerebral Revascularization; Craniocerebral Trauma; Critical Care; Electroencephalography; Humans; Intracranial Pressure; Intraoperative Period; Ischemic Attack, Transient; Monitoring, Physiologic; Oxygen; Thiopental

Topics: Animals; Barbiturates; Brain; Brain Edema; Brain Ischemia; Cerebrovascular Circulation; Dogs; Humans; Hypertension; Hypoxia, Brain; Intracranial Pressure; Ischemic Attack, Transient; Phenobarbital; Thiopental

Evidence suggests that early postischemic hyperemia is mediated by both neurological and vascular mechanisms. We hypothesized that if neuronal activity were primarily responsible for reperfusion hyperemia, then electrocerebral silence induced by intracarotid anesthetics (propofol and pentothal) would attenuate the hyperemic response. New Zealand white rabbits were subjected to 10 min of cerebral ischemia using bilateral carotid occlusion and systemic hypotension. Subsequently, carotid occlusion was released, and the mean arterial blood pressure was increased to baseline values. In the control group, intracarotid saline was periodically injected during reperfusion. In the treatment groups, intracarotid propofol or thiopental was administered to maintain electrocerebral silence for 10 min. Physiological data were measured at baseline, during ischemia, and at reperfusion. Satisfactory data were available for 16 of 19 rabbits. Mean arterial blood pressure, end-tidal CO(2), and cerebral blood flows decreased significantly in both groups during carotid occlusion. During early reperfusion, a similar percent increase in cerebral blood flow from baseline values was observed in all 3 groups (192% +/- 76%, 218% +/- 84%, and 185% +/- 101% for saline, propofol, and pentothal, respectively). These results suggest that suppression of neuronal activity during reperfusion does not affect early hyperemia after transient cerebral ischemia.. Intracarotid injection of anesthetic drugs in doses that are sufficient to produce electrocerebral silence do not obtund early cerebral hyperemia after transient cerebral ischemia. This suggests that vascular, not neuronal mechanisms, are primarily responsible for early postischemic cerebral hyperperfusion.

Topics: Anesthetics, Intravenous; Animals; Brain; Carotid Artery, Internal; Cerebrovascular Circulation; Electroencephalography; Hemodynamics; Hyperemia; Ischemic Attack, Transient; Propofol; Rabbits; Reperfusion Injury; Thiopental

Intraoperative monitoring of brain function may influence the outcome of carotid endarterectomy (CEA).. We performed transcranial Doppler (TCD) monitoring of middle cerebral artery blood flow velocities (VMCAs) and eight-channel electroencephalographic (EEG) recording simultaneously in 82 patients undergoing CEA. Thiopental narcosis limited EEG interpretation in 11 patients, thus allowing direct comparison of both methods in 71 patients.. There was a significant correlation between VMCA decrease and the frequency of EEG changes after carotid clamping (P < .001). Eight patients (11%) showed a VMCA decrease exceeding 60%, accompanied by EEG changes in 7 patients. Altogether, 16 patients (22%) showed severe or moderate EEG changes. Stenosis or occlusion of the contralateral carotid artery led to an increase of abnormal findings with both monitoring methods, which was, however, significant only for TCD (P < .05). Four patients (4.8%) suffered intraoperative transient ischemic attacks. In 3 of these patients, there were no abnormal findings with either of the methods. The events were thus unpredictable and probably of embolic origin. The fourth patient showed VMCA decrease to 0 and severe EEG changes. Nine patients had severe or moderate EEG changes without significant VMCA decrease and without complications. EEG monitoring alone in these would have led to unnecessary use of a shunt with the increased risk of embolism.. EEG and TCD monitoring are complementary techniques. Their results showed a good overall correlation but with marked differences in the individual patient. TCD monitoring alone was sensitive enough to prevent ischemic intraoperative complications. EEG findings are of limited value when barbiturates are used.

Topics: Aged; Aged, 80 and over; Blood Flow Velocity; Brain Ischemia; Carotid Stenosis; Cerebral Arteries; Cerebrovascular Circulation; Cerebrovascular Disorders; Electroencephalography; Endarterectomy, Carotid; Female; Humans; Hypnotics and Sedatives; Ischemic Attack, Transient; Male; Middle Aged; Monitoring, Intraoperative; Postoperative Complications; Predictive Value of Tests; Retrospective Studies; Thiopental; Treatment Outcome; Ultrasonography, Doppler, Transcranial

The mechanism by which barbiturates protect neurons against ischemia is unclear, particularly when they are given after ischemia or reperfusion begins. Because an excess release of excitatory neurotransmitters causes postsynaptic membrane depolarization, which triggers neuronal damage in ischemia, the effects of thiopental on histologic outcome, ischemia-induced amino acid release, and anoxic depolarization in gerbils were studied.. The effects of different doses of thiopental administered before or after ischemia were examined morphologically by assessing delayed neuronal death in hippocampal CA1 pyramidal cells produced by forebrain ischemia for 3 min in gerbils. The ischemia-induced changes in output of aspartate, glutamate, glycine, taurine, and gamma-aminobutyric acid were measured using a microdialysis-high-performance liquid chromatography procedure, and the differences among a halothane-anesthetized group, a thiopental-administered group, and a group given thiopental after a period of ischemia were evaluated. The changes induced in the direct-current potential in the hippocampal CA1 area by forebrain ischemia were compared in animals anesthetized with halothane and those given thiopental.. Preischemic administration of thiopental at all doses decreased the risks for delayed neuronal death (P < 0.01). Post-ischemic administration at a dosage of 2 mg.kg-1.min-1 for 60 min protected neurons, but the same dose for 10 min did not ameliorate the cell injury. Forebrain ischemia produced marked increases in all amino acids 3 to 6 min after the start of recirculation in the halothane-anesthetized gerbils, whereas thiopental anesthesia (2 mg.kg-1.min-1) reduced these increases throughout the experimental period, except for glycine (P < 0.01). The initiation of thiopental after reflow did not markedly diminish these increases. Thiopental anesthesia prolonged the onset of anoxic depolarization and reduced its maximal amplitude.. Thiopental helps protect the brain from ischemia, although treatment with this agent after ischemia requires a larger dose than that before ischemia. The effect of preischemic treatment may be related to the suppression of the excitatory amino acid release and the direct-current potential shift.

Topics: Animals; Brain; Chromatography, High Pressure Liquid; Dose-Response Relationship, Drug; Excitatory Amino Acids; Gerbillinae; Hemodynamics; Injections, Intravenous; Ischemic Attack, Transient; Male; Thiopental

Topics: Adult; Anesthesia, Intravenous; Anesthetics, Intravenous; Cerebral Hemorrhage; Child; Craniotomy; Fentanyl; Humans; Ischemic Attack, Transient; Male; Moyamoya Disease; Subarachnoid Hemorrhage; Thiopental

A possible cerebroprotective effect of halothane was investigated in a canine model of 5-min global cerebral ischemia. In pentobarbital-anesthetized dogs, additional inhalation of 0.5 to 1% halothane prior to ischemia prevented the post-ischemic dysfunction of the vagal component of reflex bradycardia. In contrast, pretreatment with thiopental at 10 mg/kg, i.v. failed to prevent it. The influence of ischemia in the absence of anesthetics was similar to that under barbiturate anesthesia. The results suggest that halothane, but not barbiturate, may actively protect the vagal baroreflex system from ischemia.

Topics: Administration, Inhalation; Animals; Blood Pressure; Disease Models, Animal; Dogs; Electroencephalography; Female; Halothane; Heart Rate; Ischemic Attack, Transient; Male; Pressoreceptors; Reflex; Thiopental; Vagus Nerve

Influence of drugs on the cessation time of the brain electrical activity (resistance time) during total cerebral ischaemia evoked by clamping of the aorta for 50 sec; on the duration of its reappearance during reperfusion (restitution time) and on the background activity of EEG were studied. The experiments were carried out in 7 groups. Each group contained 5 animals. Nine clampings with intermittent reperfusion periods of 10 min were performed in each animal. One group served as control. In the remaining ones after the first three clampings the animals were given Glyo-6, Nootropil, Verpamil, Epanutin, Inactin or Lidocain. The resistance and restitution times measured in the control group as well as the reproductibility of the power spectrum values of the EEG provided evidence for the stability of the model. Glyo-6 in a dose of 10 mg/kg, Nootropil in a dose of 100 mg/kg or Verpamil in a dose of 0.125 mg/kg did not alter the above-mentioned parameters. As an effect of the administration of Epanutin in a dose of 10 mg/kg, the resistance time increased slightly, whereas restitution time decreased significantly. Administration of Inactin in a dose of 15 mg/kg, or Lidocain in a dose of 100 mg/kg increased considerably resistance time for a period of about one hour. The results indicate that in the initial phase of ischaemic brain damage both the cessation of EEG activity and the restitution during reperfusion after short-term occlusion of the circulation can be influenced favourable with drugs which decrease cerebral metabolism, inhibit synaptic transmission and have membrane stabilizing effect.

Topics: Animals; Dogs; Electroencephalography; Ischemic Attack, Transient; Lidocaine; Phenytoin; Piracetam; Pyridoxine; Thiopental; Verapamil

In an attempt to determine whether one anesthetic might be clearly advantageous over another in clinical situations of temporary focal ischemia, isoflurane or thiopental (in concentrations producing equal suppression of cerebral function as measured by the electroencephalogram) were studied for their effects on neurologic outcome and cerebral infarct size in pigtailed monkeys exposed to temporary focal ischemia produced by 5 h of middle cerebral artery occlusion (MCAo). Burst suppression was produced for 15 min before MCAo and maintained throughout the ischemic period by 2.18 +/- 0.11% (mean +/- SE) end-expired isoflurane or 135 +/- 18 mg.kg-1 thiopental. Mean arterial pressure was supported with phenylephrine and maintained at approximately 90 mmHg in both groups throughout the ischemic period. At the end of the ischemic period, the isoflurane or thiopental was discontinued, allowing the animals to awaken. Intensive care was provided as needed. Neurologic function was scored for 8 days at the end of which surviving animals were killed and the brains were fixed in formalin and then examined for infarct size. There was no significant difference in final neurologic outcome between the animals receiving isoflurane and those receiving thiopental as determined by the Mann-Whitney rank sum test. Neurologic deficit scores ranged from normal (one of eight in the group receiving isoflurane and three of nine in the group receiving thiopental) to death resulting from brain injury (three in the isoflurane group and five in the thiopental-treated group). There also was no significant difference in infarct size between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Gas Analysis; Blood Glucose; Blood Pressure; Brain; Cerebral Infarction; Electroencephalography; Female; Ischemic Attack, Transient; Isoflurane; Male; Pilot Projects; Thiopental

Topics: Animals; Drug Interactions; Hypertension; Ischemic Attack, Transient; Isoflurane; Papio; Phenylephrine; Thiopental

Isoflurane has protective properties during experimental global brain ischemia or hypoxia. However, this has not been evaluated in the more common case of focal ischemia, e.g., as caused by middle cerebral artery occlusion (MCAO). The authors therefore compared the effects of isoflurane, thiopental, and N2O/fentanyl anesthesia on neurologic and neuropathologic outcome in baboons subjected to 6 h of transorbital left MCAO. Prior to MCAO, animals were assigned to one of three groups: Group 1 (n = 7) received isoflurane (in O2/air) in concentrations sufficient to maintain deep burst suppression on the EEG (2.0% +/- 0.5% inspired, mean +/- SD); group 2 (n = 6) received thiopental (O2/air) in doses adequate to maintain similar EEG suppression (3.6 +/- 0.7 g total); and group 3 (n = 6) received 60% N2O/40% O2 and fentanyl (25 micrograms/kg load, 3 micrograms X kg-1 X h-1 infusion). Efforts were made to keep mean arterial pressure (MABP) between approximately 80 and 100 mmHg, using nitroprusside/hydralazine or phenylephrine/metaraminol, with PaCO2 at approximately 30 mmHg. The selected anesthetic was established 45 min before MCAO, was maintained until 1 h after clip removal, and in decreasing concentrations for 5 h. Neurologic status was scored for 7 days and formalin-fixed brains were later sectioned for determination of infarction volume. Six of seven group 1 (isoflurane) animals were hemiplegic, and 7/7 had verified infarctions. By contrast, 4 of 6 group 2 (thiopental) animals were normal, with 2/6 having infarctions. Outcome in group 3 (N2O/fentanyl) was intermediate between groups 1 and 2 (3/6 hemiplegic, 4/6 with infarctions). Differences in the infarction rates between groups 1 and 2 was significant (P less than 0.05), while a similar comparison of neurologic outcome scores achieved a P value of 0.055. Infarctions in group 1 were more hemorrhagic in character than in group 3 (groups 1 and 2 could not be meaningfully compared). These results must be considered in light of differences in MABP during the occlusion period; MABP in group 1 was approximately 80 mm Hg in spite of vasopressor use, while that in group 2 was approximately 100 mmHg (in spite of vasodilators). Nevertheless, they fail to demonstrate any protective value of isoflurane anesthesia, at least when compared with thiopental.

Topics: Anesthesia, Inhalation; Animals; Blood Pressure; Electroencephalography; Evoked Potentials, Somatosensory; Fentanyl; Hemodynamics; Ischemic Attack, Transient; Isoflurane; Male; Nitroprusside; Papio; Phenylephrine; Thiopental

Barbiturate coma is still recommended for brain protection during periods of temporary focal ischaemia such as during carotid endarterectomy. We tested the hypothesis that a single dose of barbiturate given before a period of protracted severe focal ischaemia would protect against focal cerebral infarction. Sixteen cats had the proximal left middle cerebral artery (MCA) occluded. Eight cats received halothane alone titrated to keep their pulse and blood pressure within the normal range. Eight cats received, in addition to halothane, a bolus of thiopentone sufficient to produce an isoelectric EEG immediately prior to MCA occlusion. Six hours after the occlusions the animals were sacrificed and the brains scored histologically to assess both size and severity of ischaemia. There was no statistically significant difference in the size or severity of the infarcts between the groups. We conclude from this study that the extent of the histological injury was not reduced by a single prophylactic bolus of thiopentone given before prolonged focal cerebral ischaemia.

Topics: Animals; Brain; Cats; Cerebral Infarction; Drug Therapy, Combination; Electroencephalography; Halothane; Hemodynamics; Ischemic Attack, Transient; Thiopental

Topics: Anesthesia; Anesthesia, Inhalation; Cerebral Revascularization; Humans; Ischemic Attack, Transient; Isoflurane; Lidocaine; Male; Middle Aged; Nitrous Oxide; Oxygen; Pancuronium; Postoperative Complications; Thiopental

A review of 45 cerebral vasospasm cases for cerebral infarct under computer tomography (CT) scanner and based on activities of daily living (ADL) resulted in the finding that, of 19 cases with vasospasm of "diffuse, severe" grade, 14 cases were rated "poor (disabled)" to "dead": CT-diagnosed cerebral infarct was found in 4 out of 6 cases. From this, it was believed that indication for B-therapy was clinically significant vasospasm (diffuse, severe), which falls under the clinical grade of III or IV by Hunt and Kosnik without considering such incidental condition as severe vasospasm. After B-therapy, 45% showed ADL of at least "fair". CT-diagnosed cerebral infarct was found in 4 out of 10 cases. None died from complications as a result of B-therapy. The examination of ineffectual cases pointed to the importance of the first choice application of B-therapy, the continuation of the therapy as long as vasospasm continues, and the sustenance of cerebral perfusion pressure by the use of vasopressor (Dopamine) to offset the hypotensive effect of barbiturate. With these points of care exercised, the B-therapy is believed to achieve good results.

Topics: Adult; Aged; Anesthesia, Endotracheal; Cerebral Infarction; Dopamine; Drug Therapy, Combination; Female; Humans; Hypotension; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle Aged; Thiopental

Three patients awoke in the operating theater with a neurologic deficit after carotid endarterectomy with shunt under general anesthesia with either upper or lower extremity paralysis or both and evidence of a patent carotid artery confirmed by Doppler ultrasonography, B-mode real-time ultrasonography, or surgery. After confirmation of patency of the carotid artery, patients were anesthetized with thiopental (3 to 4 mg/kg) for 48 hours, with respiratory maintenance by ventilator. The therapeutic effect of barbiturates was monitored by prevention of spontaneous respiration without hypotension. All patients awoke approximately 36 to 48 hours after discontinuing the thiopental without the previously noted postoperative neurologic deficit or any adverse neurologic sequelae. At last follow-up more than 1 year postoperatively they were asymptomatic. Results of this study indicate that patients who undergo carotid endarterectomy and awake with a neurologic deficit and a patent operated vessel should be considered for barbiturate induced coma as a therapeutic modality.

Topics: Aged; Carotid Arteries; Cerebrovascular Disorders; Endarterectomy; Female; Follow-Up Studies; Humans; Ischemic Attack, Transient; Male; Middle Aged; Postoperative Complications; Thiopental; Time Factors

Carotid endarterectomy was performed 28 times in 27 patients. All but one patient had symptomatic carotid artery disease, 59% had bilateral disease and 59% had associated intracranial disease. Barbiturate therapy was used as a means of cerebral protection during carotid artery cross-clamping. Neurological deficit occurred in two patients, being permanent in one patient (3.5%); both patients had bilateral carotid and intracranial disease and both had carotid stump pressures greater than 55 mmHg. No morbidity could be attributed to barbiturate usage.

Topics: Adult; Aged; Anticoagulants; Blood Pressure; Brain Diseases; Carotid Arteries; Carotid Artery Diseases; Cerebrovascular Disorders; Constriction; Endarterectomy; Female; Humans; Intraoperative Complications; Ischemic Attack, Transient; Male; Middle Aged; Postoperative Complications; Risk; Thiopental

It has been shown experimentally that irreversible brain injury and death may follow after 5-7 min of cerebral ischemia and that even brief periods, 2 min or less, can produce focal damage to the nervous system. All published studies demonstrating a protective effect of barbiturates have been performed in animals. A patient is presented who recovered full neurological function after 13 min of hypovolemic hypotension. This remarkable outcome may have been due to the rapid institution of high-dose barbiturate therapy. The extent to which such therapy affected his outcome is unclear, but does add to the growing body of evidence suggesting a favorable effect from this type of barbiturate therapy.

Topics: Brain Damage, Chronic; Coronary Artery Bypass; Heart-Lung Machine; Humans; Intraoperative Complications; Ischemic Attack, Transient; Male; Middle Aged; Shock; Thiopental

Topics: Brain; Humans; Hypothermia, Induced; Intracranial Aneurysm; Ischemic Attack, Transient; Pentobarbital; Retrospective Studies; Thiopental

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.

Topics: Animals; Blood Gas Analysis; Brain Chemistry; Cerebral Cortex; Female; Hematocrit; Hydrogen-Ion Concentration; Hypoxia, Brain; Ischemic Attack, Transient; Oxygen; Oxygen Consumption; Rats; Thiopental

Topics: Aged; Barbiturates; Carotid Arteries; Electroencephalography; Endarterectomy; Humans; Ischemic Attack, Transient; Male; Thiopental

Topics: Anesthesia, Intravenous; Animals; Brain; Disease Models, Animal; Female; Haplorhini; Hypoxia, Brain; Ischemic Attack, Transient; Macaca mulatta; Thiopental; Time Factors

Topics: Animals; Barbiturates; Brain; Dogs; Haplorhini; Humans; Ischemic Attack, Transient; Monitoring, Physiologic; Oxygen Consumption; Partial Pressure; Resuscitation; Thiopental

Topics: Blood Gas Analysis; Brain Ischemia; Carbon Dioxide; Cats; Cerebral Angiography; Cerebral Infarction; Ethanol; Ischemic Attack, Transient; Mannitol; Oxygen; Pentobarbital; Pharmacology; Research; Thiopental; Trypan Blue; Urea

Topics: Animals; Brain; Brain Ischemia; Cerebral Infarction; Cyanides; Guinea Pigs; Histological Techniques; Hypoxia, Brain; Ischemic Attack, Transient; Nitrogen; Nitrous Oxide; Pathology; Research; Thiopental; Toxicology