Positive experimental demonstration of the negative brain "protective" effects of anesthetics following cardiac arrest.

The cerebral metabolic effects of a massive dose of thiopental (177 mg/kg) were investigated in seven dogs. The systemic circulation was supported with an extracorporeal circuit. At an infusion rate of 2 mg/kg/min, cerebral oxygen consumption (CMR(O(2))) decreased progressively until cerebral electrical silence was produced.

Cerebral blood flow during cardiac operations: comparison of Kety-Schmidt and xenon-133 clearance methods.

This study simultaneously compared the standard Kety-Schmidt and the modified xenon-133 (133Xe) clearance techniques for measuring cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) during cardiac operations. The validity of the CBF method is important because our management of the patient during cardiopulmonary bypass (CPB) is based, in part, on our understanding of the cerebral hemodynamics during CPB. In 20 patients undergoing coronary artery bypass grafting, CBF and CMRO2 were determined by both methods.

Cerebral vascular autoregulation and CO2 reactivity following onset of the delayed postischemic hypoperfusion state in dogs.

A small number of animal studies have suggested that during the delayed postischemic hypoperfusion state, CO2 reactivity of the cerebral vasculature is lost whereas autoregulation is retained. These findings, however, are inconsistent with the bulk of experimental evidence which demonstrates that CO2 reactivity is more robust and may be retained in pathologic circumstances which abolish autoregulation. These opposing viewpoints were therefore further evaluated in 18 dogs in which complete global ischemia was induced by cerebrospinal fluid (CSF) compression for periods of 12 (n = 12) and 18 (n = 6) min.

The effect of profound levels of hypothermia (below 14 degrees C) on canine cerebral metabolism.

The goal of this study was to determine the temperature coefficient (Q10) for canine CMRO2 at temperatures below 14 degrees C. Eight dogs were anesthetized with halothane for surgical preparation. The animals were placed on total cardiopulmonary bypass and CBF was measured by direct sagittal sinus outflow.

Detection and hemodynamic consequences of venous air embolism. Does nitrous oxide make a difference?

Volume expansion of intravascular air by nitrous oxide (N2O) may improve the sensitivity of monitors used to detect venous air embolism (VAE) and/or exacerbate hemodynamic changes following VAE. The purpose of this study was to determine if the administration of N2O alters the sensitivity (i.e.

Ischemia-reperfusion does not affect reactivity of isolated canine basilar artery.

The effect of ischemia-reperfusion on endothelium-dependent relaxations and reactivity of vascular smooth-muscle cells was studied in rings of basilar arteries obtained from six dogs exposed to 12 min of complete global cerebral ischemia followed by 100 min of reperfusion. Three sham-operated control dogs served as controls. Ischemia was induced either by an increase in intracranial pressure or by aortic occlusion.

The relationship among canine brain temperature, metabolism, and function during hypothermia.

Cerebral protection by hypothermia is commonly attributed to cerebral metabolic suppression. However, at temperatures below 28 degrees C, the relationship of temperature to cerebral metabolic rate of oxygen consumption (CMRO2) has not been well characterized. Accordingly, the relationship between brain temperature and CMRO2 was determined in eight dogs during cooling from 37 to 14 degrees C while the EEG was continuously monitored.

Postischemic canine cerebral blood flow is coupled to cerebral metabolic rate.

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO2 was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion.

Pretreatment with U74006F improves neurologic outcome following complete cerebral ischemia in dogs.

We examined the 21-aminosteroid U74006F, a potent inhibitor of lipid peroxidation, for potential neuroprotective effects in a canine model of complete cerebral ischemia. Two 1.5-mg/kg boluses were administered to six dogs, the first bolus 15 minutes prior to a 12-minute episode of complete cerebral ischemia and the second bolus after 11 minutes of ischemia, 1 minute prior to reperfusion.

Influence of intraoperative antibiotic choice on the incidence of early postcraniotomy seizures.

Because of a suspicion that intraoperative penicillin antibiotics might be causing early postoperative seizures in craniotomy patients, a deliberate effort was initiated in 1987 to avoid these agents in favor of nonpenicillin antibiotics. This permitted a retrospective comparison of the incidence of early postoperative seizures in craniotomy patients who did and who did not receive intraoperative penicillins. Records of patients treated between July 1, 1984, and July 1, 1985, and between July 1, 1987, and July 1, 1988, were reviewed, for a total of 1316 procedures.

The effects of dizocilpine maleate (MK-801), an antagonist of the N-methyl-D-aspartate receptor, on neurologic recovery and histopathology following complete cerebral ischemia in primates.

The present study was designed to determine if the noncompetitive excitatory amino acid antagonist, dizocilpine maleate, when administered after a 17 min period of complete cerebral ischemia in primates, would improve postischemic neurologic function and hippocampal histopathologic outcome when compared to placebo-treated animals. Ten pigtail monkeys were anesthetized and subjected to complete cerebral ischemia using an established neck tourniquet model. Five minutes postischemia, five monkeys received dizocilpine 300 micrograms/kg i.

Postischemic canine cerebral blood flow appears to be determined by cerebral metabolic needs.

Following a period of complete global cerebral ischemia and reperfusion there ensues a low flow state referred to as the delayed postischemic hypoperfusion state. It is unknown whether this low flow state contributes to neuronal injury or whether the magnitude of hypoperfusion correlates with the duration of ischemia. The latter question was addressed in 20 dogs in which complete global ischemia was induced by cerebrospinal fluid (CSF) compression for periods of 3, 9, 12, or 18 min.

The effect of the excitatory amino acid receptor antagonist dizocilipine maleate (MK-801) on hemispheric cerebral blood flow and metabolism in dogs: modification by prior complete cerebral ischemia.

The effect of the N-methyl-D-aspartate (NMDA) receptor antagonist dizociplipine maleate (MK-801) on cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), intracranial pressure and systemic variables was examined in 6 normal dogs (Group I). In 6 additional dogs (Group II), the effects of a prior 11 min episode of complete cerebral ischemia on the response to dizocilipine was studied. CBF was measured with a sagittal sinus outflow technique and CMRO2 was calculated as the product of CBF and the arterial to sagittal sinus O2 content difference.

Parameters affecting occurrence of paradoxical air embolism.

The effects of different patterns of ventilation and intravascular volume infusion on the occurrence of paradoxical air embolism (PAE) were evaluated in 15 pigs with a surgically created atrial septal defect (ASD). A balloon atrial septostomy was created transvenously in anesthetized pigs (mean diameter 8.6 mm +/- 1 mm).

Rates of lactate appearance and disappearance and brain lactate balance after oral glucose in the dog.

After glucose ingestion, arterial lactate concentrations increase. Although it is presumed that this is due to an increase in lactate production, rates of lactate appearance have not been measured after oral glucose nor has the major site of its production been identified. Since brain takes up a substantial portion of an oral glucose load but does not store appreciable amounts of glucose, it is possible that brain could be an important site for postprandial lactate formation.

Evaluation of the glutamate antagonist dizocilipine maleate (MK-801) on neurologic outcome in a canine model of complete cerebral ischemia: correlation with hippocampal histopathology.

This study was designed to determine if dizocilipine maleate (MK-801), administered following 11 min of complete ischemia in dogs, could favorably alter neurologic outcome and hippocampal damage. Eighteen dogs were anesthetized and subjected to complete cerebral ischemia by temporary occlusion of the ascending aorta and the venae cavae via a thoracotomy. Five min postischemia, 9 dogs were given dizocilipine 150 micrograms/kg, followed by an infusion of 1.

Comparison of the effects of isoflurane and thiopental on neurologic outcome and neuropathology after temporary focal cerebral ischemia in primates.

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.

The interaction of sodium nitroprusside, hypotension, and isoflurane in determining cerebral vasculature effects.

Eighteen mongrel dogs were anesthetized with isoflurane and prepared for determining cerebral blood flow (CBF, sagittal sinus outflow), cerebral metabolic rate (CMRO2), and ICP. Dogs were divided into three groups of six each. Group 1 dogs were maintained on 1 MAC isoflurane and, following control measurements (step 1), sodium nitroprusside (SNP) was infused to decrease mean arterial pressure (MAP) to 60 mmHg (step 2).