Cerebral effects of extended hyperventilation in unanesthetized goats

Abstract

Thirty-six adult, male unanesthetized goats were hyperventilated to a Pacoj level of 16-18 nun Hg for 6 hours. Arterial and sagittal sinus blood and cerebrospinal fluid were analyzed for pH, blood gases, bicarbonate, lactate, and pymvate before hyperventilation, during hyperventilation, and after the termination of hyperventilation. Total cerebral blood flow, regional brain blood flows, and cerebral metabolic rate for oxygen were calculated from the distribution of radioactive microspheres. Intracranial pressure was measured in either the right or left cerebral ventricle. With the initiation of hyperventilation, cerebral blood flow and cerebral metabolic rate for oxygen fell significantly (64 ± 5 ml/100 g/min to 41 ± 3; 4.6 ± 0.3 ml O2/100g/min to 3.6 ± 0.2), but both returned to prehyperventilation values within 6 hours of hyperventilation. With termination of hyperventilation, cerebral blood flow and cerebral metabolic rate for oxygen increased significantly above control levels (64 ± 5 vs. 105 ± 9; 4.6 ± 0.3 vs. 5.4 ± 0.4). Intracranial pressure was unaffected by hyperventilation or its termination. Arterial and sagittal sinus blood and cerebrospinal fluid pH increased with hyperventilation but returned to control values by 6 hours. However, pH was still significantly elevated at 6 hours. Lactate and pyruvate followed a similar pattern except in the cerebrospinal fluid, where both increased throughout the course of hyperventilation. There were no significant differences in the lactate: pyruvate ratio. On termination of hyperventilation, pH of the arterial and sagittal sinus blood and cerebrospinal fluid fell below control levels. Bicarbonate values decreased in all fluid compartments and were still below control values 2 hours after the cessation of hyper ventilat ion. Blood flows to the cerebral cortex, thalamus, hypothalamus, medulla, and cerebellum fell significantly with hyperventilation and, with the exception of the thalamus, all recovered during hyperventilation. On termination of hyperventilation, blood flows to the cortex, thalamus, medulla, and cerebellum increased significantly above control values. Only the brainstem (except the medulla) appeared unresponsive to hyperventilation. Hyperventilation had little effect on mean arterial blood pressure and heart rate. However, hyperventilation did cause a 20% reduction in cardiac output, which gradually recovered throughout the course of hyperventilation. On termination of hyperventilation, cardiac output rebounded above control values by approximately 20% and remained elevated 2 hours after hyperventilation. The results of this study indicate that in unanesthetized goats cerebral blood flow adapts to the imposition of hyperventilation and returns to normal despite continued hyperventilation. Although cerebrospinal fluid lactate levels increased, there was no evidence of cerebral hypoxia since pyruvate showed a proportionate increase. © 1987 American Heart Association, Inc.