OBJECTIVE: To study the cerebral metabolism and its relationship to cerebral blood flow (CBF) acutely after subarachnoid hemorrhage (SAH). METHODS: SAH was induced in rats by endovascular perforation of the internal carotid artery, blood injection into the prechiasmatic cistern or the cisterna magna. CBF (measured by laser Doppler flowmetry), cerebral perfusion pressure, O(2) tension, and extracellular levels of glucose, lactate, and pyruvate were monitored during 90 minutes after SAH. CBF (assessed by (125)I-antipyrine autoradiography), arteriovenous O(2) difference, and cerebral metabolic rate of O(2) were calculated at 15 or 90 minutes after SAH. RESULTS: After a transient reduction, cerebral perfusion pressure normalized within 5 minutes after SAH in all groups. There was a transient global decrease in CBF after SAH: its duration depended on the severity of the hemorrhage. CBF of less than 20% of baseline was observed for at least 15 minutes in 25% and 14% of the animals after perforation and prechiasmatic SAH, respectively. In all SAH groups, O(2) tension was suddenly reduced to approximately 40% of baseline and gradually increased, reaching 70 to 90% of baseline 90 minutes after SAH. The cerebral metabolic rate of O(2) was reduced only at 15 minutes after perforation and prechiasmatic SAH, but arteriovenous O(2) difference was normal in all groups. During 30 minutes after perforation SAH, a 50% decrease in glucose and a threefold increase in lactate and pyruvate levels were observed. CONCLUSION: The data suggest that SAH induced an acute global decrease in CBF together with a depression in the cerebral metabolism. The degree of the changes was related to the severity of the hemorrhage. The metabolic derangements were not always explained by ischemic episodes.
OBJECTIVE: To study the cerebral metabolism and its relationship to cerebral blood flow (CBF) acutely after subarachnoid hemorrhage (SAH). METHODS:SAH was induced in rats by endovascular perforation of the internal carotid artery, blood injection into the prechiasmatic cistern or the cisterna magna. CBF (measured by laser Doppler flowmetry), cerebral perfusion pressure, O(2) tension, and extracellular levels of glucose, lactate, and pyruvate were monitored during 90 minutes after SAH. CBF (assessed by (125)I-antipyrine autoradiography), arteriovenousO(2) difference, and cerebral metabolic rate of O(2) were calculated at 15 or 90 minutes after SAH. RESULTS: After a transient reduction, cerebral perfusion pressure normalized within 5 minutes after SAH in all groups. There was a transient global decrease in CBF after SAH: its duration depended on the severity of the hemorrhage. CBF of less than 20% of baseline was observed for at least 15 minutes in 25% and 14% of the animals after perforation and prechiasmatic SAH, respectively. In all SAH groups, O(2) tension was suddenly reduced to approximately 40% of baseline and gradually increased, reaching 70 to 90% of baseline 90 minutes after SAH. The cerebral metabolic rate of O(2) was reduced only at 15 minutes after perforation and prechiasmatic SAH, but arteriovenousO(2) difference was normal in all groups. During 30 minutes after perforation SAH, a 50% decrease in glucose and a threefold increase in lactate and pyruvate levels were observed. CONCLUSION: The data suggest that SAH induced an acute global decrease in CBF together with a depression in the cerebral metabolism. The degree of the changes was related to the severity of the hemorrhage. The metabolic derangements were not always explained by ischemic episodes.
Authors: Pieter M Cobelens; Ivo A C W Tiebosch; Rick M Dijkhuizen; Peter H van der Meide; René Zwartbol; Cobi J Heijnen; Jozef Kesecioglu; Walter M van den Bergh Journal: Crit Care Date: 2010-08-23 Impact factor: 9.097