Brain energetics and circulatory control after subarachnoid hemorrhage.
Ischemia-provoking factors such as vasospasm, decreased cerebral perfusion pressure, and intravascular thrombosis may be present after subarchnoid hemorrhage (SAH). When these factors were not present during controlled SAH, a primary depression of cerebral glycolysis associated with normal stores of energy-rich phosphates was found. Although cerebral blood flow usually changes in response to changes in cerebral metabolic needs, this influence on the circulation was not evident in the early hours after SAH. After 3 to 4 hours an erratic decrease in blood flow occurred, probably related to vasospasm, and there were measurable decreases in energy-rich phosphates similar to those occurring after more severe and prolonged ischemias. These findings are indicative of abnormally erratic vascular responses to metabolic cues and may play a role in producing the encephalopathy of SAH.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D004734:Energy Metabolism; D000882:Haplorhini; D006706:Homeostasis; D007427:Intracranial Pressure; D008253:Macaca mulatta; D013345:Subarachnoid Hemorrhage / Q000378:metabolism / Q000503:physiopathology*