Cerebral blood flow and metabolism in the acute phase of experimental subarachnoid bleed.
Our experiment seems to confirm the hypothesis, implying an active CBF autoregulation as one of the interacting four survival mechanisms during an intracranial hemorrhage. While our present study has indicated that the autoregulation operates during the initial bleed, it is fully conceivable that the autoregulatory capacity may be exhausted after recurrent hemorrhages. Earlier experiments (Häggendal et al. [1970]) showed that autoregulation is easily abolished for prolonged periods after periods of intracranial hypertension. Further experiments are necessary to evaluate the capacity of the cerebral autoregulation to withstand repeated intracranial bleeds.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D004285:Dogs; D004569:Electroencephalography; D010100:Oxygen / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000378:metabolism / Q000503:physiopathology*
D010100:Oxygen