The cerebral blood flow and response to cerebral venous pressure elevation was studied in pentobarbital-anesthetized dogs using the cerebral venous outflow and radiolabeled microsphere techniques. Cerebral venous pressure elevation resulted in a significant reduction in cerebral venous outflow at a pressure of approximately 2.0 mmHg (referenced at the level of the external auditory meatus). At higher pressures, cerebral venous outflow decreased at a rate of 0.5 ml.min1.mmHg-1. Mean arterial pressure was 102.0 mmHg, and thus cerebral perfusion pressure (mean arterial pressure minus cerebral venous pressure) was well within the range for cerebral autoregulation. These results were obtained regardless of whether cerebrospinal fluid pressure was allowed to rise concomitantly with cerebral venous pressure (11 dogs) or was maintained at atmospheric pressure (7 dogs). However, simultaneous measurement of cerebral venous outflow and total and regional cerebral blood flow with the radiolabeled microsphere technique with venous pressure elevation (6 dogs) produced discrepant results. As cerebral venous pressure was elevated to approximately 16.0 mmHg, cerebral venous outflow decreased to 40% of control while total and regional cerebral blood flow values remained unchanged, so that regional and cerebral vascular resistances decreased. These results suggest that cerebral venous pressure elevation opens intracranial venous anastomotic channels and diverts blood flow from the measured venous drainage through other drainage sites. In addition, our results suggest that the dominant mechanism of cerebral autoregulation is metabolic, not myogenic.
|American Journal of Physiology - Heart and Circulatory Physiology
|Published - 1983
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)