Increased venous pressure causes myogenic constriction of cerebral arterioles during local hyperoxia.
The responses of cerebral (pial) arterioles to increased venous pressure were examined in anesthetized cats equipped with cranial windows for the observation of the cerebral microcirculation. Increased venous pressure was induced by occlusion of the superior vena cava. Intracranial pressure was kept constant. Increased venous pressure when the window was filled with stationary cerebrospinal fluid caused 9-12% arteriolar dilation. Cerebral arteriolar dilation of equal magnitude (8-12%) was also seen when the space under the cranial window was perfused with fluorocarbon FC-80 equilibrated with 100% nitrogen. Increased venous pressure when the cranial window space was perfused with fluorocarbon equilibrated with 100% oxygen caused a small (5%) but significant arteriolar constriction. These results show that the dominant mechanism of autoregulation in the cerebral arterioles is metabolic, and that it involves an oxygen-sensitive mechanism. Myogenic vasoconstriction is unmasked during venous hypertension when the dominant metabolic mechanism is eliminated by increased local supply of oxygen.
D000818:Animals; D001158:Arteries / Q000187:drug effects*; D001160:Arterioles / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D002560:Cerebrovascular Circulation; D005466:Fluorocarbons / Q000494:pharmacology; D008833:Microcirculation; D010100:Oxygen / Q000494:pharmacology*; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects*; D014690:Venous Pressure
D005466:Fluorocarbons; D010100:Oxygen