Autoregulation of Cerebral Blood Flow in Response to Adenosine-Induced Hypotension in Dogs

During induced hypotension for surgical procedures, cerebral blood flow (CBF) autoregulation and cerebrovascular responsivity to CO2 may be impaired-changes that appear to be agent-specific. Adenosine is a potent endogenous systemic vasodilator and has been investigated as a hypotensive agent. In this study in dogs we investigated cerebral vascular responses to graded decreases of cerebral perfusion pressure (CPP) (100%, 60%, 45%, and 35% of control CPP) during normocapnia (PaCO2 = 37 mm Hg) and hypocapnia (PaCO2 = 21 mm Hg). CBF was measured using the venous outflow technique. Six mongrel dogs were anesthetized with halothane (0.6% inspired) and nitrous oxide (70%) in oxygen and studied during both normocapnic and hypocapnic hypotension. The entry sequence was randomized with >/= 1 h of recovery between normocapnia and hypocapnia. Hypocapnia reduced control CBF from 60.6 +/- 7.1 to 45.1 +/- 5.4 ml 100 g min (mean +/- SEM, p <0.05) during normotension. CBF was unchanged from control values during both graded normocapnic and hypocapnic hypotension until CPP reached 60% of control CPP (50 and 47 mm Hg for normocapnia and hypocapnia, respectively). Thereafter CBF decreased significantly from control values at 45% (37 mm Hg for both groups) and 35% (29 mm Hg for both groups) of control CPP. The lower limit of CBF autoregulation derived by applying linear regression analysis to the CBF-CPP relationship above and below the inflexion point was similar under both experimental conditions (60 +/- 1% of control CPP during normocapnia and 63 +/- 3% of control CPP during hypocapnia). CBF was significantly greater during normocapnia compared with hypocapnia at all levels of CPP, except at 35% of control when the values were similar. Cerebral metabolic rate was unchanged throughout the study. We conclude that neither CBF nor CO2 responsivity is appreciably altered during adenosine-induced hypotension when GPP remains above the lower limit of autoregulation of CBF.