THE RESPONSE OF THE CANINE CEREBRAL-CIRCULATION TO HYPERVENTILATION DURING ANESTHESIA WITH DESFLURANE

Arterial CO2 tension (Pa(CO2) is an important factor controlling cerebral blood flow (CBF) and cerebral vascular resistance (CVR) in animals and humans. The normal responsiveness of the cerebral vasculature to Pa(CO2) is approximately 2 ml.min-1.100g-1.mmHg-1. This study examined the effect of desflurane, a new volatile anesthetic, on the responsiveness of the cerebral vasculature to changes in Pa(CO2). Mean arterial pressure (MAP), CBF, CVR, intracranial pressure (ICP), and cerebral metabolic rate for O2 (CMR(O)2) were measured in five dogs anesthetized with desflurane (0.5-1.5 MAC) at normocapnia (Pa(CO2)) = 40 mmHg) and at two levels of hypocapnia (Pa(CO2)) = approximately 30 and approximately 20 mmHg). Under desflurane anesthesia, similar changes in CBF and CVR occurred with hyperventilation at all MAC levels of desflurane. At 0.5 MAC, CBF decreased significantly, from 81 +/- 6 to 40 +/- 3 ml. min-1.100 g-1 (P < 0.05, mean +/- SE) when Pa(CO2) was decreased from 40 to 24 mmHg; i.e., the CBF decreased approximately 2.6 ml.min-1.100 g-1.mmHg-1. At 1.0 MAC desflurane, CBF decreased significantly, from 79 +/- 10 to 43 +/- 5 ml.min-1.100 g-1 with hyperventilation (2.0 ml.min-1.100 g-1.mmHg-1); at 1.5 MAC desflurane, CBF decreased from 65 +/- 6 to 38 +/- 2 ml.min-1.100 g-1 with hyperventilation (1.6 ml.min-1.100 g-1.mmHg-1). Despite the significant decreases in CBF with hyperventilation, there was no significant change in ICP. Dose-dependent decreases in MAP were observed with increasing concentrations of desflurane but were not significantly affected by ventilation. It can be concluded that the cerebral vasculature remained responsive to changes in Pa(CO2) at all concentrations of desflurane studied, even in the presence of moderate hypotension.