Trigeminal Cardiac Reflex and Cerebral Blood Flow Regulation
The trigeminal depressor response (TDR) is characterized with profound hypotension caused by sympathetic outflow decreases. The purpose of this study was: (1) to compare the hemodynamic changes during acute hypotension induced by the TDR with those induced by electrical stimulation of the vagal nerve (VS) as models of sympathetic inhibition and vagal activation and (2) to investigate the effects of nitrous oxide (N2O), a well-known sympathomimetic, on the hemodynamic changes during the TDR. Male Japan White rabbits were anesthetized with halothane in oxygen and mechanically ventilated. The electrode pair for the TDR was inserted into the submucosal tissue of the animal's tongue. The pair for the VS was applied to the isolated left vagal trunk. Both the TDR and the VS produced similar decreases in mean arterial pressure (MAP) and cerebral cortex regional blood flow (rCBF), although the decreases in heart rate (HR) and aortic blood flow were greater during the VS. Cerebral cortex tissue oxygen tension in both groups decreased slightly. 50% N2O, producing MAP elevation and HR decrease, ameliorated the hemodynamic changes including rCBF reduction during the TDR. A sudden diminution of sympathetic tone following noxious stimulation of the orofacial area, as in the case of the TDR, may be a possible trigger mechanism for vasodepressor reactions in dental patients. The sympathomimetic and possible antinociceptive effects of N2O may explain, at least in part, the preventive effects on vasodepressor reactions during dental procedures.