[Effects of volatile anesthetics on the cervical sympathetic nerve activity during acute hypoxemia or hypercarbia in dogs].

Either hypoxemia or hypercarbia produces a significant change in the autonomic nervous system activity. Responses of the cervical sympathetic nerve activity (CSA) to acute hypoxemia and/or hypercarbia were studied in the absence and the presence of either halothane (H), enflurane (E), isoflurane (I) or sevoflurane (S). Multifiber potentials of CSA, EEG, ECG, heart rate, arterial blood pressure, arterial oxygen saturation (SaO2) and endtidal carbon dioxide concentration (FETCO2) were continuously monitored. CSA increased responding to acutely induced hypoxemia at a speed of -6-9% (SaO2)/min. The response of CSA was estimated in two ways as a function of SaO2; the threshold was determined at which CSA increased by 3% over the base level and the gain was determined by the slope of CSA increase divided by the SaO2 span. They were 92% and -1. 88 (Mean) in the absence of volatile anesthetics, respectively. The threshold and the gain decreased markedly in the presence of volatile anesthetics in a dose dependent fashion. They were 89.2% and -1.16; 81% and -0.74; 84.2% and -1.16 and 86.2% and -0.94 with 1MAC of H, E, I and S. At 1MAC, E and S suppressed CSA response significantly compared to equipotential H and I. CSA also increased responding to acutely induced hypercarbia at FETCO2 of 10%. The peak level increased 34% above the control value responding to hypercarbia in the absence of volatile anesthetics, though it was less than a half value of that induced by hypoxemia. The tonic levels of CSA were suppressed with increasing concentrations of volatile anesthetics. The base level and the peak level were 68.3% and 75%; 50.7% and 51.8%; 70.3% and 76.7%, and 55.5% and 63.2% with 1MAC of H, E, I and S. The inhibitory effects of 1MAC E on the CSA was significantly stronger than that of equipotential H or I. CSA did not respond against hypoxemia following bilateral sinus nerve block with 2% lidocaine 4 ml. Since EEG was silent while SaO2 was lower than 30%, vigorous CSA at these levels of hypoxemia should be maintained by strong afferent activity of the chemoreceptor site. These combined stimulation of both acute hypoxemia and hypercarbia seem to suggest that CSA response are additive each other. In conclusion, it is indicated that the depressant effects of volatile anesthetics on the CSA responses to acutely induced hypoxemia and hypercarbia can cause depression of the control activity on the autonomic nervous system against hypoxemia and hypercarbia, and conceal the manifestation of clinical signs of hypoxemia and hypercarbia, per se.