The effects of sevoflurane, isoflurane or enflurane on the pattern of phrenic nerve discharge in rabbits
Nakamura, S.; Hayashi, K.; Genda, T.; Nagasaka, H.; Aikawa, K.; Matsumoto, N.; Hori, T.
Masui. Japanese Journal of Anesthesiology 47(10): 1166-1172
1998
ISSN/ISBN: 0021-4892 PMID: 9834586 Document Number: 493222
In order to estimate primary action of anesthetic agents on the central neural mechanisms of respiratory control and the ventilatory response to an acute increased ETCO2, the effect of sevoflurane (SEV), isoflurane (ISO) or enflurane (ENF) on the pattern of phrenic nerve discharge (Phr.N.A.) was studied in adult rabbits which had been vagotomized, paralyzed and ventilated artificially with 100% oxygen. Throughout the course of experiment, ETCO2, and the rectal temperature of animals were maintained around physiological values. Depressant effects of these anesthetics on Phr. N.A. which consisted of inspiratory slope (SLO), peak amplitude (AMP), inspiratory (Ti) and expiratory (Te) time, I/E ratio (I/E) and respiratory cycle (Tc) were evaluated and compared with each anesthetic. At 0.5 MAC administration, SEV and ISO reduced SLO and AMP without a remarkable change in Tc, but ENF did with a prolongation in Tc. Inhalation of each anesthetic with 1 MAC caused a marked respiratory slowing with a more reduction of SLO and AMP than those occurred at 0.5 MAC; SEV increased Te more than Ti, but ENF prolonged Ti more than Te, while ISO enhanced both Ti and Te without any change of I/E. An acutely increased ETCO2, after the respiratory arrest (RA test) induced the change of Phr.N.A which was characterized by a marked prolongation in Tc with a prolonged Te, an increased SLO and an augmented AMP. The prolonged Tc induced by RA test was diminished by the inhalation of anesthetics, and a new response, shortening in Ti was produced by ENF and ISO. Based on these results, it might be concluded that there are both quantitative and qualitative differences in these anesthetic effects on the central pattern generator of respiration and the mechanism of CO2 responses at equipotent anesthetic concentrations.