PULMONARY VASODILATOR RESPONSE TO ADENOSINE TRIPHOSPHATE-SENSITIVE POTASSIUM CHANNEL ACTIVATION IS ATTENUATED DURING DESFLURANE BUT PRESERVED DURING SEVOFLURANE ANESTHESIA COMPARED WITH THE CONSCIOUS STATE

Background: The objective of this study was to investigate the effects of sevoflurane and desflurane anesthesia on the pulmonary vasodilator response to the adenosine triphosphate-sensitive potassium channel ag onist, lemakalim, compared with the response measured in the conscious state. Zn addition, the authors assessed the extent to which sympathe tic alpha(1)-adrenoreceptor inhibition and cyclooxygenase pathway inhi bition modulate the vasodilator response to lemakalim. Methods: Twenty -four conditioned male mongrel dogs were chronically instrumented to m easure the left pulmonary vascular pressure-flow relationship. After p reconstriction with the thromboxane analogue, U46619, dose-response re lationships to lemakalim were assessed on separate days in the conscio us state and during sevoflurane (approximate to 3.5% end-tidal) and de sflurane (approximate to 10.5% end-tidal) anesthesia (similar to 1.5 m inimum alveolar concentration for each anesthetic agent). The effects of sympathetic alpha(1)-adrenoreceptor inhibition (prazosin) and cyclo oxygenase inhibition (indomethacin) on the pulmonary vasodilator respo nse to lemakalim also were assessed in the conscious and desflurane-an esthetized states. Results: Neither sevoflurane nor desflurane had a n et effect on the baseline left pulmonary vascular pressure-flow relati onship compared with the conscious state. The magnitude of the pulmona ry vasodilator response to lemakalim was preserved during sevoflurane anesthesia but was attenuated (P < 0.05) during desflurane anesthesia compared with the conscious state. The attenuated lemakalim-induced va sodilator response during desflurane anesthesia was partially reversed (P < 0.05) by pretreatment with prazosin but not indomethacin. Conclu sion These results indicate that adenosine triphosphate-sensitive pota ssium channel-mediated pulmonary vasodilation is preserved during sevo flurane anesthesia but is attenuated during desflurane anesthesia. The attenuated response to adenosine triphosphate-sensitive potassium cha nnel activation during desflurane anesthesia is partially mediated by reflex sympathetic alpha(1)-adrenoreceptor vasoconstriction.