Saeki S, Shimosato S, Kosaka F
Department of Anesthesiology, Resuscitology University of Okayama School of Medicine, Okayama, Japan.
J Anesth. 1991 Oct;5(4):338-43. doi: 10.1007/s0054010050338.
Using 22 isolated rat ventricular muscle preparations, we investigated whether or not the increase in preload and/or contraction frequency may counteract the negative inotropy of both isoflurane (2.0%) and halothane (1.0%). Increases in preload from 94% of Lmax (the length where muscles produce the maximal tension) to Lmax did not alter significantly the percent decrements in tension development caused by either isoflurane or halothane. The increases in contraction frequency from 0.1 to 0.6 Hz augmented the depressant effect of isoflurane significantly ( P < 0.001), while the depressant effect of halothane was not altered at these contraction frequencies. Small but significant counteraction occurred in the depressant effects of halothane at 0.8 and 1.6 Hz ( P = 0.002). These changes in intracellular mechanism(s), resulted from the increase in contraction frequency, interacted with the two anesthetics on tension development, while these may not be the case for the increase in preload.
我们使用22个分离的大鼠心室肌标本,研究了前负荷和/或收缩频率的增加是否可以抵消异氟烷(2.0%)和氟烷(1.0%)两者的负性肌力作用。前负荷从最大张力(Lmax,即肌肉产生最大张力的长度)的94%增加到Lmax,并未显著改变异氟烷或氟烷引起的张力产生百分比下降。收缩频率从0.1 Hz增加到0.6 Hz显著增强了异氟烷的抑制作用(P < 0.001),而在这些收缩频率下氟烷的抑制作用未改变。在0.8 Hz和1.6 Hz时,氟烷的抑制作用出现了微小但显著的抵消作用(P = 0.002)。收缩频率增加引起的这些细胞内机制变化,与两种麻醉药在张力产生方面相互作用,而前负荷增加可能并非如此。