丙泊酚对大鼠和豚鼠离体心肌小梁收缩性的差异作用。

The differential effect of propofol on contractility of isolated myocardial trabeculae of rat and guinea-pig.

van Klarenbosch J, Stienen G J, de Ruijter W, Scheffer G J, de Lange J J

Department of Anaesthesiology, Academisch Ziekenhuis, Vrije Universiteit, Amsterdam, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.

Br J Pharmacol. 2001 Feb;132(3):742-8. doi: 10.1038/sj.bjp.0703849.

Abstract

The effects of propofol on myocardial contractility were studied in rat, in which the contractile activation mainly depends on calcium derived from the sarcoplasmic reticulum (SR), and guinea-pig, in which transsarcolemmal influx of calcium plays a major role. 2. Intact and chemically skinned trabeculae from the right ventricle were studied. Intact trabeculae were electrically stimulated and force development during steady state and post rest contractions was measured. In saponin skinned trabeculae Ca(2+) uptake and release by the SR was studied. In Triton skinned trabeculae the influence of propofol on calcium sensitivity of the myofilaments was studied. 3. In intact rat trabeculae propofol in concentrations of 28, 112 and 280 microM did not change peak force development nor the pattern of post rest contraction. In guinea-pig trabeculae propofol significantly reduced peak force to respectively 64, 40 and 23% of control values and the post rest contractions were potentiated. In skinned trabeculae propofol did not affect Ca(2+) handling by the SR, nor did it change force production and Ca(2+) sensitivity of the myofilaments. 4. This study shows that, in contrast to rat, in guinea-pig propofol directly depresses myocardial contractility, probably by decreasing transsarcolemmal Ca(2+) influx. There is no significant influence of propofol on Ca(2+) handling by the SR, nor on the contractile proteins.

摘要

在大鼠（其收缩激活主要依赖于肌浆网（SR）释放的钙）和豚鼠（其钙经肌膜内流起主要作用）中研究了丙泊酚对心肌收缩力的影响。2. 研究了右心室完整和经化学处理使肌膜通透的小梁。对完整小梁进行电刺激，并测量稳态和休息后收缩期间的力发展。在皂角苷处理使肌膜通透的小梁中研究了SR对Ca(2+)的摄取和释放。在曲拉通处理使肌膜通透的小梁中研究了丙泊酚对肌丝钙敏感性的影响。3. 在完整的大鼠小梁中，浓度为28、112和280微摩尔的丙泊酚既不改变峰值力发展，也不改变休息后收缩模式。在豚鼠小梁中，丙泊酚显著降低峰值力，分别降至对照值的64%、40%和23%，且休息后收缩增强。在肌膜通透的小梁中，丙泊酚不影响SR对Ca(2+)的处理，也不改变肌丝的力产生和Ca(2+)敏感性。4. 本研究表明，与大鼠不同，在豚鼠中丙泊酚直接抑制心肌收缩力，可能是通过减少钙经肌膜内流实现的。丙泊酚对SR对Ca(2+)的处理以及收缩蛋白均无显著影响。