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The differential effect of propofol on contractility of isolated myocardial trabeculae of rat and guinea‐pig
Author(s) -
Klarenbosch J van,
Stienen G J M,
Ruijter W de,
Scheffer G J,
Lange J J de
Publication year - 2001
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703849
Subject(s) - contractility , myofilament , calcium , contraction (grammar) , ventricle , guinea pig , chemistry , propofol , muscle contraction , biophysics , anatomy , endoplasmic reticulum , medicine , endocrinology , biology , myosin , pharmacology , biochemistry
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. 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. In intact rat trabeculae propofol in concentrations of 28, 112 and 280 μ M 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. 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.British Journal of Pharmacology (2001) 132 , 742–748; doi: 10.1038/sj.bjp.0703849