Myocardial metabolism for the toxicologist.
Drug effects on myocardial contractile function are obviously of considerable practical importance for the toxicologist. The basic mechanism of such actions must reside at some point in the metabolism of cardiac muscle. Interference in the liberation of energy from the fuels that the heart uses may be implicated. It is possible that drugs may interfere with the storage (conservation) of that energy as the high energy phosphates (ATP and CP). Finally, the utilization of that stored energy by the contractile proteins themselves may be altered. The latter process is highly dependent on intracellular calcium ion kinetics. Anesthetic drugs, which produce reversible depression of myocardial contractile function is a dose-dependent fashion, have been shown to interfere to some extent with all three processes. However, the most important mechanism probably involves utilization of energy and intracellular calcium ion movement. A basic knowledge of the biochemistry of cardiac muscle is necessary for the understanding of drug action and toxicity at the subcellular level.
D000255:Adenosine Triphosphate / Q000378:metabolism; D003326:Coronary Circulation; D004734:Energy Metabolism / Q000187:drug effects; D006003:Glycogen / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D010101:Oxygen Consumption; D014280:Triglycerides / Q000378:metabolism
D014280:Triglycerides; D000255:Adenosine Triphosphate; D006003:Glycogen