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-Myosin heavy chain myocytes are more resistant to changes in power output induced by ischemic conditions

Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri

Submitted 7 March 2005 ; accepted in final form 9 September 2005

During ischemia intracellular concentrations of P_i and H⁺ increase. Also, changes in myosin heavy chain (MHC) isoform toward -MHC have been reported after ischemia and infarction associated with coronary artery disease. The purpose of this study was to investigate the effects of myoplasmic changes of P_i and H⁺ on the loaded shortening velocity and power output of cardiac myocytes expressing either - or -MHC. Skinned cardiac myocyte preparations were obtained from adult male Sprague-Dawley rats (control or treated with 5-n-propyl-2-thiouracil to induce -MHC) and mounted between a force transducer and servomotor system. Myocyte preparations were subjected to a series of isotonic force clamps to determine shortening velocity and power output during Ca²⁺ activations in each of the following solutions: 1) pCa 4.5 and pH 7.0; 2) pCa 4.5, pH 7.0, and 5 mM P_i; 3) pCa 4.5 and pH 6.6; and 4) pCa 4.5, pH 6.6, and 5 mM P_i. Added P_i and lowered pH each caused isometric force to decline to the same extent in -MHC and -MHC myocytes; however, -MHC myocytes were more resistant to changes in absolute power output. For example, peak absolute power output fell 53% in -MHC myocytes, whereas power fell only 38% in -MHC myocytes in response to elevated P_i and lowered pH (i.e., solution 4). The reduced effect on power output was the result of a greater increase in loaded shortening velocity induced by P_i in -MHC myocytes and an increase in loaded shortening velocity at pH 6.6 that occurred only in -MHC myocytes. We conclude that the functional response to elevated P_i and lowered pH during ischemia is MHC isoform-dependent with -MHC myocytes being more resistant to declines in power output.

ischemia; inorganic phosphate; loaded shortening velocity; power output

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