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Am J Physiol Heart Circ Physiol 274: H580-H590, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 2, H580-H590, February 1998

Endotoxemia-induced myocardial dysfunction is not associated with changes in myofilament Ca2+ responsiveness

Sherri L. Rigby1, Polly A. Hofmann2, Juming Zhong1, H. Richard Adams1,3, and Leona J. Rubin1,3

1 Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, and 3 Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211; and 2 Department of Physiology and Biophysics, University of Tennessee, Memphis, Tennessee 38163

Myocardial contractile function is depressed after onset of endotoxemia and is intrinsic to the ventricular myocyte. We tested the hypothesis that decreased Ca2+ responsiveness of the contractile myofilaments underlies this inotropic depression. Specifically, we evaluated the relationship between Ca2+ and unloaded cell shortening and isometric tension development of skinned guinea pig ventricular myocytes. Myocytes were isolated 4 h after intraperitoneal injection of 4 mg/kg Escherichia coli lipopolysaccharide (LPS) or saline (control; Ctl). Myofilament Ca2+ responsiveness assessed by image analysis of shortening of skinned myocytes at pH 7.0 was not different between Ctl [pCa value that resulted in half-maximal shortening (pCa50): 5.78 ± 0.04] and LPS (pCa50: 5.72 ± 0.02). Similarly, myofilament Ca2+ responsiveness measured by isometric tension of skinned myocytes was not different between Ctl (pCa50: 5.73 ± 0.02) and LPS (pCa50: 5.76 ± 0.02). Maximal tension generated by LPS myocytes (2.89 ± 0.23 g/mm2) was significantly less (P < 0.05) than Ctl (3.75 ± 0.34 g/mm2). However, when myocytes were isolated and skinned in the presence of protease inhibitors, maximal tension generated by LPS myocytes (3.53 ± 0.98 g/mm2) was similar to Ctl (3.01 ± 0.80 g/mm2). We conclude that in vivo administration of LPS resulting in endotoxemia without shock does not alter myofilament Ca2+ responsiveness of ventricular myocytes. Rather, reduced contractility is more likely a result of decreased Ca2+ availability because systolic Ca2+ transients of fura 2-loaded LPS myocytes were significantly decreased (P < 0.05) compared with Ctl myocytes.

lipopolysaccharide; sepsis; sarcomere; saponin; myocyte; endotoxemia


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