Sepsis-induced depressed contractile function of isolated ventricular myocytes is due to altered calcium transient properties

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Chronic peritoneal sepsis in a rodent model produces myocardial dysfunction characterized by decreased rates of ventricular contraction and relaxation in the isolated heart preparation. However, it remains controversial whether the ventricular contractility is altered during sepsis. In the present study, we determined the effect of chronic peritoneal sepsis on the mechanical properties and intracellular Ca2+ handling of cardiac myocytes isolated from septic rats at 24 or 48 h. Mechanical properties were evaluated by use of an IonOptix MyoCam system. Myocytes were electrically stimulated at 0.5 Hz. The contractile properties analyzed included peak shortening (PS), time-to-peak shortening (TPS), time-to-90% relengthening (TR90), and maximal velocities of shortening and relengthening (±dL/df). Intracellular Ca2+ handling was evaluated with fura-2 fluorescent dye. Myocytes obtained from 24-h postseptic animals exhibited a depressed PS (85% of control), normal TPS, prolonged TR90 (147% of control), and reduced ±dL/df (both 79% of control). Myocytes from 48-h postseptic animals also exhibited a reduced peak of intracellular Ca2+ sequestration (55% of control), but resting intracellular Ca2+ and Ca2+-transient decay were comparable with the values seen in myocytes from untreated rats. Myocytes from septic and control animals were equally responsive over a range of stimulation frequencies (0.1-5 Hz). Myocytes from septic animals were unresponsive (5% of control) to increase of extracellular Ca2+ (0.5-3 mM). These results demonstrate that sepsis produces substantial deficits in cardiac myocytes function that can be attributed to altered calcium transient properties.

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This article was published in Shock, Volume 18, Issue 3, Pages 285-288.

The published version is available at http://ovidsp.tx.ovid.com/sp-3.15.1b/ovidweb.cgi?&S=IDGMFPFLKLDDFLMANCKKKFGCJPHOAA00&Link+Set=S.sh. .

Copyright © 2002 Ovid.

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