CYTOSOLIC Ca2+ CONCENTRATION AND CONTRACTION-RELAXATION PROPERTIES OF VENTRICULAR MYOCYTES FROM ESCHERICHIA COLI ENDOTOXEMIC GUINEA PIGS

Abstract
Hearts isolated from a guinea pig model of Escherichia coli endotoxemia exhibit decreased systolic contractile function and reduced diastolic compliance of the left ventricle within 4 h after injection of endotoxin. Fluid resuscitation prevented the endotoxin-induced decrease in diastolic compliance without affecting systolic contractile depression. Because intrinsic myocardial dysfunction after endotoxemia may result from alterations in intracellular Ca2+ handling, we tested the hypothesis that in vivo fluid resuscitation improved diastolic function by altering Ca2+ handling of the myocardium. We tested this hypothesis by measuring cell shortening and intracellular Ca2+ of ventricular myocytes isolated from endotoxemic guinea pigs. E. coli endotoxin (LPS, 1 mg/kg)-injected guinea pigs were divided into resuscitated and nonresuscitated groups. Fluid resuscitated animals received a Ringer's infusion (8 mL·kg−1·h−1) intravenously (i. v.) beginning immediately after endotoxin injection. Four hours later, ventricular myocytes were isolated enzymatically and loaded with fura-2/AM. When myocytes were field stimulated at .8 Hz, peak systolic Ca2+ transients of LPS-resuscitated (619 ± 75 nM) and LPS-nonresuscitated (599 ± 60 nM) myocytes were not significantly different from each other, but both were significantly less than values from control myocytes (1187 ± 118 nM, p <.05). The percentage of cell shortening of LPS-resuscitated (6.2 ±.9%) and LPS-nonresuscitated (6.2 ±.3%) myocytes were also less than control (11.8 ±.5%, p < .05). In contrast to improved diastolic compliance of fluid-resuscitated hearts, diastolic [Ca2+], of myocytes (at .8 Hz) from LPS-resuscitated animals (138 ± 47 nM) was not statistically different from LPS-nonresuscitated animals (129 ± 19 nM). Diastolic values of both LPS groups were consistently lower than control value (251 ± 38 nM, p <.05). These data suggest that improved diastolic compliance of LPS hearts following fluid resuscitation is not associated with improved myocyte contractility or myoplasmic Ca2+ handling.

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