| Abstrakt: |
Endotoxin depresses left ventricular (LV) contractility independently of alterations in loading conditions, acidosis, or hypoxia (Hung and Lew, 1993a). We evaluated if endotoxin-induced LV depression is associated with a decrease in functionall-type calcium channels, as reflected by the number of dihydropyridine receptors measured by [3H]-PN200-110 binding. New Zealand white rabbits were instrumented with sonomicrometers to measure the end-systolic pressure–volume relationship after i.v. saline (group I,n=6), 5μg/kg endotoxin (group II,n=6), or 10μg/kg endotoxin (group III,n=6). The end-systolic volume (ESV) measured at a matched end-systolic pressure did not change significantly over 6 h in group I (ESV changed by <5±2%s.e.) and group II (ESV changed by <3±2%), but increased markedly in group III (ESV increased 70±24%,P<0.05), indicating LV systolic depression. We measured [3H]-PN200-110 binding in crude membrane homogenates from the left ventricle. There was a dose-dependent decrease in Bmax: 75±5 fmol/mg protein in group I, 62±3 fmol/mg in group II, and 56±5 fmol/mg in group III (P=0.02 by ANOVA). Since the majority of dihydropyridine receptors are functionall-type calcium channels in rabbits (Lewet al., 1991), we conclude that a decreased number of dihydropyridine receptors contributes to endotoxin-induced LV depression. |
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