Reduced myocardial response to calcium during endotoxin shock in the cat.

The hemodynamic effects of short intravenous infusions of calcium chloride were examined in anaesthetized cats before and during shock induced with E coli endotoxin (2 mg/kg). In normal cats calcium (5 mg kg-1 min-1 or 10 mg kg-1 min-1 infused for 5 minutes) increased left ventricular (LV) dP/dtmax, LVdP/dt at fixed isovolumic pressures, systemic arterial blood pressure and, usually, cardiac output. These hemodynamic changes lasted approximately 20 minutes. During endotoxin shock the calcium response (cardiac output, LVdP/dt, blood pressure) was greatly reduced. This diminished responsiveness was evident as early as 0.5--1 hour after endotoxin and lasted throughout the 4-hour shock period. The duration of the hemodynamic response was also decreased during shock. Reduced myocardial sensitivity to a number of cardiac stimulants, including beta-adrenoceptor stimulants and agents augmenting cellular cAMP/levels, occurs in this and other shock models. The present results suggest that this altered sensitivity is attributable to changes in the actual contraction processes rather than beta-adrenoceptor desensitization or a defect in the cAMP system. Since this altered calcium response does not occur in vitro the results might suggest the presence, in shock, of a circulating agent acting at the level of cellular calcium exchange.