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/dt(max), 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 β-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 β-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.
|Number of pages||8|
|Publication status||Published - jan. 1 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine