title: Reduced myocardial response to calcium during endotoxin shock in the cat.
abstract: 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.
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects; D002415:Cats; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D012769:Shock / Q000209:etiology*; D013997:Time Factors
chemical_list: D004731:Endotoxins; D002118:Calcium