The effects of aging on the cardiac contractile response to unresuscitated thermal injury.

Abstract

Isolated coronary perfused guinea pig hearts were used to determine if aging alters left ventricular (LV) intrinsic contractile response to unresuscitated burn shock. We first compared control hearts from both young (N = 10) and aged (N = 10) guinea pigs. Compared with young control hearts, aged control hearts showed significantly lower left ventricular performance (LVP) (84.2 +/- 1.6 v 76.0 +/- 1.5; P less than 0.003), +dP/dtmax (1417.5 +/- 52.4 v 1048 +/- 48.7; P less than 0.001), and -dP/dtmax (1079 +/- 79 v 916 +/- 27; P less than 0.001) at a left ventricular end-diastolic pressure (LVEDP) of 10 mmHg. A 43% +/- 2% third-degree burn (Walker model) was studied in 20 young and 10 aged guinea pigs. The aged burn hearts showed significantly lower LVP (57.1 +/- 2.1 v 65.5 +/- 2.0; P less than 0.01) and +dP/dtmax (1026 +/- 66.4 v 1219 +/- 59.9; P less than 0.001) at an LVEDP of 10 mm Hg. In addition, LV function curves for the aged burn hearts were shifted downward and to the right of curves obtained from the young burn hearts (P less than 0.05). Contractile defects in the aged group were neither related to altered beating frequency nor to maximally effective increases in diastolic stretch. While increased extracellular calcium concentration (from 1 to 8 millimolar [mM]) increased LVP, +dP/dtmax, and -dP/dtmax in a dose-dependent manner in both young and aged burn hearts, absolute values of measured contractile performance were consistently less in the aged hearts compared with the young hearts at identical calcium concentrations. Finally, we examined the effects of thermal injury on contractile function within the aged group. Peak LVP and maximal rate of relaxation were uniformly decreased in all burn hearts compared with control aged hearts. The +dP/dtmax was not significantly altered by burn in this age group (burn: 1026 +/- 66; control: 1048 +/- 49). This study suggests that severe myocardial contractile changes resulting from a major thermal insult in subjects with already compromised hearts is likely a significant limiting factor in the response to burn shock.