Cardiac dysfunction occurs after a major burn injury regardless of age; whether burn trauma causes greater myocardial contractile depression in the older subject due to reduced cardiac reserves that normally occur with adult aging is not known. The cellular basis for burn-induced cardiac dysfunction is not known, but several studies have suggested that alterations occur in the rate of Ca2+ delivery to the contractile proteins as well as in the rate of Ca2+ removal from the sarcoplasm by the sarcoplasmic reticulum (SR). To determine if agerelated differences in the cardiac contractile response to burn injury are associated with differences in SR Ca2+ transport, an isolated heart preparation was used to examine mechanical function, and myocardial homogenate preparations were used to assess SR Ca2+ transport. Guinea pigs from both age groups (adult, 6-8 months, and senescent, 34-36 months of age) were divided into two subgroups-control and 45% cutaneous scald burn. Cardiac dysfunction associated with adult aging alone was indicated by lower systolic pressure and lower rates of left ventricular (LV) pressure rise and fall, as well as decreased responses to isoproterenol, exogenous Ca2+, increased coronary flow rate, and electrical pacing. Myocardial depression in senescent control hearts was accompanied by a decreased maximal Ca2+ uptake in myocardial homogenates, suggesting that altered SR calcium transport may contribute to the diminished contractile function associated with aging. Burn injury impaired cardiac function in all animals regardless of age as evidenced by a leftward shift of LV function curves and altered responses to receptor- and nonreceptor-mediated inotropic interventions. However, the percentage change in cardiac function after burn injury was similar in both age groups compared to those of their respective controls. Significant alterations in SR Ca2+ transport were observed in myocardial homogenates isolated from both adult and senescent hearts after burn injury. Our data confirm that burn injury induced cardiac contractile dysfunction as well as alterations in SR Ca2+ transport function regardless of age, and we conclude that altered SR Ca2+ transport function contributes, in part, to the diminished cardiac function after burn injury.
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