DIMINISHED CARDIAC CONTRACTILE RESPONSE TO BURN INJURY IN AGED GUINEA-PIGS

Previous studies have shown that regulation of the cardiovascular system progressively deteriorates with adult aging, limiting cardiovascular adaptive mechanisms to stress such as aerobic exercise or trauma. This present study examined cardiac contractile performance as a function of adult aging in a guinea pig model and secondarily examined the effects of adult aging on cardiac contractile responses to burn injury. In a total of 39 adult and 49 senescent animals, a cutaneous full-thickness burn comprising 45% of the total body surface area was obtained using a template device (Walker model); a sham burn was produced in 38 adult and 35 senescent animals by immersion in room temperature water. Adult aging altered cardiac contraction and relaxation as indicated by significantly lower left ventricular pressure and +/-dP/dt max, as well as diminished left ventricular responsiveness to increases in preload, perfusate calcium, isoproterenol, and calcium channel blockade. Burn injury caused significant hypotension, hypothermia, and a rise in hematocrit regardless of age. Cardiac contractile dysfunction occurred in all hearts after burn injury regardless of age, as indicated by a rightward and downward shift of left ventricular function curves for both burn groups compared with their respective controls. The failure of increasing perfusate calcium to overcome burn-mediated contractile deficits in both age groups suggested that burn injury disrupts sarcolemma-bound calcium. The burn-induced decrease in negative inotropic potency of a calcium channel blocker suggests that burn injury specifically targets the calcium slow channel of the sarcolemma. Finally, the burn-mediated diminution in cardiac responsiveness to isoproterenol in both age groups supports previous work from our laboratory showing that burn injury alters beta-adrenergic receptor function. Our data suggest that burn injury alters cardiac contractile performance regardless of age by altering subcellular events and structures that regulate intracellular calcium availability to the myofilaments.