ABSTRACTIschemia causes significant damage to the heart as manifested by decreases in ventricular performance. Several different methods have been shown to protect the heart from ischemic injuryndash;one is operative over a short period (an hour) and the other over longer periods (a day). The latter form of protection has been demonstrated in rats after induction of Gram-negative sepsis or administration of endotoxin or cytokines. In the present study we determined whether guinea pigs would also show induction of cardiac protection subsequent to a dose of endotoxin. Male guinea pigs were injected with 1 mg of endotoxin and studied the following day. Hearts were perfused at a constant perfusion pressure and studied in an isovolumic mode. Left ventricular developed pressure was significantly lower in the endotoxin-treated group than in the control group. After 35 min of total ischemia and 25 min of reperfusion, recovery of left ventricular developed pressure was complete in the endotoxin group but significantly decreased in the control group such that after ischemia and reperfusion, there was no significant difference in left ventricular performance between the two groups. Coronary flow was significantly greater in the endotoxin group than in the control group both prior to and after ischemia. Hearts from endotoxin-treated guinea pigs resumed spontaneous contractile activity sooner and released less lactate upon reperfusion than did the control group. Thus prior treatment of guinea pigs with endotoxin resulted in depression of the isolated heart but also resulted in protection of the isolated heart from further damage due to ischemia/reperfusion injury.
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