McDonough, Kathleen H.; Causey, Karen M.
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Gram-negative sepsis as well as administration of agents that simulate or occur naturally subsequent to a septic challenge, can present as an oxidant stress to the myocardium. These stresses may then induce the development of protection of the heart from future stresses. This protection of the heart may occur in spite of the fact that sepsis itself induces myocardial dysfunction. In the present study we determined if sepsis is protective of a 50 min ischemic episode, one in which some degree of irreversible damage may occur. In addition we determined if sepsis-induced protection was still present when this ischemic challenge was imposed upon the heart of the alcoholic septic animal in which the chronic alcoholic state can lead to a potentiation of sepsis induced cardiac depression. Thus animals were fed an ethanol containing diet or a control diet for 8-10 weeks and were then made septic by the administration of Escherichia coli into the dorsal subcutaneous space. Control animals received sterile saline. The following day, hearts were studied in the isovolumic beating preparation and, after basal function was assessed, hearts were made globally ischemic for 50 min and reperfused for 30 min. Left ventricular pressure was continuously monitored and coronary flow was measured at specific intervals. After ischemia and reperfusion, hearts from control- and alcohol-fed animals that were nonseptic showed significantly decreased left ventricular performance. Ventricular pressure development of hearts from septic and alcoholic septic rats was not significantly decreased after ischemia and reperfusion compared to preischemia although preischemic function was significantly lower in the sepsis groups compared to their nonseptic control groups. Recovery of coronary flow tended to be more rapid in the two septic groups and to show a hyperemia compared to recovery of flow in the control and alcohol nonseptic groups. Thus sepsis-induced protection of the heart was effective even after 50 min ischemia.

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