TY - JOUR
T1 - Substrate utilization and high energy phosphate levels of hearts from hyperdynamic septic rats
AU - McDonough, K. H.
AU - Henry, J. J.
AU - Lang, C. H.
AU - Spitzer, J. J.
PY - 1986
Y1 - 1986
N2 - Experiments were conducted to test the hypothesis that the previously demonstrated depression in ventricular function of rats with hyperdynamic sepsis was a result of depressed high energy phosphate levels or altered myocardial substrate utilization. Rats were inoculated with a pooled fecal homogenate, and 48 hr later their hearts were removed and studied using the Langendorff preparation. The coronaries were perfused with a hydrostatic pressure of 90 mmHg, and hearts were paced at 310-320 beats/min. Substrate oxidation was determined by supplying 14C-labeled glucose, lactate, or palmitate in physiologic concentration, ie, 5.5, 1, and 0.6 mM, respectively. Hearts were frozen either in situ or after 40-50 min of perfusion for the determination of tissue metabolite levels. Myocardial content of high energy phosphates, total adenine nucleotides, and creatine were similar in septic animals and time-matched controls both in situ and after perfusion. Oxidation of exogenous substrates accounted for the total myocardial O2 consumption in both groups of perfused hearts. Palmitate oxidation was responsible for approximately 50% of the total O2 consumption of the heart, with glucose accounting for approximately 20% and lactate for the remainder. The percentage contribution of the three substrates to oxidative metabolism was similar in hearts from septic and time-matched controls; therefore, myocardial substrate preference was not altered by sustained sepsis. These studies also indicate that ischemia and the concomitant fall in high energy phosphates do not contribute to the myocardial dysfunction of hyperdynamic sepsis.
AB - Experiments were conducted to test the hypothesis that the previously demonstrated depression in ventricular function of rats with hyperdynamic sepsis was a result of depressed high energy phosphate levels or altered myocardial substrate utilization. Rats were inoculated with a pooled fecal homogenate, and 48 hr later their hearts were removed and studied using the Langendorff preparation. The coronaries were perfused with a hydrostatic pressure of 90 mmHg, and hearts were paced at 310-320 beats/min. Substrate oxidation was determined by supplying 14C-labeled glucose, lactate, or palmitate in physiologic concentration, ie, 5.5, 1, and 0.6 mM, respectively. Hearts were frozen either in situ or after 40-50 min of perfusion for the determination of tissue metabolite levels. Myocardial content of high energy phosphates, total adenine nucleotides, and creatine were similar in septic animals and time-matched controls both in situ and after perfusion. Oxidation of exogenous substrates accounted for the total myocardial O2 consumption in both groups of perfused hearts. Palmitate oxidation was responsible for approximately 50% of the total O2 consumption of the heart, with glucose accounting for approximately 20% and lactate for the remainder. The percentage contribution of the three substrates to oxidative metabolism was similar in hearts from septic and time-matched controls; therefore, myocardial substrate preference was not altered by sustained sepsis. These studies also indicate that ischemia and the concomitant fall in high energy phosphates do not contribute to the myocardial dysfunction of hyperdynamic sepsis.
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M3 - Article
C2 - 3698211
AN - SCOPUS:0022621381
SN - 0092-6213
VL - 18
SP - 161
EP - 170
JO - Circulatory Shock
JF - Circulatory Shock
IS - 3
ER -