Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

Abstract

SUMMARY. The following studies were carried out to examine energy metabolites and cardiac performance of the failing heart (hereditary cardiomyopathy) of the Syrian hamster (strain UM-X7.1) perfused either by normal or stress conditions, and to determine whether cyclical changes in energy-related metabolites occurred in the glucose-perfused hearts of both normal and heart failure animals. Hamster hearts from 250-day-old animals with moderate heart failure were removed and perfused either as nonworking hearts (Langendorff method, an afterload pressure of 90 mm Hg and 2.5 rriM calcium in the perfusate) or as working hearts with stress conditions [an afterload of 110 mm Hg, high calcium concentrations in the perfusate (3.5 ITIM), and 10~8 M isoproterenol]. Mechanical parameters (developed pressure and max dP/dt) and measurements of oxygen consumption indicated that both contractility and oxygen consumption had fallen 50% in myopathic hearts, compared with those of normal hamsters perfused with either of the two conditions. By means of a specially designed stimulator-triggered freeze clamp, hearts were terminated at systole and diastole, and tissue content of ATP, ADP, AMP, adenosine, phosphocreatine, creatine, pyruvate, lactate, and inorganic phosphate were analyzed. A 50% reduction in cardiac performance of the cardiomyopathic hamster hearts was associated with a corresponding reduction in systolic ATP, adenosine, and phosphocreatine values, while inorganic phosphate and lactate increased. With glucose as the sole substrate, the high energy phosphates, ATP and phosphocreatine, reached maximum values during diastole and minimum values during systole. The phase alternate was observed with creatine, ADP, AMP, and inorganic phosphate. Cyclical changes were less obvious in the cardiomyopathic hearts due to less ATP utilization per cycle. A decrease in high energy phosphates, a low level in the free energy of ATP hydrolysis, augmented levels of lactate, increased inorganic phosphate, and a depressed purine nucleotide pool all of which occur concurrently, may cause the decrease in cardiac performance in the failing heart of the cardiomyopathic Syrian hamster. (Circ Res 53: 759-766, 1983)

Biological activity of angiotensin-(1-7) heptapeptide in the hamster heart.

“…Our data regarding cardiac performance in the isolated perfused hearts of 200 -day-old hamsters are similar to those data of Sievers et al 15 and Wikman-Coffelt et al, 16 who studied 240-250-day-old hamsters, using the Langendorff preparation with a perfusion pressure of 90-100 mm Hg. We used a perfusion pressure of 50 mm Hg in our studies to reduce cardiac tissue edema during perfusion throughout the duration of our experiments.…”

“…Under these conditions, we identified a depressed baseline cardiac performance in the CMH. Baseline MFR was not different between CMH and NH, as also shown by Sievers et al 15 At a constant perfusion pressure, angiotensin-(1-7) decreased MFR in both CMH and NH. The decrease in LVP and LV +dP/dt, however, was significant only in the NH hearts.…”

The preventive effect of verapamil on ethanol-induced cardiac depression: phosphorus-31 nuclear magnetic resonance and high-pressure liquid chromatographic studies of hamsters.

“…Adenosine was quantitated in a similar manner, except peak height instead of integration of peaks was used. 24 …”

Nitric Oxide Modulates Mitochondrial Respiration in Failing Human Heart

“…Abnormalities of mitochondria in cardiomyocytes in heart failure have been well documented in both animals [1][2][3][4] and human studies, [5][6][7] which provided structural and metabolic evidence of mitochondrial dysfunction. Mitochondrial DNA damage with increased mitochondrial DNA deletion in patients with heart failure has also been reported, 8,9 a defect associated with the impairment of oxidative phosphorylation.…”