Oxygen sufficiency in working rabbit papillary muscle at 35 degrees C.
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Biomedical subjects
Publications and source records attributed to T R Snow.
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The effect of insulin was examined with emphasis on the alteration in the force-frequency relation. The results show that insulin does not change the time to peak tension nor the time of contraction. The inotropic effect was significant and did not depend upon the frequency of stimulation. However, there was a definite dependence of the magnitude of the inotropic effect on temperature. Previous studies have indicated that the inotropic effect is not a result of increased substrate availability or changes in cAMP phosphodiesterase activity. These results and those reported here are consistant with the hypothesis that insulin's inotropic effect is due to increases in intracellular Ca++.
The fluorescence of pyrenebutyric acid is quenched by oxygen and the quenching is a linear function of the oxygen concentration. In addition, pyrenebutyric acid has been shown to be readily taken up by the cell with a partition coefficient of approx. 200. Results are presented on the effect of pyrenebutyric acid on oxidative metabolism in rabbit heart mitochondria. 1. Pyrenebutyric acid is readily taken up by heart mitochondria: 0.843 +/- 0.087 nmol pyrenebutyric acid taken up by Mr/mg dried weight. 2. Pyrenebutyric acid does not alter the steady-state redox levels (State 1, 2, 4 or 5) of any member of the respiratory chain. 3. Pyrenebutyric acid does not alter the response of cytochrome b, cytochrome c or NADH in the State 4-3-4 transition induced by the addition of ADP. Thus pyrenebutyric acid would appear to be non-toxic to oxidative metabolism.
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Experiments were performed to examine the response of cyt a,a3 to transient ischemic and hypoxic episodes in the empty, fibrillating canine heart in situ. Using a dual wavelength, differential spectrophotometer, reaction spectra show an absorption peak at approximately 605 nm consistent with that obtained from purified cyt a,a3. The characteristics of the averaged reaction spectrum in the interval 590 nm to 610 nm indicate that hemoglobin/myoglobin contribute no more than 23% to the signal measured at 605 nm. A regimen of one 30 sec global ischemia (GI) repeated once every 3 minutes over a 90 min period showed no appreciable signal deterioration. Therefore, five such interventions were subsequently used as the test perturbation. Studies of the effects of ischemic episodes of 30 and 60 min show that the response of cyt a,a3 to this test intervention was smaller (90 +/- 6% and 89 +/- 7%) than that observed prior to the ischemic episode. Changes in coronary perfusion pressure (+/- 10 Torr) produced an immediate oxidation/reduction of cyt a,a3. In the working heart, just prior to fibrillation, 6 sec to interrupted ventilation resulted in a continuous reduction of cyt a,a3. The data from these studies show: 1) The redox state of cyt a,a3 may be continuously monitored in the canine heart in situ. 2) Following ischemias of 30 and 60 min duration, respiratory chain function may be impaired; and 3) The well-perfused epicardium is extremely sensitive to small changes in oxygen delivery.
This study was designed to test whether use of allopurinol could improve lung preservation after 6 hours of cold storage. Thirty-two rabbits were divided into four groups (n = 8 each group): (1) the control group received no flush or storage, (2) the EC group received Euro-Collins (EC) solution for both flush and storage, (3) the Allo-F group received Euro-Collins solution with allopurinol (1 mmol/L) for both flush and storage, and (4) the Allo-R group received Euro-Collins solution to which allopurinol (1 mmol/L) was added only to the reperfused blood. For groups 2 through 4, the lungs were flushed (40 ml/kg) in situ, excised, and then stored at 4 degrees C. After storage, the lungs were reperfused for 1 hour with an in vitro blood-perfused ventilated model. Lung function was measured during reperfusion with mean pulmonary arterial pressure, end-inspiratory airway pressure, and blood gas data. The lung wet/dry weight ratio was used to measure lung edema. The lungs in the EC group had a significant increase in mean pulmonary arterial pressure, airway pressure, and wet/dry weight ratio when compared with the control group. The mean pulmonary arterial pressure in either of the groups receiving allopurinol was consistently lower than that in the EC group. The airway pressure in the Allo-R group also significantly decreased compared with the EC group.(ABSTRACT TRUNCATED AT 250 WORDS)
Fourteen donor hearts were assessed by measurement of dopamine requirement, basic hemodynamic parameters (for example, systolic blood pressure), and the left ventricular pressure-volume relationship. The latter function was measured by a combination microtipped manometer/conductance catheter placed in the left ventricle through the ascending aorta. With an isoproterenol dose 24 hours after transplantation as the measure of cardiac performance, multiple linear regression analysis indicated that the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), ventriculoarterial coupling (Ea/Ees), and myocardial ischemic time were good predictors of posttransplantation cardiac performance. Dopamine requirement and basic hemodynamic data were not. Twelve implanted hearts showed an Ea/Ees of less than 1.0 and showed good early (less than 24 hours) and late function. Two hearts considered on clinical grounds to be unsuitable for transplantation showed an Ea/Ees of more than 1.0. The data suggest that measurement of the left ventricular pressure-volume relationship would appear to be a clinically useful predictor of donor-heart performance after transplantation.
BACKGROUND: The goal of organ preservation is maintenance of physiologic functions during extended extracorporeal storage. METHODS: This study was designed to evaluate the efficacy of using low-potassium (4 mmol/L) dextran (1%) solution on lung function after 30 hours hypothermic (10 degrees C) storage and to compare this with lung function after no storage. With low-potassium dextran solution rabbit lungs were flushed (10 degrees C, 40 ml/kg, 60 cm H2O), excised, inflated (with room air), and either not stored (control; no preservation; n = 9) or stored in low-potassium dextran solution (10 degrees C) 30 hours (experimental group; n = 9). RESULTS: During the flush the infusion pressure and pulmonary vascular resistance for the two groups did not differ (17.56 +/- 1.3 versus 16.74 +/- 1.5 mm Hg/ml/sec). After either no preservation or after 30 hours of storage, the lungs were first reperfused with low-potassium dextran solution (37 degrees C) for 4 minutes and then with blood (37 degrees C) for 30 minutes at 100 ml/min. During the reperfusion period the mean pulmonary artery pressure and end-inspiratory airway pressure for the control and experimental groups did not differ. After reperfusion the wet and dry weights of the left lung were determined. The wet/dry ratio for the two groups did not differ (5.32 +/- 2.20 versus 4.70 +/- 2.70, respectively). CONCLUSIONS: These data suggest that cold flush, cold storage, and initial warm perfusion with low-potassium dextran solution crystalloid preserve lung function after 30 hours of storage.
BACKGROUND: To achieve successful lung transplantation, it is essential to minimize reperfusion injury occurring as a result of metabolite accumulation during the preservation period or at the time of initial interaction of blood with constricted pulmonary vasculature. Initial reperfusion with warm crystalloid solution may be advantageous in preventing this injury. METHODS: This study was designed to evaluate the effect of low-potassium (4 mmol/L) dextran (1%) solution as the initial warming solution after 6 hours of hypothermic storage. In 23 New Zealand White rabbits the lungs were flushed with low-potassium dextran solution (10 degrees C, 40 ml/kg, 600 cm H2O), excised, inflated with room air, and stored in a low-potassium dextran solution (10 degrees C) for 6 hours. After storage, the lungs were divided into two groups. Group 1 (n = 8) was reperfused with warm low potassium dextran for 4 minutes, at 37 degrees C followed by blood reperfusion for 30 minutes at 37 degrees C. Group II (n = 15) was reperfused only with blood for 30 minutes at 37 C. The mean pulmonary vascular resistance measured during cold flush and prior to storage was similar in both groups (group I = 20.0 +/- 5.9 mm Hg.sec/ml, group II = 19.3 +/- 1.9 mm Hg.sec/ml). RESULTS: During reperfusion, only 4 of the 15 lungs in group II maintained an acceptable (< 80 mm Hg) mean pulmonary artery pressure; six failed immediately. All eight lungs in group I completed the 30-minute reperfusion (p < 0.005). The mean pulmonary artery pressure was significantly less, and effluent oxygen tension was significantly greater in group I during reperfusion. CONCLUSIONS: In this experimental model, initial warm reperfusion with low-potassium dextran ameliorated the deleterious effects of reperfusion, thus providing an environment to improve lung preservation.