In vitro influence of biologic components of ischemia on canine cardiac mitochondrial oxidative phosphorylative abilities

In vitro influence of biologic components of ischemia on canine cardiac mitochondrial oxidative phosphorylative abilities

64 IN VITRO INFLUENCE OF BIOLOGIC COMPONENTS OF ISCHEMIA ON CANINE CARDIAC MITOCHONDRIAL OXIDATIVE PHOSPHORYLATIVE ABILITIES. A. Mukherjee, T.M. Wong,...

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64 IN VITRO INFLUENCE OF BIOLOGIC COMPONENTS OF ISCHEMIA ON CANINE CARDIAC MITOCHONDRIAL OXIDATIVE PHOSPHORYLATIVE ABILITIES. A. Mukherjee, T.M. Wong, L. M. Buja, and J. T. Willerson. Departments of Medicine and Pathology. University of Texas Health Science Center, Dallas, TX. The influence of certain biological components of the ischemic process on --in vitro mitochondrial (M) oxidative phosphorylation (OP) has been Specifically, OP of isolated canine myocardial M has been evalstudied. uated after exposure to different concentrations of phosphate (5-50 mM), lactate ion in excess (40 mM, pH 7.4), calcium (50-200 WM), lactic acidosis (pH 6.3) and to M protein dilution "edema") for 10 minutes --(in vitro to 8 hours. The influence of phosphate and lactate ion addition, lactic acidosis and --in vitro volume expansion on M function were studied in the isolation medium (0.18 M KCl, 0.5% BSA with or without Tris EDTA, pH 7.4) prior to evaluation of M function in the assay medium (0.25 M sucrose, 10 mM Tris HCl and 10 mM inorganic phosphate, pH 7.4). The effect of calThe results of these cium addition was assessed in the assay medium. studies demonstrate that each of these interventions detrimentally alter OP ability. The M functional alterations resulting from these intervenbut the detrimental effect of phostions persisted after their removal, phate addition and --in vitro volume expansion was partially corrected by the addition of cytochrome C. The data obtained are consistent with the possibility that each of these biological components of the ischemic process is capable of altering M function of myocardial cells but suggest that phosphate and calcium ion accumulation exert.the most important detrimental effect (40% or greater) on OP in isolated M.

CARDIAC RESPONSE To ORTHOSTASIS UNDER ALTITUDE STRESS. W.S. Murthy, R.K. Saxena, N. Krishnamurthy and H.S. Napar. Defence Institute of Physiology and Allied Sciences, Delhi Cantt., India. The study has been conducted on 40 healthy soldiers, between the age of 2D - 30 years, to evaluate the effect of altitude adaptation on the cardiac responses to orthostasis. Of these 40 soldiers, 10 were lowlanders (LL), 10 were high altitude natives who were brought to the plains during the study (HAN-I) and 10 were HAN who had never been to plains (HAN-II). The cardiac responses to orthostasis were assessed by monitoring heart rate (HR) electrocardiogram (ECG) and blood pressure before, during and after 15 minute period of 70" head-up passive tilt. The sea level studies were conducted at Delhi (260 m alt) in LL and Hani, and thereafter these subjects were airlifted to an altitude of 3500 meters in Western Himalayas where further studies were conducted for a period of 5 weeks. For comparison, these responses were also measured in AL and HAN-II. The LL showed orthostatic intolerance in the initial phase of induction to high altitude due to transient cardiac insufficiency as manifested by a fall in systolic B.P. attenuation of cardio-acceleration, reduction in the voltage of QNS complex and T-wave, depression of STsegment, and also due to poor vasoconstrictor response. A few subjects showed inversion of T-wave. There was 30% of cases showing syncope during tilt.