The American journal of physiology
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The intracellular supply of O2 to mitochondria was studied in single-cell suspensions of rat hepatocytes by measuring the O2 dependence of oxidation of cytochromes. Values were obtained by adding standardized O2-containing solutions to anaerobic cell suspensions and observing absorbance changes at wavelength pairs specific for cytochromes a + a3, c + c1, and b561 + b566. ⋯ Analysis of these data indicate that the diffusion coefficient in the region of mitochondria in situ is considerably smaller than the extracellular diffusion coefficient and suggests that a significant O2 gradient in the vicinity of mitochondria occurs under hypoxic conditions. These results suggest that the rate of O2 diffusion may be a critical factor for intracellular O2 supply to mitochondria during hypoxia.
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Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 mueq.cm-2.h-1. OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3(-)-free nutrient solution. In Na+ solutions, increasing nutrient, [HCO3(-)] augmented OH- and Isc linearly while resistance (R) decreased. ⋯ In the absence of secretory Cl-, OH- and Isc were linearly related to varying nutrient [Cl-]. In tissues with nutrient solutions on the secretory side and vice versa, apparent OH- was 0.4-0.5 mueq.cm-1.h-1 and was dependent on secretory [HCO3(-)] but was not affected by DNP, DIDS, or replacement of Cl- on secretory or nutrient solutions. We conclude that 1) OH- secretion is dependent on nutrient HCO3(-) and Na+ and oxidative metabolism, 2) endogenous HCO3(-) does not contribute significantly, and 3) adequate tissue Cl- must be present for normal OH-.
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Monocrotaline, a pyrrolizidine alkaloid derived from Crotalaria spectabilis, is known to be toxic to a variety of domestic and laboratory animals and to humans. Major pathological effects induced by monocrotaline poisoning include hepatic cirrhosis and megalocytosis, venocclusive disease, pulmonary hypertension, and right ventricular hypertrophy. The present investigation explored the structural and functional relationships that exist between pulmonary artery pressure, small pulmonary artery medial thickness, and right ventricular hypertrophy. The results of this physiological and histological study on monocrotaline-intoxicated rats has demonstrated that there is a positive correlation between progressive pulmonary hypertension, thickening of the medical wall of small pulmonary vessels, and right ventricular hypertrophy as a function of time.