The American journal of physiology
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The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. ⋯ Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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Preconditioning myocardium with brief episodes of ischemia reduces energy demand and delays cell death during a subsequent ischemic episode. We hypothesized that postischemic contractile dysfunction after the brief ischemic episodes ("stunning") causes this reduced energy demand. If this hypothesis is correct, then cardioprotection should persist as long as mechanical function still is depressed at the onset of sustained ischemia. ⋯ Despite persistently severe stunning in the 120-min reflow group, infarct size was intermediate, averaging 12.3 +/- 2.7% (P less than 0.05 vs. 5-min reflow; P less than 0.01 vs. control), and the infarct vs. flow regression had returned toward control. Thus the cardioprotective effect of preconditioning was attenuated when the intervening reperfusion time was extended, even though severe contractile dysfunction persisted. We conclude that myocardial stunning, per se, is insufficient to cause preconditioning.
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Cardiac fibroblasts synthesize large amounts of procollagens, yet only a small fraction of mature collagens accumulate in the extracellular matrix. To determine the roles of intracellular degradation of newly synthesized procollagens and extracellular degradation of mature collagens during normal growth and during thyroxine-induced left ventricular hypertrophy, in vivo left ventricular procollagen synthetic rates were assessed in control rats and rats treated with L-thyroxine for 1, 2, 4, and 8 wk (1 mg.kg-1.day-1). A modification of the flooding infusion method was developed using measurements of cardiac prolyl-tRNA, and tissue-free and protein-bound hydroxyproline specific radioactivities 60 min after intravenous administration of a massive dose of [3H]proline. ⋯ Despite increased procollagen synthesis, disproportionate accumulation of fibrillar collagens (assessed as the relative concentration of protein-bound hydroxyproline in left ventricular tissue) did not occur. Derived left ventricular degradative rates for newly synthesized procollagens as well as for mature collagens were increased in thyroxine-treated animals. Increased procollagen synthesis, enhanced flux of newly synthesized procollagens through intracellular degradative pathways, and extensive extracellular matrix remodeling without disproportionate collagen accumulation are characteristics of this form of "physiological" left ventricular hypertrophy.
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Although a four-wavelength method for cryospectrophotometric measurement of intravascular oxyhemoglobin (HbO2) saturations has previously been described, the relationship between experimental measurements and theory has not been clearly detailed. The current work utilizes an empirical relationship between HbO2 saturation measurements and reflected light oximetry, which is consistent with the two-flux theory of Kubelka and Munk (Z. Tech. ⋯ Therefore, equibestic wave-length pairs were used at which optical density differences were invariant with saturation. This allows numerous wavelength sets over the range 540-600 nm to be selected, rather than the limited choices of isosbestic wavelengths. Finally, the effects of freeze rate, freeze depth, Hb concentration, and vessel diameter are each discussed in terms of their influence on experimental measurements.
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Sequential 31P nuclear magnetic resonance (NMR) spectra were measured in adult dogs to determine the relationship between cardiac function and myocardial intracellular pH (pHi) and phosphorylated energy metabolites during 2 h of hemorrhagic shock. Simultaneous measurements of coronary blood flow (radioactive microspheres), arterial and coronary sinus pH, blood gases, and oxygen content were performed. ⋯ Return of shed blood and crystalloid fluid resuscitation improved cerebral and coronary perfusion and returned cardiac contractile function to near baseline values. We conclude that severe and sustained hemorrhagic shock produced significant alterations in brain and heart phosphorylated metabolites as well as significant intracellular acidosis; however, these changes in energy metabolites were reversible with adequate fluid resuscitation from shock.