The Journal of clinical investigation
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Hemodynamics and myocardial metabolism were evaluated in 18 patients in cardiogenic shock following acute myocardial infarction. The response to l-norepinephrine was studied in seven cases and the response to isoproterenol in four cases. Cardiac index (CI) was markedly reduced, averaging 1.35 liters/min per m(2). ⋯ Myocardial lactate metabolism deteriorated uniformly; lactate production increased or extraction shifted to production. In the acute state of coronary shock the primary therapeutic concern should be directed towards the myocardium and not towards peripheral circulation. Since forward and collateral flow through the severely diseased coronary bed depends mainly on perfusion pressure, l-norepinephrine appears to be superior to isoproterenol; phase-shift balloon pumping may be considered early when pharmacologic therapy is unsuccessful.
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The metabolism of FFA and ketone bodies was studied in fasted rats by infusing at a constant rate tracer amounts of FFA-(3)H, beta-hydroxybutyrate-(14)C or acetoacetate-(14)C for periods up to 2 hr. Blood that was removed for analyses was replaced by continuous transfusion. The rates of turnover of FFA, beta-hydroxybutyrate, and acetoacetate in rats fasted for 2 days were, respectively, 3.2, 5.6, and 2.5 mumoles/100 g body weight per min. ⋯ Insulin injection (20 mU i.v.) lowered the plasma ketone body concentration in these animals. Studies using beta-hydroxybutyrate-(14)C showed that insulin (50 mU i.v.) decreased ketogenesis in the presence of a sustained high plasma FFA concentration and had no effect on uptake of circulating ketone bodies. The results indicate that plasma FFA concentration is not the sole determinant of plasma ketone body concentration and that insulin can suppress ketone body production through some means other than lowering plasma FFA concentration.
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Measurements of gas exchange in dogs with granulomatous lung disease resembled those which have been made in similar disorders of man. The minute volume of ventilation was large, the oxygen extracted from each liter of ventilation was low, and the arterial blood oxygen saturation tended to be subnormal despite hyperventilation. ⋯ Whether the agreement of the flows is causally related to the alveolar tension remains an open question. A possible explanation may lie in the effect of alveolar tension on the oxygen consumed by the diseased lung.
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The mechanical properties of the lungs in seven patients with chronic obstructive pulmonary disease (COPD) were measured before and during dyspnea on exertion, as well as when relief with added oxygen was obtained. Mean pulmonary dynamic compliance was 0.091 liters/cm of H(2)O before dyspnea, 0.057 during dyspnea, and 0.101 liters/cm H(2)O during relief. ⋯ In five similar patients a progressive increase in the instantaneous rate of change of transpulmonary pressure (dP/dt) was observed during exercise and this was markedly increased during dyspnea. These changes in dP/dt during exercise could explain the observed fall of pulmonary dynamic compliance.
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Rats were made acutely hyper- or hyponatremic by infusion of hypertonic saline or water, respectively. Other rats were maintained in these states from 1 to 7 days to observe the effects of time. Brain tissue water, Na, Cl, and K were compared with serum Na and Cl concentration (Na(E) and Cl(E)). ⋯ These characteristics are interpreted to mean that significant quantities of Na and K in brain are osmotically inactive. The brain protects itself from acute volume changes in response to change in Na(E) by the freedom for Na and Cl to move from the Cl space, by V(i) not changing acutely to the degree predicted from osmotic properties of cells in general, and by significant quantities of Na + K in V(i) being osmotically inactive. With sustained changes in osmolality, V(i) approaches normal values and brain K changes to account for part of this later adjustment.