The Journal of clinical investigation
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Most patients with stable cirrhosis of the alcoholic have "target" red cells; however, a minority have "spur" cells and severe hemolytic anemia. These two syndromes were studied in 27 patients with target cells and 17 patients with spur cells, all of whom had advanced cirrhosis. The cholesterol and phospholipid content of red cell membranes effectively distinguished target cells from spur cells. ⋯ Lecithin: cholesterol acyltransferase (LCAT) activity was decreased in most patients with target cells and spur cells; however, the relationship between this activity and the lipid abnormalities observed was weak. Serum bile acid levels also correlated poorly with serum and cell lipids. However, in patients with target cells the amount of cholic and deoxycholic acids in serum was approximately equal to the amount of chenodeoxycholic acid, whereas in patients with spur cells chenodeoxycholic acid (the precursor of lithocholic acid) predominated.
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When physiological dead space (Vd(p)) is calculated for a patient who has alveolar dead space, e.g., after pulmonary vascular occlusion, less than the full volume of attached mechanical dead space (Vd(m)) appears in the measured dead space (Vd(n)). Under these conditions the traditional subtraction of Vd(m) from Vd(n) leads to underestimation of Vd(p) and can give a falsely small ratio of Vd(p) to tidal volume (Vt) when, in fact, an abnormally large Vd(p)/Vt exists. To make the proper correction for Vd(m), two equations have been derived and validated with seven subjects having Vd(p)/Vt from 0.29 to 0.87, using Vd(m)'s from 120 to 322 ml. ⋯ The fraction of Vd(m) subtracted from Vd(n) is the square of the ratio of effective alveolar to total alveolar ventilation and is never > 1. This fraction is (Pa(CO2)/Pa(CO2))(2), where Pa(CO2) and Pa(CO2) are the mean partial pressures of expired alveolar and of arterial CO(2); in the other equation this fraction is [Pe(CO2)/Pa(CO2) (Vt - Vd(an) - Vd(m))](2) where Pe(CO2) is mixed expired Pco(2) and Vd(an) is anatomical dead space. The second equation requires an estimated Vd(an) and is applicable when Pa(CO2) is not measured or does not plateau (as in exercise).
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In 10 patients with severe, acute respiratory failure we studied the effects of positive end-expiratory pressure when intermittent positive pressure ventilation (IPPV) with inspired oxygen (F(IO2)) up to 0.5 failed to maintain arterial oxygen tension (P(aO2)) above 70 torr. Positive end-expiratory pressures (PEEP) of 0, 5, 10, and 15 cm H(2)O were applied for 30-min periods each and in random order. Blood gas exchange, lung volumes, compliance, and hemodynamics were studied at each level of PEEP. ⋯ Dynamic lung compliance decreased progressively with rising levels of PEEP except for an increase with 5 and 10 cm H(2)O PEEP in patients with initial values of 0.06 liter/cm H(2)O or higher. Cardiac index fell in some patients and rose in others and there was no correlation of mean cardiac index, systemic blood pressure, or peripheral vascular resistance with level of PEEP. The most probable explanation for the effect of PEEP on P(aO2) and compliance is recruitment of gas exchange airspaces and prevention of terminal airway closure.
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The present study was undertaken to examine whether the beta adrenergic agonist, isoproterenol, increases plasma renin activity (PRA) by activation of intrarenal or extrarenal pathways. The effects of intravenous (i.v.) and renal arterial infusion of isoproterenol on PRA and renin secretion rate (RSR) were compared in anesthetized dogs. In 12 studies in 9 dogs i.v. infusion of isoproterenol (0.009-0.018 mug/kg per min) was associated with an increase in PRA from 14.7 to 35.7 ng/ml per 3 hr (P < 0.001). ⋯ These results do not provide evidence for a role of intrarenal beta adrenergic receptors in the control of renin release and indicate that the effect of beta adrenergic stimulation with isoproterenol to increase the release of renin is mediated by an extrarenal mechanism. Since the effect of i.v. isoproterenol occurred in the absence of changes in plasma potassium concentration, renal perfusion pressure, glomerular filtration rate, renal plasma flow, and electrolyte excretion and was not abolished by renal denervation, the possibility must be considered that the effect on renin secretion is mediated by circulatory factors. The changes in systemic hemodynamics which occurred with i.v. but not renal arterial infusion of isoproterenol may be involved in the initiation of such a pathway.
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Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. ⋯ These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.