Phenylephrine-induced hyperkalemia: role of the liver.
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Biomedical subjects
Publications and source records attributed to R L Vick.
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Other investigators have shown that infusion of glucagon causes the concentration of potassium, [K+], in the arterial plasma to increase rapidly, then to decrease to less than the beginning value. In studies on anesthetized dogs, we found that the magnitude of the initial, rapid rise of [K+] was increased by nephrectomy but not affected by pancreatectomy. The subsequent decline of [K+] and the persistent hypokalemia were not affected significantly by nephrectomy. Plasma [K+] decreased in the nephrectomized-pancreatectomized dogs, as it did in the nephrectomized and the control groups, but the effect was temporary, and [K+] began to increase again, even though the infusion of glucagon continued; after the infusion was ended, plasma [K+] became significantly higher than the beginning value. These data suggest that the hypokalemia caused by infusion of glucagon initally depends on extrarenal factors other than insulin, and, later, depends on insulin.
The isolated left lower lobes of 15 dogs' lungs were perfused by means of a roller pump with blood at hematocrit values ranging from 31 to 80 per cent. Pressure-flow curves were constructed at blood flow rates from one half to three times the normal flow for the left lower lobe at each hematocrit level. The perfusion pressure was normalized with reference to the normal hematocrit(38 to 48 per cent) and normal blood flow for the left lower lobe (20 ml. per kilogram per minute). From these normalized pressure-flow curves, normalized resistance-flow curves were constructed at different mean hematocrit levels. Regression lines were drawn relating normalized pulmonary vascular resistance to hematocrit at different rates of pulmonary blood flow which might be found in patients with congenital heart disease. It was found that pulmonary vascular resistance rose in an exponential fashion as the hematocrit was increased, and that the blood viscosity determined both the shape of the resistance-flow curve and magnitude of the increase in resistance to pulmonary blood flow, especially when the pulmonary blood flow was less than normal and the hematocrit was greater than 54 per cent. The family of regression lines relating pulmonary vascular resistance to hematocrit at different flow rates may be used clinically in patients with congenital heart disease and polycythemia to determine if an elevated pulmonary vascular resistance is due to increased blood viscosity or obstructive pulmonary vascular disease. It is concluded that an increased blood viscosity due to polycythemia significantly alters the pulmonary hemodynamics of patients with congenital heart disease with either increased or decreased pulmonary blood flow. Increased blood viscosity may play an important part in the early initiation and development of pulmonary arteriosclerosis in patients with transposition of the great arteries.
Potassium chloride was administered by constant, intravenous infusion in splenectomized, but otherwise normal, dogs. The concentration of potassium, [K+], and of insulin, [insulin], in the arterial plasma was measured at frequent intervals. To assess the relative contributions of extrarenal and renal mechanisms toward the maintenance of normal plasma [K+], the results were compared with data obtained previously in splenectomized, nephrectomized dogs. During the infusion, plasma [K+] increased in the dogs with kidneys intact at a mean rate slightly less than that in the nephrectomized dogs. After the infusion was stopped, plasma [K+] declined to about 0.75 meq/liter above control values in both groups of animals. The results indicate the operation of both renal and extrarenal homoeostatic mechanisms. The renal mechanisms contributed measurably during the infusion of KCl, but not immediately after the infusion was stopped. Simultaneous measurements of plasma [K+] and plasma [insulin] indicate that insulin may be involved in the extrarenal homeostatic response.
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