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Analysis of the chemical events and their interrelationships with alterations in ECG during respiratory acidosis and alkalosis
144
Southern
Society for Clinical Research
insipidus have been compared with those values observed during various constant rates of infusion of pitressin,@ in healthy young adult males. A positive balance of water of approximately 1 L. was maintained throughout each study. At relatively constant rates of solute excretion, the changes in the rates of excretion of urine (AV) and clearance of free water (AC,,,) are approximately equal and represent the increased rate of renal reabsorption *of water resulting from the administered pitressin. At rates of infusion of pitressin between one and twenty milli-units per hour, the increase in rate of renal tubular reabsorption of water appears to vary as an exponential function of the rate of administration of pitressin according to the equation: ACazo = 2.7 (pitressin rate)0.62. Although not yet established unequivocally, the generality of this or a similar relationship is suggested by the high degree of statistical significance with which the data fit this equation. It is inferred that, in the range studied, the increase in renal tubular reabsorption of water promoted by pitressin is approximately a function of the square root of the rate of administration of pitressin. ABSORPTION,TRANSPORTAND EXCRETIONOFCUDS IN THE NORMAL HUMAN AND IN PATIENTS WITH WILSON’S DISEASE. W. N. Jensen and H. Kamin (introduced by T. B. Schwartz. *) Depts. of Medicine and Biochemistry, Duke Univ. School of Medicine, and V. A. Hospital, Durham, N. C. Non-isotopic copper studies have shown that there is a constant increase in brain and liver hypocupremia and hypercontent, copper cupuria in Wilson’s disease. CLIMBwas administered orally to four normal subjects and three patients with Wilson’s disease. Radiocopper content of blood, plasma, urine and feces was measured over a sixty-hour period. All normals had an initial peak of plasma non-globulin-bound radiocopper, a decline during the next six to eight hours; followed by a second, progressive increase present during the remainder of the study. The secondary rise consists of globulin-bound radiocopper. In Wilson’s disease there was no secondary rise in total plasma or globulin-bound radiocopper. Urinary excretion correlated with the increased plasma non-globulin radiocopper. Fecal excretion of radiocopper was decreased. It is suggested that copper is transported from
the intestine to the liver; incorporated into a copper-globulin complex and released to the plasma. The initial peak of non-globulin-radiocopper represents leakage around the copperglobulin binding mechanisms when these are presented with increased quantities of copper. One defect in Wilson’s disease consists of a metabolic block at the copper globulin synthesis in and/or release stage. Other abnormalities copper metabolism may be secondary to this defect. ANALYSIS OF THE CHEMICAL EVENTS AND THEIR INTERRELATIONSHIPS WITH ALTERATIONSIN ECG DURING RESPIRATORYACIDOSISAND ALKALOSIS. S. B. Joyner, D. A. Davis, D. T. Young, E. Craige and L. G. Welt. * Univ. of North Carolina School of Medicine, Chapel Hill, N. C. The chemical alterations induced by respiring high concentrations of COZ, and hyperventilation with room air, have been studied in three groups of dogs as follows: (1) simultaneous arterial and central venous blood, (2) simultaneous arterial, peripheral and hepatic venous blood, and (3) arterial blood samples in experiments conducted forty-eight hours following nephrectomy and injection with inulin. The effects of hypercapnia are: decrease in pH, increase in pCO*, increase in inulin space, and an accession of sodium, potassium, glucose and phosphorus to the inulin space. The increment of sodium and potassium appears to be derived from the muscles, glucose from the liver (splanchnic area), and phosphorus from both. Hyperventilation promotes: an increase in pH, and a decrease in pCO*, an increase in the inulin space is again observed, and larger increments of sodium and potassium, with smaller accessions of glucose, and inconstant increments of phosphorus to the inulin space. Sodium appears to leave muscle and liver, potassium is lost from liver but gained by muscle. The liver releases glucose, and both liver and muscle release phosphorus. The alterations in the ECG are not consistently predictable in terms of pH, pC0~ or the concentrations of potassium in serum. RENAL SODIUM REGULATION: A COMPARISONOF THE EFFECT OF RECUMBENCY AND NECK COMPRESSION. G. A. Kelser, Jr., H. L. klar, E. H. Estes, Jr. and J. V. Warren. * Dept. of Medicine, Duke Univ. School of Medicine, and V. A: Hospital, Durham, N. C. AMERICAN
JOURNAL
OF
MEDICINE
Southern
Society for Clinical Research
insipidus have been compared with those values observed during various constant rates of infusion of pitressin,@ in healthy young adult males. A positive balance of water of approximately 1 L. was maintained throughout each study. At relatively constant rates of solute excretion, the changes in the rates of excretion of urine (AV) and clearance of free water (AC,,,) are approximately equal and represent the increased rate of renal reabsorption *of water resulting from the administered pitressin. At rates of infusion of pitressin between one and twenty milli-units per hour, the increase in rate of renal tubular reabsorption of water appears to vary as an exponential function of the rate of administration of pitressin according to the equation: ACazo = 2.7 (pitressin rate)0.62. Although not yet established unequivocally, the generality of this or a similar relationship is suggested by the high degree of statistical significance with which the data fit this equation. It is inferred that, in the range studied, the increase in renal tubular reabsorption of water promoted by pitressin is approximately a function of the square root of the rate of administration of pitressin. ABSORPTION,TRANSPORTAND EXCRETIONOFCUDS IN THE NORMAL HUMAN AND IN PATIENTS WITH WILSON’S DISEASE. W. N. Jensen and H. Kamin (introduced by T. B. Schwartz. *) Depts. of Medicine and Biochemistry, Duke Univ. School of Medicine, and V. A. Hospital, Durham, N. C. Non-isotopic copper studies have shown that there is a constant increase in brain and liver hypocupremia and hypercontent, copper cupuria in Wilson’s disease. CLIMBwas administered orally to four normal subjects and three patients with Wilson’s disease. Radiocopper content of blood, plasma, urine and feces was measured over a sixty-hour period. All normals had an initial peak of plasma non-globulin-bound radiocopper, a decline during the next six to eight hours; followed by a second, progressive increase present during the remainder of the study. The secondary rise consists of globulin-bound radiocopper. In Wilson’s disease there was no secondary rise in total plasma or globulin-bound radiocopper. Urinary excretion correlated with the increased plasma non-globulin radiocopper. Fecal excretion of radiocopper was decreased. It is suggested that copper is transported from
the intestine to the liver; incorporated into a copper-globulin complex and released to the plasma. The initial peak of non-globulin-radiocopper represents leakage around the copperglobulin binding mechanisms when these are presented with increased quantities of copper. One defect in Wilson’s disease consists of a metabolic block at the copper globulin synthesis in and/or release stage. Other abnormalities copper metabolism may be secondary to this defect. ANALYSIS OF THE CHEMICAL EVENTS AND THEIR INTERRELATIONSHIPS WITH ALTERATIONSIN ECG DURING RESPIRATORYACIDOSISAND ALKALOSIS. S. B. Joyner, D. A. Davis, D. T. Young, E. Craige and L. G. Welt. * Univ. of North Carolina School of Medicine, Chapel Hill, N. C. The chemical alterations induced by respiring high concentrations of COZ, and hyperventilation with room air, have been studied in three groups of dogs as follows: (1) simultaneous arterial and central venous blood, (2) simultaneous arterial, peripheral and hepatic venous blood, and (3) arterial blood samples in experiments conducted forty-eight hours following nephrectomy and injection with inulin. The effects of hypercapnia are: decrease in pH, increase in pCO*, increase in inulin space, and an accession of sodium, potassium, glucose and phosphorus to the inulin space. The increment of sodium and potassium appears to be derived from the muscles, glucose from the liver (splanchnic area), and phosphorus from both. Hyperventilation promotes: an increase in pH, and a decrease in pCO*, an increase in the inulin space is again observed, and larger increments of sodium and potassium, with smaller accessions of glucose, and inconstant increments of phosphorus to the inulin space. Sodium appears to leave muscle and liver, potassium is lost from liver but gained by muscle. The liver releases glucose, and both liver and muscle release phosphorus. The alterations in the ECG are not consistently predictable in terms of pH, pC0~ or the concentrations of potassium in serum. RENAL SODIUM REGULATION: A COMPARISONOF THE EFFECT OF RECUMBENCY AND NECK COMPRESSION. G. A. Kelser, Jr., H. L. klar, E. H. Estes, Jr. and J. V. Warren. * Dept. of Medicine, Duke Univ. School of Medicine, and V. A: Hospital, Durham, N. C. AMERICAN
JOURNAL
OF
MEDICINE