Henry O. Heinemann
York University
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Featured researches published by Henry O. Heinemann.
The American Journal of Medicine | 1959
Henry O. Heinemann; Felix E. Demartini; John H. Laragh
Abstract Chlorothiazide was given intravenously to a group of normal human subjects and to one patient with diabetes insipidus, and its effects on renal function were compared with those of meralluride administered under similar circumstances. Following the administration of chlorothiazide, the urine flow and solute output increased but the free water clearance did not increase. Administration of meralluride was followed by a comparable increase in urine flow, a lesser rise in solute output, and an increased excretion of free water. Chlorothiazide produced a considerably greater increase in solute (sodium chloride) excretion than did meralluride. This difference was particularly evident in a sodium-depleted subject. The natriuretic effects of Chlorothiazide occurred despite an average reduction in the glomerular filtration rate of 16.9 per cent. Chlorothiazide also promoted the excretion of potassium, whereas meralluride had little effect on potassium excretion. When given together, the response to meralluride and chlorothiazide appeared to be additive in respect to total solute excretion. However, the potassium diuresis of chlorothiazide was prevented by previous administration of a mercurial agent. The findings perhaps suggest the presence of more than one renal transport mechanism concerned with the reabsorption of strong monovalent electrolytes. The observations can be explained by the hypothesis that meralluride acts only in the proximal tubule, while chlorothiazide affects solute (sodium and chloride) reabsorption both in the proximal and in the distal segments of the nephron.
Annals of Internal Medicine | 1970
Franco M. Muggia; Henry O. Heinemann
Abstract Hypercalcemia frequently complicates the course of patients with neoplastic disease. The clinical manifestations of this electrolyte imbalance may overshadow those of the underlying disord...
The American Journal of Medicine | 1971
Roberta M. Goldring; Gerard M. Turino; Henry O. Heinemann
Abstract In patients with stable mechanical ventilatory limitation and chronic hypercapnia, chloride depletion by administration of diuretics leads to elevations in extracellular bicarbonate levels which are inordinate for the carbon dioxide tension (PaCO 2 ). Chloride replacement returns this bicarbonate-PaCo 2 relationship o a predicted level. Ammonium chloride induces an inordinate reduction in extracellular bicarbonate concentrations for the levels of PaCO 2 in arterial blood. The ventilatory responsiveness to inhalation of 5 per cent carbon dioxide following these interventions is related exponentially to the extracellular bicarbonate concentration and not to the level of extracellular hydrogen ion activity measured prior to carbon dioxide inhalation. However, the increase in ventilation per unit increment in extracellular hydrogen ion activity induced by carbon dioxide inhalation (ΔVEΔH+) is constant. This suggests that the extracellular bicarbonate concentration acts to modulate the ventilatory response to stimulation with carbon dioxide whereas the changes in hydrogen ion activity during carbon dioxide inhalation act as the determinants of the ventilatory response to inhaled carbon dioxide.
The American Journal of Medicine | 1974
Gerard M. Turino; Roberta M. Goldring; Henry O. Heinemann
Abstract Alkalosis in hypercapneic patients caused by abrupt respirator-induced reduction of the partial pressure of carbon dioxide leads to bicarbonate diuresis. Potassium is the predominant cation accompanying bicarbonate loss in the urine. The determining variable for induction of proportional changes in renal bicarbonate and potassium excretion is the partial pressure of carbon dioxide. The reduction of the partial pressure of carbon dioxide modifies bicarbonate regeneration directly by limiting the hydration reaction and facilitates potassium loss indirectly by reducing extracellular, and by inference intracellular, hydrogen ion activity.
Annals of Internal Medicine | 1966
Henry O. Heinemann; John H. Laragh
Excerpt Sodium balance is normally regulated by the interaction of the kidneys, the adrenal cortex, and one or several additional regulatory mechanisms, at present poorly defined (1-3). Excessive r...
Annals of Internal Medicine | 1966
Henry O. Heinemann; Sue Buckingham; Sheldon C. Sommers
Excerpt It is now apparent that the mammalian lung is not solely concerned with the physical-chemical process of gas exchange but has other, nonrespiratory, functions. One of these functions, which...
JAMA | 1958
John H. Laragh; Henry O. Heinemann; Felix E. Demartini
The American Journal of Medicine | 1977
Henry O. Heinemann
The American Journal of Medicine | 1974
Henry O. Heinemann; Roberta M. Goldring
The American Journal of Medicine | 1976
Henry O. Heinemann; James B. Lee