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Reperfusion of acutely ischemic myocardium results in deficient energy production and abnormal Ca2+deposition. This study evaluates mitochondrial energy production in ishemic reperfused myocardium following an in vivo infusion of a Ca2+antagonist, ruthenium red. Results are summarized as follows: (1) In vivo infusion of ruthenium red increases adenosine diphosphate-induced respiration threefold and adenosine triphosphate (ATP) production fivefold compared with those mitochondria derived from myocardium which had been occluded 2 hr and reperfused 2 hr without ruthenium red. (2) Infusion of ruthenium red improves state 3 respiration and ATP production to nearly normal levels by mitochondria isolated from myocardium which had been occluded 30 min and reperfused 2 hr. However, mitochondrial respiration and ATP production from nonischemic myocardium are not altered by in vivo ruthenium red infusion. (3) Ruthenium red infusion decreases both tissue and mitochondrial Ca2+content in ischemic-reperfused myocardium. (4) The partial improvement in energy production in ischemic-reperfused myocardium by ruthenium red is probably related to a decrease in intracellular Ca2+concentration.

It has been documented that biogenic amines can stimulate Na,K-ATPase from various tissue preparations. However, it is unclear whether or not this stimulation occurs in myocardial tissues. We have evaluated possible catecholamine stimulation of purified Na,K-ATPase preparations utilizing a bovine ventricular microsomal preparation. We have studied the dose response of the enzyme to ouabain and digitoxigenin in the presence and absence of propranolol and norepinephrine. Our results indicate that propranolol increases the sensitivity of Na,K-ATPase to inhibition by digitalis, and that stimulation of Na,K-ATPase in bovine myocardium is not mediated via an adrenergic mechanism. In addition, our results indicate that in myocardial tissue, both stereoisomers of propranolol produce a direct, nonspecific membrane effect which can modify Na, K-ATPase activity.

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus.(Arch Intern Med 139:86-88, 1979)