The acute vascular effects of frusemide in heart failure.

Abstract

Diuretics effectively treat the sodium and water retention found in the syndrome of heart failure. When given intravenously, the loop diuretic frusemide brings about rapid symptomatic relief, an effect preceding the increase in urinary sodium and water output by up to 30 min. In 1966, Weinstein & Solis-Gil [1] reported that the use of frusemide led to symptomatic improvement shortly after its administration. They proposed that a ‘diuresis’ was occurring through the skin, as their patients did not exhibit increased urine output before the improvement was noted, but instead seemed to sweat excessively. In 1967, Biagi & Bhapat [2] put forward the hypothesis of pulmonary venous dilatation as the mechanism of frusemide's action. In 1969, Bhatia et al. [3] studied this hypothesis by administering intravenous frusemide to patients with altitude induced pulmonary oedema. Yet it was not until the study by Dikshit et al. [4] in 1973 that this beneficial effect was shown to be due to the dilatation of peripheral capacitance vessels. Since these early case reports and studies, the events preceding diuresis after frusemide administration have been widely studied. A venodilatory response has been reproduced with and without success. Any such effect is widely believed to occur due to the release of prostaglandins by the veins. The effect of frusemide on veins has been shown to be mostly an indirect one, but frusemide may also display direct venodilator properties.