Renal and cardiac function during alpha1-beta-blockade in congestive heart failure.

UNLABELLED: The kidney and the neurohormonal systems are essential in the pathogenesis of congestive heart failure (CHF) and the physiologic response. Routine treatment of moderate to severe CHF consists of diuretics, angiotensin-converting enzyme (ACE) inhibition and beta-blockade. The need for control of renal function during initiation of ACE-inhibition in patients with CHF is well known. The aim of this study was to investigate whether supplementation by a combined alpha1-beta-blockade to diuretics and ACE-inhibition might improve cardiac function without reducing renal function. METHODS: Fourteen patients treated for moderate to severe CHF with diuretics and ACE inhibitors were investigated at baseline, after 4 months of maximum carvedilol treatment and after withdrawal of carvedilol. RESULTS: Carvedilol lowered blood pressure and heart rate but increased left and right ventricular ejection fractions without changing cardiac output or pulmonary blood volume. At the same time, a minor fall was seen in glomerular filtration rate (GFR). but renal blood flow was unchanged and effective renal plasma flow slightly increased. Carvedilol also lowered the plasma levels of angiotensin II and aldosterone. All changes were reversed after withdrawal of carvedilol. CONCLUSIONS: Carvedilol augments ACE-inhibitor-induced vasodilation by lowering blood pressure, and angiotensin II beside reducing heart rate. The heart adapts to the haemodynamic alterations without changes in cardiac output and pulmonary blood volume. GFR is slightly lowered despite no changes in renal blood flow and a slight increase in effective renal plasma flow. The study emphasizes the need for control of renal function during treatment with carvedilol in patients with CHF.

Characteristics of resistance vessels in pre-eclampsia and normotensive pregnancy.

Isolated omental resistance vessels from women with pre-eclampsia had an increased media thickness/lumen diameter ratio compared to similar vessels from normotensive pregnant women. The active and passive tension length curves for the two groups of vessels were similar and like the classical tension length curve for skeletal muscles. The maximal media stress (force per media cross-section) was also similar; however, calculating in terms of equivalent pressure (on basis of Laplaces law) indicated that the vessels in vivo would have been able to contract against an increased blood pressure. The results indicate that pre-eclampsia is associated with structural alterations of the resistance vessels which might be of importance for the haemodynamics of pre-eclampsia.