Intravenous hydralazine, 0.15, 0.30 or 0.60 mg/kg, was administered to 11 supine hypertensives on two occasions: once after pretreatment with intravenous propranolol, 0.1 mg/kg, and once after pretreatment with intravenous placebo. The average fall in mean arterial pressure for each dosage of hydralazine was no different with or without propranolol, even though propranolol inhibited rises in plasma renin activity and pulse due to hydralazine. However, in each of four patients who had high supine baseline plasma renin activity, propranolol enhanced the fall in blood pressure caused by hydralazine. A second group of patients was given an infusion of 0.01 or 0.02 mg/kg per minute phentolamine, which did not change baseline blood pressure. Subsequent administration of intravenous hydralazine, 0.15 mg/kg, resulted in a fall in blood pressure which was larger than previously observed with intravenous hydralazine alone, regardless of supine baseline plasma renin activity. These data are consistent with the hypothesis that reflex catecholamine release interferes with the hypotensive effect of intravenous hydralazine. Pretreating with propranolol weakens homeostatic defenses against hydralazine such as rises in pulse rate and plasma renin activity. However, propranolol appears to enhance the alpha-adrenergic effect of released catecholamines, and the antihypertensive response to hydralazine is unaltered. In patients with high supine plasma renin activity, propranolol potentiates the fall in blood pressure induced by hydralazine, perhaps because the hypertension in such patients is renin dependent.

Adult↗

PubMedDate not supplied

The effect of oxidants on biomembranes and cellular metabolism.

During the reductive process in the tissues, the aerobes generate a number of oxidants. Unless these oxidants are reduced, oxidative damage and cell death would occur. Oxidation of plasma membrane lipids leads to autocatalytic chain reactions which eventually alter the permeability of the cell. The role of oxidative damage in the pathophysiology of diabetic complications and ischemic reperfusion injury of myocardium, especially the changes in the channel activity which may lead to arrhythmia have been studied. Hyperglycemia activates aldose reductase which could efficiently reduce glucose to sorbitol in the presence of NADPH. Since NADPH is also aldose required by glutathione reductase for reducing oxidants, its diversion would lead to membrane lipid oxidation and permeability changes which are probably responsible for diabetic complications such as cataractogenesis, retinopathy, neuropathy etc. Antioxidants such as butylated hydroxy toluene (BHT) and also reductase inhibitors prevent or delay some of these complications. By using patch-clamp technique in isolated frog myocytes, we have shown that hydroxy radicals generated by ferrous sulfate and ascorbate as well as lipid peroxides such as t-butyl hydroperoxide facilitate the entry of Na+ by oxidizing Na+-channels. Increased intracellular Na+ leads to an increase in Na+/Ca2+ exchange. The increased Na+ concentration by itself may produce electrical disturbance which would result in arrhythmia. Increased Ca2+ may affect proteases and may help in the conversion of xanthine dehydrogenase to xanthine oxidase, consequently increased production of super oxide radicals. Increased membrane lipid peroxidation and other oxygen free-radical associated membrane damage in myocytes has been demonstrated.

Aldehyde Reductase↗

PubMedDate not supplied

Stratified multiphase model for blood flow in a venular bifurcation.

Available in vitro and in vivo experimental observations suggest that red cell aggregation and blood vessel geometry are important determinants of the flow characteristics of blood in venules. However, no consistent relationship has been observed between red blood cell aggregation and vascular resistance. The present work attempts to understand this relationship by evaluating computationally the effect of red cell aggregation on the flow characteristics of blood in a converging vessel bifurcation. The proposed mathematical model considers blood as a two-phase continuum, with a central core region of concentrated red cell suspension that is surrounded by a layer of plasma adjacent to the vessel wall. In the central core region, blood is described by Quemada's non-Newtonian rheological model, in which local viscosity is a function of both the local hematocrit and a structural parameter that is related to the size of red blood cell aggregates. Fluids from the two feeding branches are immiscible, which results in a stratified multiphase flow in the collecting venule. Calculations predict a complex, three-dimensional pattern of blood flow and generally nonaxisymmetric distribution of velocity, hematocrit, and shear stress in the collecting venule. The calculations are a first step toward a realistic model of blood flow in the venous microcirculation.

Erythrocyte Aggregation↗

PubMedDate not supplied

New type of cholera.

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Cholera↗

PubMedDate not supplied

Ribavirin in clinical practice.

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Child↗