Clinical evidence suggests that vascular damage plays a key role in the pathophysiology of dengue hemorrhagic fever (DHF). In this study, the authors tested this hypothesis by examining the levels of soluble intercellular adhesion molecule and vascular cell adhesion molecule (sICAM-1 and sVCAM-1), and the presence of circulating endothelial cells (CECs), as evidence of vascular damage, in peripheral blood from DHF patients (n=13). A significant increase in plasma levels of sICAM-1 (n=12) and sVCAM-1 (n=13) was detected by enzyme-linked immunosorbent assay (ELISA) in DHF patients, compared with healthy individuals. Increased numbers of CECs, as detected by the expression of endothelial cell markers (ICAM-1, platelet cell adhesion molecule [PCAM]-1, and CD36) with flow cytometry, were observed in DHF patients (n=4), compared to healthy subjects. The high levels of sICAM-1 and sVCAM-1, together with the presence of CECs in DHF patients, provide further evidence of endothelium damage and activation in DHF patients.

The present study was designed to evaluate the renal haemodynamic pattern of never-treated microalbuminuric and normoalbuminuric patients with essential hypertension. A total of 19 never-treated essential hypertensive patients with microalbuminuria were selected and, as control subjects, 24 never-treated essential hypertensive patients without microalbuminuria (determined on three 24-h urine collections) were recruited. In the two groups, we compared blood pressure values, standing plasma noradrenaline, plasma renin activity, plasma aldosterone, urinary aldosterone, lipid profile, serum glucose and uric acid, glomerular filtration rate and renal plasma flow. In comparison with normoalbuminuric patients, microalbuminuric patients showed significantly higher systolic blood pressure values (P < 0.05), higher renal vascular resistances (P < 0.05) and lower plasma renin activity values (P < 0.01). Urinary albumin excretion showed a significant positive correlation with systolic (r = 0.46, P < 0.005) and mean blood pressure (r = 0.38, P < 0.05), serum uric acid (r = 0.43, P < 0.005) and triglyceride values (r = 0.36, P < 0.005), and a significant negative correlation with plasma renin activity (r = -0.34, P < 0.05). The present data are consistent with the occurrence of renal vasoconstriction in microalbuminuric never-treated essential hypertensive patients.

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To evaluate the acute hemodynamic, both systemic and renal, and humoral effect of three increasing doses of Iloprost, a prostacyclin analogue, eight uncomplicated untreated hospitalized patients with mild to moderate essential hypertension, while on a constant sodium and potassium intake, received, after oral hydration, three doses of Iloprost (1,2 or 4 ng/kg/body weight for 45 min) in a single-blind randomized sequence. Each dose was preceded by placebo (saline infusion for 45 min) with a 48 h interval between each study. Iloprost significantly (P less than .05) reduced blood pressure, and increased heart rate, filtered sodium, urinary sodium excretion, fractional sodium excretion, noradrenaline, adrenaline, and plasma renin activity (PRA). The blood pressure lowering effect as well as the heart rate, renal plasma flow and noradrenaline increases were significantly greater on the 4 ng dose. Glomerular filtration rate and adrenaline showed a dose-dependent increase; urinary sodium excretion and fractional sodium excretion were similarly increased by the three doses. No correlation was found between urinary sodium excretion and either glomerular filtration rate or renal plasma flow. The data obtained indicate that Iloprost causes reduction of blood pressure with a reflex activation in the sympathetic nervous system and stimulation of renin secretion, renal vasodilation mainly at the level of the afferent arteriole, and natriuresis. This latter effect is probably due to a direct inhibition of tubular reabsorption, which, at variance with the other effects, is dose-independent.