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Biomedical subjects

S G Chrysant

Publications and source records attributed to S G Chrysant.

At least 91 records · Page 5Linked to original sources
PubMed1977

Action of Nitroglycerin and amyl nitrite in labile and essential hypertension: hemodynamic differences.

Seventeen patients with labile hypertension received nitroglycerin and 18 received amyl nitrite. Twelve patients with established essential hypertension received nitroglycerin and 12 received amyl nitrite. Nitroglycerin reduced the systolic and mean arterial pressures and cardiac output in both groups, but had no effect on diastolic pressure and total peripheral resistance. Amyl nitrite decreased systolic, diastolic, and mean arterial pressures and peripheral vascular resistance and increased heart rate and cardiac output in labile hypertensives. In established hypertensive patients, amyl nitrite decreased systolic, diastolic, and mean arterial pressures and cardiac output, and had little effect on peripheral vascular resistance. Nitroglycerin reduced arterial pressure in labile and established hypertensives through venodilation and peripheral venous pooling. Amyl nitrite and effects similar to nitroglycerin in established hypertensives; in labile hypertensives it reduced arterial pressure through arterial dilation and a decrease in peripheral vascular resistance.

Adult↗
PubMed1976

Systemic and renal hemodynamic effects of bupicomide: a new vasodilator.

The systemic and renal hemodyanmic effects of bupicomide were studied in 10 male patients with uncomplicated essential hypertension of moderate severity. Bupicomide significantly reduced systolic, diastolic, and mean arterial pressure and peripheral vascular resistance and this hypotensive effect was associated with a reflexive increase in heart rate, left ventricular ejection rate, and cardiac index; it had no effect upon other reflexive sympathetic adjustments induced by upright tilt and the Valsalva maneuver. Bupicomide also increased renal blood flow and decreased renal vascular resistance, but it had no effect upon the glomerular filtration rate. The hypotensive mechanism of bupicomide therefore is mediated by peripheral arteriolar dilation, through vascular smooth muscle relaxation. The more immediate clinical side effects of bupicomide are related to its strong vasodialting action and include headaches, cutaneous flushing, and tachycardia.

Clinical Trials as Topic↗
PubMed1976

Effects of diuretics on lipid metabolism in patients with essential hypertension.

Available clinical evidence indicates a high prevalence of hyperuricemia in patients with essential hypertension; this becomes accentuated with diuretic therapy. Since there is an association of hyperlipidemia with hyperuricuria and hypertension and since hyperuricemia is a feature of diuretic therapy, we explored whether these relationships might be provoked by prolonged diuretic therapy. Eighteen male patients with uncomplicated essential hypertension of mild severity were treated for 9 months with hydrochlorothiazide and supplemental potassium chloride, 100 mg and 45 mEq/day, respectively. Arterial pressure, renal function, and serum electrolyte, uric acid, blood glucose, and lipid concentrations were measured several times before and during therapy. Arterial pressure remained significantly reduced during therapy (P less than 0.001); this was associated with reduced serum potassium (P less than 0.01) and increased blood glucose and serum uric acid concentrations (P less than 0.005, P less than .025, respectively). Blood urea nitrogen, serum creatinine, sodium, cholesterol and triglyceride levels did not significantly change with treatment. Thus, although diuretics increase serum uric acid and blood glucose, their effect on serum lipid concentration is negligible.

Adult↗
PubMed1975

Systemic hemodynamic effects of bethanidine in essential hypertension.

Although available elsewhere, bethanidine remains under study in the U.S. and its hemodynamic effects are unreported. Therefore, 29 patients with moderately severe essential hypertension received one of four oral dose levels (0.10, 0.25, 0.35, or 0.50 mg/kg) of the postganglionic sympatholytic drug. Blood pressure was reduced only in the 14 patients receiving the highest dose. This was demonstrated within three hours, first by a significant postural hypotension (upright tilt: +14 before vs -19 mm Hg after, P less than 0.001). This orthostatic hypotension effect was associated with a greater fall in cardiac output (13 vs 22%, P less than 0.025) and a diminished reflective increase in total peripheral resistance (19 vs 6%, P less than 0.01); an attenuated Valsalva maneuver overshoot in the supine position was also observed (42 vs 10%, P less than 0.001). Eight of these 14 patients demonstrated supine hypotension associated with either reduced output and/or resistance. Hence, bethanidine is a rather rapidly acting oral sympatholytic agent which reduces blood pressure by producing: (1) decreasec venous return (especially in upright position), suggesting venodilation; (2) arteriolar dilation (supine and upright) reducing peripheral vascular resistance; and (3) attenuated cardiovascular sympathetic reflective adjustments.

Administration, Oral↗
PubMed1975

Natriuresis and carbohydrate-induced antinatriuresis in fasted, hydrated hypertensives.

After an overnight fast and oral hydration with water, hypertensive subjects developed a significant natriuresis (mean urine sodium excretions increased from 130 to 291 mueq/min. The incidence of a natriuresis (greater than 200 mueq sodium excreted per minute) was 75% in the hypertensive group (16 subjects) compared to 27% in a previously studied normotensive group (22 subjects). The incidence of a carbohydrate-induced antinatriuresis (greater than 30% decrease in urinary sodium excretion) was 62% in the hypertensive group compared to 41% in the normotensive group. No decrease in plasma volume (131I-labeled albumin concentration) due to a shift of solute and water intracellularly could be documented to explain the antinatriuretic effect of glucose. An incidental observation was a significant decrease in plasma zinc concentrations after glucose ingestion.

Adult↗
PubMed1975

Direct renal hemodynamic effects of two vasodilators: diazoxide and acetylcholine.

The direct renal hemodynamic effect of two different vasodilators, diazoxide and acetylcholine, in the anesthetized dog, were studied. In 12 dogs (Group 1), diazoxide was given first directly into the renal artery and was followed by the addition of acetylcholine. In 6 dogs (Group 2) the order of drug administration was reversed. The glomerular filtration rate (GFR), the effective renal plasma flow (ERDF), and the excretion of sodium, potassium, chloride, and urine output were determined for both control and experimental (infused) kidneys. Both drugs when given alone resulted in a significant increase of all parameters tested on the experimental kidney, except the ERPF which was spuriously decreased by diazoxide. The addition of either drug upon the first given did not produce and further effect. It was, therefore, concluded that the hemodynamic changes, as well as the handling of electrolytes and water by the kidney, were solely due to the vasodilating properties of both compounds. A local renal tubular effect by diazoxide concerning sodium excretion could not be substantiated by our studies.

Acetylcholine↗
PubMed1975

Direct renal hemodynamic effects of clonidine.

The renal hemodynamic and excretory effects of clonidine were tested in 2 groups of dogs. In one group, the drug was given directly into the renal artery at a rate of 1.2 mug/min and resulted in a significant decrease of the effective renal plasma flow (ERPF) in both kidneys, an increase in filtration fraction (F.F.), urine volume (U.V.), and free water clearance (CH2O) and had no effect upon the glomerular filtration rate (GFR), osmolar clearance (Cosm) and the excretion of sodium (UNa+V), chloride (UC1-V), potassium (UK+V), calcium (UCa++V) and phosphorous (UP04V). In the second group of animals it was given intravenously at a rate of 12.0 mug/min and resulted in a significant decrease of ERPF, UNa+V, UC1-V, and an increase in F.F., U.V. and CH2O and had no effect upon GFR, Cosm, UK+V, UCa++V and UPO4V. Systemically, it decreased heart rate (H.R.) and respiratory rate (R.R.) in both groups of animals; it increased blood pressure (BP) in Group I and had no effect on BP in Group II.

Animals↗
PubMedDate not supplied

Fixed low-dose drug combination for the treatment of hypertension.

The goal of treating hypertension is to maximize therapeutic efficacy without untoward side effects. The accepted approach is to start treatment with a low dose of a single drug and then titrate it upward as needed to achieve a better therapeutic effect. However, higher doses of administered individual drugs increase the frequency and severity of side effects. A rational combination of individual drugs administered in low doses is preferable because it is associated with a high degree of efficacy, low incidence or severity of side effects, and high patient compliance. The most commonly used drug combinations are as follows: (1) diuretics with potassium-sparing agents; (2) beta-adrenergic blockers with diuretics; (3) angiotensin-converting enzyme inhibitors with diuretics; (4) angiotensin II receptor blockers with diuretics; and (5) angiotensin-converting enzyme inhibitors with calcium-channel blockers.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Comparative efficacy of olmesartan, losartan, valsartan, and irbesartan in the control of essential hypertension.

In a multicenter, randomized, double-blind trial, the authors compared the antihypertensive efficacy of once-daily treatment with the new angiotensin II type 1 receptor blocker (ARB) olmesartan (20 mg) with recommended starting doses of losartan (50 mg), valsartan (80 mg), and irbesartan (150 mg) in 588 patients with a cuff diastolic blood pressure (DBP) of greater than or equal to 100 and less than or equal to 115 mm Hg and a mean daytime DBP of greater than or equal to 90 mm Hg and less than 120 mm Hg, as measured by ambulatory blood pressure monitoring. Cuff and ambulatory blood pressures were monitored at baseline and after 8 weeks of treatment. All groups were predominantly white and approximately 62% male, and their mean age was approximately 52 years. In all groups, mean baseline DBP and systolic blood pressure (SBP) were approximately 104 and 157 mm Hg, respectively. The reduction of sitting cuff DBP with olmesartan (11.5 mm Hg), the primary efficacy variable of this study, was significantly greater than with losartan, valsartan, and irbesartan (8.2, 7.9, and 9.9 mm Hg, respectively). Reductions of cuff SBP with the four ARBs ranged from 8.4-11.3 mm Hg and were not significantly different. The reduction in mean 24-hour DBP with olmesartan (8.5 mm Hg) was significantly greater than reductions with losartan and valsartan (6.2 and 5.6 mm Hg, respectively) and showed a trend toward significance when compared to the reduction in DBP with irbesartan (7.4 mm Hg; p=0.087). The reduction in mean 24-hour SBP with olmesartan (12.5 mm Hg) was significantly greater than the reductions with losartan and valsartan (9.0 and 8.1 mm Hg, respectively) and equivalent to the reduction with irbesartan (11.3 mm Hg). All drugs were well tolerated. The authors conclude that olmesartan, at its starting dose, is more effective than the starting doses of the other ARBs tested in reducing cuff DBP in patients with essential hypertension.

Analysis of Variance↗