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Biomedical subjects

C Cottier

Publications and source records attributed to C Cottier.

30 records · Page 2Linked to original sources
PubMed1983

Pressured pattern or type A behavior in patients with peripheral arteriovascular disease: controlled retrospective exploratory study.

The question as to whether a specific behavior or type A pattern is limited to patients with coronary artery disease, or is found in atherosclerotic disease, in general, is explored. The interrelationship between a pattern of "pressured" behavior, assessed by open ended interviews, type A behavior, determined by the Bortner test, and peripheral atherosclerotic disease was investigated in a controlled retrospective study which compared three groups of 13 patients each: intermittent claudication (IC), intermittent claudication combined with coronary artery disease (CADIC) and a control group of patients without vascular disease (WVD). A pressured behavior pattern, assessed by interview, was found to be most prominent in the CADIC group, and least in the control group. The subjects with arteriovascular disease tended to exert more control over people compared to the WVD patients (Fisher's exact probability test, p = 0.05). The tendency to type A behavior, measured by means of the Bortner scale, also differentiated the three groups with CADIC scoring highest and WVD scoring lowest (analysis of variance, F = 3.944, p less than 0.05). IC patients present personality features of proneness to coronary disease. The pattern of "pressured" and type A behavior seem to correlate with the number of vascular areas involved in atherosclerotic disease.

Coronary Disease↗
PubMed1983

Use of clonidine and propranolol as monotherapy in borderline hypertension.

The effect of clonidine (average 0.24 mg/day) and propranolol (average 105 mg/day) on home blood pressure readings in 16 patients with borderline hypertension was investigated in a randomized, double-blind, placebo crossover design. Patients could detect small but significant decreases of blood pressure with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). The larger mean blood pressure decrease from clonidine vs propranolol was significant (p less than 0.015). Small doses of sympatholytic agents might control the blood pressure in patients with borderline hypertension, and the home blood pressure technique is a convenient tool to detect and monitor such changes. Biochemical predictors of the responsiveness to clonidine were investigated. There was no difference in placebo norepinephrine and renin values between better and lesser responders to clonidine. Plasma norepinephrine fell with clonidine treatment, but with no relationship to the blood pressure response. Plasma norepinephrine response to clonidine might reflect not only the central withdrawal of sympathetic tone, but also, in part, the effect of clonidine on peripheral presynaptic alpha 2-receptors.

Adult↗
PubMed1983

Cardiopulmonary mechanoreceptors and renin release in humans.

We investigated the hemodynamic determinants of the reflex release of renin to changes in posture and blood volume distribution in healthy humans to determine the relative contribution of arterial and cardiopulmonary mechanoreceptors to the reflex release of renin under physiological circumstances. In the first experiments, we induced a selective decrease of right atrial pressure by inflation of cuffs around the thighs. Renin increased and returned toward baseline on decompression. The renin increase was neurogenic because plasma norepinephrine increased, the response was abolished by beta blockade, and renin did not increase in patients with denervated transplanted kidneys. The second experiments were performed with tilting and later filling a pressure suit to counteract the effect of tilting on gravitational pooling of the blood. Tilting elicited increases of renin and norepinephrine; filling the suit abolished these increases. Right atrial pressure fell with tilting and rose after filling the suit. Because the neck was elevated above the heart equally in both conditions, it is concluded that the increase and decrease of renin reflected decrease and increase of the stretch of cardiopulmonary receptors. The third experiments were performed by elevating the upper trunk with the legs remaining in a horizontal position (sitting). This caused a heart-to-neck pressure difference and an increased sympathetic outflow through unloading arterial baroreceptors. Norepinephrine increased but renin did not. Cardiopulmonary receptors exhibit an important influence on the reflex release of renin.

Blood Pressure↗
PubMed1982

Usefulness of home BP determination in treating borderline hypertension.

This study explores whether home BP self-determination can be used to assess the effect of treatment in patients with borderline hypertension. Sixteen untreated patients underwent a double-blind trial of propranolol hydrochloride (average dose, 105 mg), clonidine hydrochloride (0.24 mg), and placebo. Home BP readings decreased with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). During placebo, the readings increased to levels identical to untreated values. This study demonstrates that patients with borderline hypertension are consistently capable of detecting small average changes in home BP. It is also shown that sympatholytic monotherapy can be effectively used to lower the BP in such patients.

Adult↗
PubMed1982

Antihypertensive mechanism of the diuretic muzolimine in mild renal failure. Roles of sodium and cardiovascular norepinephrine responsiveness.

Eighteen patients with mild impairment of renal function (glomerular filtration rate 65 +/- 5 ml/min:m +/- SEM) and hypertension (168/105 +/- 6/3 mmHg) were shown on average to have abnormally increased cardiovascular pressor responsiveness to infused norepinephrine (NE; p less than 0.05), whereas plasma and urinary NE, exchangeable body sodium and blood-volume did not differ significantly from normal. A slightly increased pressor responsiveness to angiotensin II was associated with a tendency to low plasma renin activity (PRA). Compared to placebo conditions, treatment with the loop-diuretic muzolimine in a mean dose of 35 +/- 2 mg/day for six weeks decreased blood-pressure and exchangeable sodium (p less than 0.05), and NE pressor responsiveness was restored to normal values, whilst plasma and urinary NE were not significantly changed. This was consistent with improvement of the initially abnormal relationship between NE levels and NE responsiveness factors. In contrast, the pressor dose of angiotensin II and PRA were increased to an approximatively similar extent during muzolimine treatment. These observations suggest that removal of body sodium and a decrease in NE reactivity without an equivalent increase in sympathetic nervous activity may be important complementary factors in the antihypertensive mechanisms of diuretic treatment in patients with mild renal functional impairment.

Adult↗
PubMed1982

Enhanced cardiovascular pressor reactivity to norepinephrine in mild renal parenchymal disease.

The cardiovascular pressor responsiveness to infused norepinephrine (NE) or angiotensin II (AII) as related to endogenous plasma NE or renin levels was assessed in 20 patients with mild parenchymal kidney disease (plasma creatinine 2.20 +/- 0.58 mg/dl, +/- SEM) and in 20 normal subjects approximately matched for sex and age. The two groups did not differ significantly in mean body weight, heart rate, blood volume, plasma electrolytes, exchangeable or urinary sodium, plasma aldosterone, epinephrine and renin levels, or AII threshold or pressor doses. Basal (including pre-infusion) plasma NE levels, the relationship between plasma NE measured during NE infusion and the corresponding NE infusion rate, as well as the total plasma clearance of NE (5.0 +/- 0.8 vs. 5.5 +/- 0.5 liter/min) also did not differ significantly between the two groups. In contrast, the threshold or pressor doses of infused NE decreased significantly in the patients with kidney disease (94 +/- 11 vs. 134 +/- 14 ng/kg/min and 21 +/- 3 vs. 40 +/- 7 ng/kg/min; P less than 0.05). Moreover, based on analysis of covariance, the individual pressor doses as related to basal plasma NE levels were distributed differently (P less than 0.01) between the patients and normal subjects. These findings suggest that the kinetics of plasma NE are unaltered largely in early stage kidney disease. However, such patients tend to develop an exaggerated pressor responsiveness to NE in the presence of normal plasma NE levels. This disturbance may favor the development of hypertension.

Adult↗
PubMedDate not supplied

Role of cardiovascular receptors on the neural regulation of renin release in normal men.

Although factors influencing renin release have been studied extensively, one facet of renin release remains controversial, namely, neural regulation by arterial high-pressure receptors and cardiopulmonary low-pressure receptors. We therefore designed four studies to investigate systematically the separate and combined effects of unloading (decreased stretch) high- and low-pressure receptors on renin release in normal men. Selective unloading of cardiopulmonary receptors was induced by impeding the venous return with tourniquets around the thighs. A predominant unloading of arterial (carotid) baroreceptors was elicited with upright posture and simultaneously preventing the venous pooling in the legs. Unloading of both high- and low-pressure receptors was achieved by both upright standing and tilting. During postural experiments to predominantly unload arterial baroreceptors, the heart rate increased and the veins constricted, but renin failed to increase. The postural increase of renin occurred only if we allowed venous pooling in the legs. Selective unloading of cardiopulmonary receptors elicited substantial increases of renin. When both the cardiopulmonary and arterial baroreceptors were unloaded, renin increased more than with isolated unloading of cardiopulmonary receptors. We conclude that: 1) in intact humans it is possible to demonstrate an independent role of cardiopulmonary receptors in the control of renin release; 2) there Is evidence for interaction between the two receptor systems in renin control; but 3) an independent role for arterial baroreceptors in the control of renin release could not be demonstrated under the conditions of this experiment.

Adolescent↗
PubMedDate not supplied

Glycerol and dextran combined in the therapy of acute stroke. A placebo-controlled, double-blind trial with a planned interim analysis.

The results of clinical trials investigating various therapies in acute ischemic stroke have been inconsistent. The effect of glycerol therapy and a combination therapy of glycerol and dextran was evaluated in a double-blind, placebo-controlled study. Repeated neurologic examinations (Day 0, Weeks 1, 6, 12, and 24) according to a modified Mathew score were performed on 62 patients. Statistical analysis showed no superiority of either treatment compared with placebo in acute ischemic stroke. A retrospective estimation of the Type II error of the study yielded approximately p = 0.25. A major side effect was hemolysis in 98% of patients treated with glycerol.

Acute Disease↗
PubMedDate not supplied

Role of cardiac factors in the initial hypotensive action by beta-adrenoreceptor blocking agents.

The blood pressure decrease after beta-blockade is delayed and there are little data on the hemodynamic events associated with the initial decrease in blood pressure. The present study measured the hemodynamics of the initial hypotensive action of timolol maleate, a nonselective beta-adrenoreceptor blocking agent, in 10 patients with essential hypertension. Frequent measurements were made for the first 30 hours of treatment, and follow-up measurements made at 3 and 6 weeks. Before treatment, mean arterial blood pressure, cardiac output, and arteriovenous oxygen difference were 115.9 +/- 9.1 mm Hg, 4.65 +/- 1.05 liter/min, and 55.0 +/- 9.6 ml/liter, respectively. At 3 hours after the first dose of timolol, blood pressure had fallen 13.5 +/- 8.2 mm Hg (p less than 0.05). This was preceded by an initial decrease in cardiac output, which was not associated with a simultaneous decrease in blood pressure, and by an increase of arteriovenous oxygen difference. The early, statistically significant, decrease in cardiac output was followed by a return to normal output, which coincided with the onset of blood pressure reduction. The magnitude of the initial decrease of cardiac output and of the initial increase in arteriovenous oxygen difference was significantly correlated to the later decrease in blood pressure (7 hours after first dose). These hemodynamic observations are consistent with the notion that early underperfusions of tissue play a role in the initial hypotensive action of beta-blockers. After 6 weeks, the blood pressure remained lower but the cardiac output was again decreased at that point. As with many antihypertensive agents, there was a difference between the early and late hemodynamic pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗