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Biomedical subjects

G Muiesan

Publications and source records attributed to G Muiesan.

At least 55 records · Page 3Linked to original sources
PubMed1986

Adrenergic activity and left ventricular function during treatment of essential hypertension with calcium antagonists.

The effects of 2 calcium antagonist drugs, verapamil and nifedipine, on blood pressure, heart rate (HR), plasma catecholamines, plasma renin activity and some echocardiographic indexes of left ventricular anatomy and function were studied in 67 patients with essential hypertension. The short- and long-term antihypertensive effect of verapamil was not associated with significant changes in HR, plasma catecholamines or plasma renin activity; the decrease in blood pressure after nifedipine was associated with a significant increase in HR and plasma catecholamines (mainly noradrenaline) (p less than or equal to 0.05). These findings were confirmed in a crossover comparison in 12 hospitalized patients treated with verapamil and nifedipine for 8 days each. The dose of isoproterenol that increased HR by 25 beats/min was significantly increased during verapamil treatment (p less than 0.05) and decreased during nifedipine treatment (p less than 0.01). Stroke volume and shortening fraction increased slightly but significantly (p less than 0.05) with 3 months of nifedipine treatment, while no change was detected with verapamil treatment. Left ventricular mass was significantly decreased after effective antihypertensive treatment for 3 months with verapamil or nifedipine (p less than or equal to 0.05).

Adult↗
PubMed1986

Similarities and differences in the antihypertensive effect of two calcium antagonist drugs, verapamil and nifedipine.

The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.

Adult↗
PubMed1986

Renal noradrenergic and dopaminergic activity in patients with borderline essential hypertension.

An opposite modulatory influence of renal noradrenergic and dopaminergic activities on sodium excretion has been suggested. In this study urinary noradrenaline (UNA) and dopamine (UDA) excretion were evaluated in patients with borderline essential hypertension (BH; n = 9) and in patients with established essential hypertension (EH; n = 11) as well as in normal subjects (NT, n = 8), during normal sodium and potassium intake. Measurements were performed on fractionated urine collections on two separate days: on the first day under basal conditions and on the second day after saline infusion (SAL), 2L/2h, i.v. In BH, basal UNA and UDA were higher with respect to NT and EH. The difference was significant (p less than 0.05) in urine collected between 8 and 14 h. In all three groups, SAL induced a significant decrease in UNA and a significant increase in UDA; the decrease in UNA after SAL was significantly lower in EH in respect to BH and NT. In conclusion, the increased UDA in BH may represent a compensatory mechanism to a defect in sodium excretion, possibly due to elevated renal and/or systemic noradrenergic activity; the normal response to volume and salt loading suggests that the physiological modulation of sympathetic tone is still preserved in BH.

Adult↗
PubMed1986

Comparison of captopril and digoxin in mild to moderate heart failure.

Captopril 25 mg every 8 hours for 1 month appeared to improve dynamic effort tolerance and cardiac function under the stress of isometric exercise in patients with chronic heart failure, functional class II-III NYHA. The improvement was comparable to that obtained in the same subjects with digoxin 0.25 mg once a day given for a similar period of 1 month. Therefore, captopril with its lower toxicity and wider therapeutic range, might be considered as a valid alternative to digoxin for treatment of patients in sinus rhythm with mild to moderate heart failure.

Adult↗
PubMed1986

Effect of captopril on left ventricular mass and function in hypertensive patients and in the rat.

Twenty-seven mild to moderate essential hypertensive patients were treated with captopril alone or combined with hydrochlorothiazide and left ventricular echocardiographic changes were evaluated after 1, 3 and 6 months. The left ventricular mass decreased slightly after 3 months, together with mean wall stress and total peripheral resistance, while the cardiac performance, as measured by fractional shortening and cardiac output, was unaffected. A high degree of individual variability was observed, and only 9 out of 20 patients examined after 3 months had a consistent reduction in left ventricular mass. The effect of captopril on the isomyosin composition was also evaluated in 4 normotensive rats after 12 weeks of drug administration. No interference with the physiological pattern was observed and no modifications of the biochemical and structural properties of the myocardium were detected.

Adult↗
PubMed1985

Effect of pinacidil on blood pressure, plasma catecholamines and plasma renin activity in essential hypertension.

Pinacidil, a new cyanoguanidine derivative, is an antihypertensive agent with arteriolar vasodilating properties, which acts on precapillary resistance vessels. A trial was carried out in 30 patients with essential hypertension WHO I-II. The treatment period was divided into three phases. Hydrochlorothiazide (HCTZ) and amiloride were administered for 4 weeks in Phase 1 and supine and standing blood pressure decreased significantly. During Phase 2 pinacidil was added to HCTZ/amiloride for the following 3 months. A further significant reduction in blood pressure was obtained. In the next period of treatment (Phase 3) patients were divided into two groups. For 1 month Group A (15 patients) received pinacidil alone and Group B (15 patients) received HCTZ/amiloride. Conventional laboratory blood tests in all patients remained unchanged during treatment. Reported side effects during Phase 2 were headache (2 patients), dizziness (3 patients), palpitations (2 patients) and ankle oedema (2 patients). Plasma renin activity was slightly increased at the end both of Phases 1 and 2. Plasma catecholamines were increased but not significantly at the end of Phase 2 as compared to Phase 1. The results indicate that pinacidil is effective in lowering blood pressure in mild to moderate essential hypertension.

Adult↗
PubMed1985

Possibility of cardiac output monitoring from the intra-arterial blood pressure profile.

A method for estimating cardiac output (CO) from the intra-arterial blood pressure profile ("contour method") was tested in 8 patients: 6 with essential hypertension, 1 with a pheochromocytoma and 1 with orthostatic hypotension. CO (1/min) was derived by the following formula: PSA (1+St/Dt) X HR 10(-3), where PSA is the area under the systolic portion of the pressure curve, St is the systolic and Dt the diastolic time, X is a correction factor, HR is the heart rate and 10(-3) is a conversion factor from ml/min to 1/min. The "contour method" was compared to the thermodilution CO method. The correlation between the 2 methods was highly significant: the r value in all patients during different conditions (supine, tilt, dynamic and static exercise) ranged from 0.91 to 0.97 with an intercept close to 0 and a slope close to 1. These results indicate that CO is properly measured from the intra-arterial blood pressure profile by the "contour method". A continuous hemodynamic monitoring can be derived applying the "contour method" to the intra-arterial blood pressure profile obtained with the Oxford technique.

Adrenal Gland Neoplasms↗
PubMed1985

Autonomic nervous system control of heart rate in essential hypertension.

In order to evaluate the role of the autonomic nervous system in controlling heart rate (HR) in essential hypertensive patients (EH), we studied 13 untreated EH, WHO I-II, aged 21-68 years, and 10 normotensive subjects (N), aged 20-68 years. The average variation of heart period (VHP) during regular breathing was used as an index of parasympathetic control of HR. Measurements were carried out supine and during tilting, before and after propranolol (0.15 mg/kg intravenously). A sympathetic control index of HR was derived from the ratio HR before/HR after propranolol. A parasympathetic control index of HR was also obtained from the ratio HR before/HR after atropine (0.03 mg/kg intravenously). The VHP was constantly lower in EH than N (P < 0.001) before and after propranolol, supine and standing. The parasympathetic control index of HR was significantly higher in EH (P < 0.001). A significant negative correlation was found between VHP and the parasympathetic control index (r = -0.73) plotting together all values found in EH and N. The sympathetic control index of HR did not differ between EH and N. These results indicate a lower parasympathetic influence on HR in this group of EH compared with N, while sympathetic control was similar in the two groups. This difference in vagal control of HR persists in the presence of increased sympathetic activity (tilting) and after beta-blockade.

Adult↗
PubMed1985

Interrelations of cardiac and arterial vascular wall hypertrophy in essential hypertension.

Structural vascular changes in the calf arteries and left ventricular mass were measured in 52 essential hypertensive patients (WHO I and II, 35 men and 17 women, age range 21-63 years). Left ventricular mass was measured on M-mode echocardiographic tracings. Structural vascular changes were evaluated indirectly by studying the minimal vascular resistance, calculated from mean arterial pressure and maximal (post-ischaemic) blood flow, measured by venous occlusion plethysmography. A statistically significant correlation between left ventricular mass and minimal vascular resistance was observed (r = 0.33, P < 0.05). The low correlation suggested that structural changes in the heart and in the systemic arteries did not develop simultaneously. In the subgroup of patients with minimal vascular resistance in the normal range, left ventricular hypertrophy was found in 15 out of 30 patients (50% of cases) whereas, in the subgroup of patients with high minimal vascular resistance, absence of left ventricular hypertrophy was found in six out of 22 patients (27% of cases). These results suggest that left ventricular hypertrophy more often precedes arterial structural changes in the calves.

Adult↗
PubMed1985

Continuous haemodynamic ambulatory monitoring in essential hypertension.

Haemodynamic ambulatory monitoring was derived from the intra-arterial blood pressure (BP) profile in 10 patients with essential hypertension. Stroke volume (SV) was computed beat by beat according to the following formula: X x PSA x (1 + St/Dt), where X is a correction factor, PSA is the area under the systolic portion of the pressure curve, St is the systolic and Dt the diastolic time. The X value was obtained in each patient by predetermining SV by thermodilution and solving the previous formula by X. The correlation between SV calculation and SV measured independently by thermodilution was highly significant: r values ranged from 0.85 to 0.92 (intercepts close to 0 and slopes close to 1) during different situations (supine, tilt, dynamic and static exercise). In five patients continuous haemodynamic ambulatory monitoring was obtained by applying the formula above to the intra-arterial tracing recorded with the Oxford technique. A computer program was developed in order to get BP, heart rate (HR), SV, cardiac output (CO) and total peripheral resistance (TPR) simultaneously. In these patients, the morning increase of BP was determined by an increase of both CO and TPR. Stroke volume increased slightly during the night, probably as a consequence of a reduced HR.

Adult↗
PubMed1985

Adrenergic activity and myocardial anatomy and function in essential hypertension.

In hypertension, changes of cardiac anatomy and function are not just a simple consequence of the increased pressure load. The sympathetic nervous system activity is one of the factors which may influence the cardiac performance, and possibly also the cardiac anatomy of hypertensive patients. Several clinical studies have provided evidence of a subset of patients, usually with mild or borderline hypertension, with an increased cardiac performance, higher plasma catecholamine concentrations and/or greater response to beta-adrenergic stimulation. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy (LVH). In man, plasma catecholamines are usually higher in hypertensive patients with LVH, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and in patients with LVH. Several studies have also suggested that reversal of LVH may be more easily induced by those antihypertensive drugs that reduce, or at least do not stimulate, the sympathetic activity, although exceptions to this statement may be observed.

Animals↗
PubMed1985

[Hypotension during ventricular pacing. A study of the vagal reflex component].

It has been suggested that hypotension during ventricular pacing (V) could be caused by a parasympathetic vasodilating reflex. In order to evaluate this hypothesis, we studied 10 patients who had wide fluctuations of arterial pressure during V. Intra-arterial pressure, right atrial pressure, EKG and cardiac index (thermodilution) were determined in the following conditions: basal rhythm (B), V, atrioventricular pacing (A-V) and ventricular-atrial pacing (V-A). The same investigations have been carried out in the same conditions (B,V,A-V,V-A) after atropine 0.03 mg/Kg intravenously. The arterial blood pressure during V decreased markedly simultaneously with the appearance of cannon waves in the right atrial pressure tracing. During A-V the arterial pressure remained stable at the highest level observed during V. The start of V-A pacing induced a marked drop of arterial pressure, which, however, gradually increased to a level slightly lower than during A-V pacing. After atropine the arterial blood pressure during V decreased again in all patients concomitantly to the appearance of cannon waves in the atrium as before atropine. The values of arterial blood pressure during B, A-V and V-A were not different from those measured before atropine. Therefore, an increase of parasympathetic activity during V is not responsible for the wide fluctuation of arterial blood pressure. A possible role of sympathetic failure must be considered.

Adult↗