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Biomedical subjects

N De Luca

Publications and source records attributed to N De Luca.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Techniques for the diagnosis of kidney diseases. Is there a role for the immunoperoxidase method in the evaluation of immunologic glomerulopathy on biopsy specimens, including those in paraffin? Our experience: preliminary results].

Firstly an extensive summary of the diagnostic power and limits in renal glomerular pathology of light microscopy even corroborated by all the special histochemical stains is made. Secondly a complete list of all those renal glomerular diseases in which electron microscopy is unanimously considered necessary for the diagnosis is given as well as the main and most updated references pertinent to those rare and recently recognized pathological entities in which EM proved as a fundamental diagnostic tool are provided. Thirdly the authors focus on the importance of immunohistochemistry (IIC) in the diagnosis of immune-mediated renal glomerular diseases. The advantages and disadvantages of immunofluorescence microscopy (IF) and immunoperoxidase method (I-perox) are respectively discussed. The value of I-perox staining method applied to sections from paraffin blocks is emphasized and some technical suggestions in order to optimize results are given. Among the latter the choice of the used fixative for the purpose of preserving antigenicity of immunoglobulins and complement fractions, the timing of tissue fixation as well as the quantitation of enzymatic pretreatment relative to the duration of fixation, and the repeated washings with phosphate-buffer saline to minimize background staining. Ultimately the authors report on their preliminary personal results with the use of I-perox staining on sections from paraffin embedded renal core biopsies. Although if is their favourite diagnostic microscopy for evaluating renal immunopathology the authors underline I-perox method as a helpful tool to rely on at least in those circumstances when frozen material for IF is not available due to the scarcity of core biopsy, when glomeruli are absent in frozen sections, or when due to a technical lab accident the frozen tissue devoted to IF has been ruined or lost, and the only available material is the one which lies embedded in paraffin. The LSAB ("labelled streptavidin biotin") complex and PAP ("peroxidase-antiperoxidase") working procedures are provided in detail.

Biomarkers↗
PubMed1994

[Effects of antihypertensive treatment on carotid vascular changes].

The carotid artery is one of the most important sites in the progression of atherosclerotic lesions. Atherosclerosis is known to be determined by a variety of factors, among which arterial hypertension is one of the most important. Blood pressure control by antihypertensive treatment is thus of great benefit in management of atherosclerosis, particularly in view of the direct action of some classes of antihypertensive agents on atheromatous lesions. Today, modern diagnostic technique allow a non-invasive examination of the artery wall (B-mode ultrasound and pulsed-Doppler), so that early detection of structural and functional alterations is possible. In order to evaluate the efficacy of the long term blood pressure reduction in the progression and/or in the regression of cardiovascular structural abnormalities, we studied intima-media thickness and arterial compliance during one-year antihypertensive treatment with a new calcium-antagonist, lacidipine, or a diuretic hydrochlorothiazide. In both groups we observed a comparable blood pressure reduction (lacidipine: from 166 +/- 5/100 +/- 1 to 142 +/- 4/88 +/- 2 mmHg; hydrochlorothiazide: from 154 +/- 5/102 +/- 2 to 140 +/- 4/88 +/- mmHg; both p < 0.01). On the contrary, only in patients treated with lacidipine did we obtain a significant improvement in carotid blood flow (383 +/- 16 vs 411 +/- 16 ml/min p <) and in arterial compliance (0.8 +/- 0.1 vs 1.2 +/- 0.2 cm/dyne p < 0.01). Indeed, we observed a different behaviour of the intima-media thickness in the two groups (lacidipine: 1.11 +/- 1.4 vs 1.13 +/- 1.5 mm n.s.; hydrochlorothiazide: 1.15 +/- 0.15 vs 1.21 +/- 0.17 mm p < 0.06). Our results demonstrate that an effective antihypertensive treatment with calcium antagonists may influence the progression of carotid vascular abnormalities.

Aged↗
PubMed1994

[Carotid vascular structural changes and left ventricular hypertrophy].

In the literature there are few studies evaluating carotid vascular atherosclerotic involvement in patients with essential arterial hypertension. Nowadays with new non-invasive methodological methods, such as Doppler-echotomography, it is possible to evaluate accurately structural vascular and cardiac changes. In this study we evaluated the relationship between carotid vascular structural changes and cardiac left ventricular mass index in 15 normotensive subjects and in 15 patients with essential hypertension. We performed a B-mode echotomography (7.5 MHz) of a common carotid in order to measure the diameter of the vessel and intima-media wall thickness. In the same subjects we determined echocardiographic left ventricular mass index and we measured arterial pressure by sphygmomanometric method. There was no statistical significant difference in the two groups except that in systolic, diastolic and mean arterial pressure (96 +/- 2 vs 123 +/- 2 mmHg, p < 0.01), left ventricular mass index (102 +/- 3 vs 118 +/- 3 g/m2, p < 0.01) and in the common carotid intima media wall thickness (0.91 +/- 0.01 vs 2.23 +/- 0.02 mm). In the normotensive subject mean arterial pressure correlated significantly with age (r = 0.699) and with common carotid arterial diameter (r = 0.523) (both p < 0.05). In hypertensive patients, on the contrary, mean arterial pressure correlated with left ventricular mass index (r = 0.523), carotid arterial diameter (r = 0.627) and common carotid intima media wall thickness (r = 0.847). These results demonstrate that in hypertensive patients cardiac abnormalities accompanied vascular structural changes.

Carotid Arteries↗
PubMed1994

[The effects of plasma cholesterol reduction on vasoconstriction due to sympathetic activation in patients with moderate primary hypercholesterolemia].

Recent studies have demonstrated that hypercholesterolemia is one of the major factor involved in the progression of coronary heart disease and that the reduction in plasma cholesterol reduces mortality for cardiovascular events. Indeed, recent experimental studies have demonstrated alterations in vascular reactivity in atherosclerosis. The aim of this study was to evaluate in patients with primary hypercholesterolemia the consequences of an effective of chronic treatment with inhibitor of HMG-CoA reductase on vascular responsiveness to cold pressure test. We observed a significant reduction in total plasma cholesterol during the study that was accompanied by a significant decrease in the response of peripheral vascular resistances to cold pressure test (55 +/- 4% vs 73 +/- 5% p < 0.01). There was also a significant relationship between the reduction of total cholesterol and the response of vascular resistance to the cold pressure test (r = 0.853, p < 0.05). Our results demonstrate that the reduction in total plasma cholesterol may influence the haemodynamic response induced by the activation of the sympathetic system.

Adult↗
PubMed1993

Effects of the single and repeated administration of benazepril on systemic and forearm circulation and cardiac function in hypertensive patients.

The hemodynamic and cardiac effects of the new angiotensin-converting enzyme inhibitor, benazepril, were studied in 28 hypertensives in a double blind, placebo-controlled, between-patient study. Hemodynamic studies were performed noninvasively by means of M-mode echo (central hemodynamics and left ventricular systolic function), 2-D echo-Doppler (left ventricular diastolic function), and pulsed Doppler flowmetry (forearm circulation). Examinations were done at the end of a placebo run-in period and 3 hours after benazepril administration, both on the first day and after 6 weeks of treatment (10 or 20 mg once daily, according to patient response). In comparison with placebo, benazepril reduced systolic (p = 0.04) and diastolic (p = 0.003) blood pressure, because of a significant reduction in systemic vascular resistance (p = 0.03), while cardiac output was unchanged. Forearm vascular resistance was reduced and brachial artery compliance increased, although not to a statistically significant level (both p = 0.07). Both systolic and diastolic left ventricular function were positively influenced by the afterload reduction: End-systolic stress was reduced by 12% (p = 0.07), as was the late diastolic peak flow velocity (p = 0.02). All hemodynamic changes were evident after acute benazepril administration, and no differences was observed between acute and repeated treatment. We conclude that, similar to other ACE-inhibitors, benazepril reduces blood pressure through a reduction in vascular resistance, while cardiac output and heart rate are unaffected. These hemodynamic effects occur as early as after the first administration and exert a favorable influence on left ventricular dynamics.

Adult↗
PubMed1993

Digitalis restores the forearm sympathetic response to cardiopulmonary receptor unloading in hypertensive patients with left ventricular hypertrophy.

OBJECTIVE: To investigate whether the impaired reflex response to cardiopulmonary baroreceptor unloading in hypertensive patients with left ventricular hypertrophy can be promptly improved by a pharmacological challenge. For this purpose we studied the effects of acute digitalis administration on cardiopulmonary baroreflex, evaluated by forearm noradrenaline spillover. METHODS: Eleven hypertensives with left ventricular hypertrophy and 10 age- and sex-matched normotensives underwent the application of -5 and -10 mmHg lower-body negative pressure (LBNP) before and after the administration of digitalis. Forearm noradrenaline spillover, measured using a tracer technique, was used to estimate the reflex sympathetic response. RESULTS: Under control conditions LBNP evoked a similar fall in right atrial pressure in the two study groups. In the normotensives there was a significant increase in forearm noradrenaline spillover. In the hypertensives no significant changes in forearm noradrenaline spillover were found. Intravenous administration of 0.02 mg/kg lanatoside C was associated with an increase in systolic blood pressure and a reduction in forearm noradrenaline spillover in both groups. In the normotensives the percentage change in forearm noradrenaline spillover induced by LBNP increased significantly in response to digitalis administration. However, digitalis restored the response of forearm noradrenaline spillover to LBNP in the hypertensives, so that no significant difference in this response was detected between the two study groups. Digitalis did not modify the effects of LBNP on cardiac pressures in either group. CONCLUSIONS: The present results demonstrate that administration of lanatoside C restores the response of forearm noradrenaline spillover to cardiopulmonary baroreceptor unloading in hypertensive patients with left ventricular hypertrophy. This indicates that the impairment of cardiopulmonary baroreflexes in these patients can be reversed by acute pharmacological treatment. Therefore, impairment of this reflex response seems to be related to functional rather than to structural abnormalities of the hypertrophied ventricle.

Digitalis Glycosides↗
PubMed1993

Indapamide reduces hypertensive left ventricular hypertrophy: an international multicenter study.

The effect of 6 months of treatment with indapamide (IND, 2.5 mg/day) on regression of left ventricular hypertrophy (LVH), an independent predictor of poor prognosis in hypertension, was compared by echocardiography to that of nifedipine (NFD, 40 mg/day), enalapril (ENL, 20 mg/day), atenolol (ATL, 100 mg/day), and hydrochlorothiazide (HCTZ, 25 mg/day) in four parallel double-blind studies in 151 hypertensive patients with a diastolic blood pressure between 95 and 120 mm Hg and a raised left ventricular mass index (LVMI) (mg/m2) (Devereux). Patients were randomized to IND or comparator following a 2-week washout (1 month in the IND vs. ATL study). Respective baseline and 6-month LVMI values (mg/m2) were: IND (n = 20) vs. HCTZ (n = 20): 151.4 +/- 6.3 and 125.70 +/- 4.6 (p < 0.001) vs. 141.3 +/- 6.6 and 135.6 +/- 8.3 (p = N.S.); IND (n = 22) vs NFD (n = 19): 144.1 +/- 5.3 and 125.1 +/- 4.3 (p < 0.001) vs. 170.4 +/- 6.6 and 148.2 +/- 6.2 (p < 0.001); IND (n = 9) vs. ENL (n = 9): 155.1 +/- 6.3 and 143.4 +/- 5.2 (p < 0.001) vs. 142.0 +/- 6.7 and 130.0 +/- 5.9 (p < 0.001); IND (n = 17) vs. ATL (n = 12): 146.2 +/- 5.1 and 130.8 +/- 6.5 (p < 0.001) vs. 156.7 +/- 8.4 and 142.9 +/- 10.3 (p < 0.01). All drugs significantly reduced diastolic blood pressure, and all except HCTZ induced a significant and similar reduction in left ventricular mass.

Adult↗
PubMed1993

[Dose-response study of bunazosin in the treatment of light-to-moderate arterial hypertension].

INTRODUCTION: The antagonists of alpha-adrenergic receptors were introduced in the therapy of arterial hypertension in 1950, but have had limited use due to the poor efficacy and safety of some drugs belonging to this pharmacological class. A recent molecule from this class, bunazosin, is a highly selective alpha 1-antagonist, whose long half-life allows a single daily administration. The aim of this study was to identify the minimum effective dose of bunazosin in the treatment of mild-moderate arterial hypertension. MATERIALS AND METHODS: Patients of both sexes, aged over eighteen years, suffering from mild/moderate essential arterial hypertension were admitted to the study. The experimental design was controlled between patients; and the study was carried out in accordance with the principles of Helsinki anf Tokyo. Dosage was of 3 and 6 mg/day per os; after 2 weeks' treatment, if DBP in clinostatism > or = 95 mmHg, the dose was doubled. Treatment lasted four weeks. RESULTS: At the end of treatment, in the group of patients initially treated with 3 mg/day, SBP, in clinostatism fell by 10.0% and DBP by 8.4% (p < 0.01 between times); in the group of patients initially treated with 6 mg/day, the reductions were of 9.2% and 6.5% respectively (p < 0.01 between times). Heart rate, electrocardiograph traces and laboratory parameters showed no clinically significant modifications. The safety profile of the treatment was excellent in 80% of the patients treated overall. DISCUSSION: This study allowed the minimum effective dose of bunazosin, equal to 3-6 mg/day, to be identified, as well as confirming the antihypertensive efficacy of the drug and its ample safety margin. In fact, this range of daily dosage led to a fall in pressure values, without causing clinically significant alterations of heart rate, electrocardiograph traces and laboratory parameters. CONCLUSIONS: In conclusions, in mild/moderate arterial hypertension, bunazosin in monotherapy at the dosage of 3-6 mg/day, is an effective and safe treatment.

Adrenergic alpha-Antagonists↗
PubMed1992

Reversal of cardiac and large artery structural abnormalities induced by long-term antihypertensive treatment with trandolapril.

In 15 patients with untreated mild to moderate essential hypertension and left ventricular hypertrophy, we assessed blood pressure, echocardiographic left ventricular mass index, brachial artery compliance (pulsed doppler flowmetry), and calculated forearm vascular resistance (strain gauge plethysmography) before, during (6 and 12 months) and after (1 month washout period) 1 year of satisfactory (blood pressure < or = 140/90 mm Hg) antihypertensive therapy with the angiotensin-converting enzyme inhibitor trandolapril (2.0 mg orally once daily). During the antihypertensive effective treatment, we observed a significant reduction of systolic and diastolic blood pressures, left ventricular mass index, and forearm vascular resistance at both 6 and 12 months. In addition, brachial artery compliance was significantly increased. After washout, systolic (156 +/- 3 mm Hg) and diastolic (102 +/- 1 mm Hg) blood pressures returned to levels comparable to baseline. However, left ventricular mass index (132 +/- 4; p < 0.01) and brachial artery compliance (1.53 +/- 0.01; p < 0.01) were still different from baseline. These results demonstrate that chronic antihypertensive treatment with trandolapril is associated with a stable regression of cardiac and vascular abnormalities, which is partially unrelated to the blood pressure lowering effect.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Abnormal hormonal and renal responses to saline load in hypertensive patients with parental history of cardiovascular accidents.

BACKGROUND: Acute cardiac and cerebrovascular accidents are more frequent in hypertensive subjects with a family history of acute vascular accidents. The mechanisms underlying the susceptibility to vascular disease in these subjects are unknown. We investigated whether a parental history of premature heart attack or stroke in hypertensive subjects is associated with abnormalities of sodium handling. METHODS AND RESULTS: Patients with mild, uncomplicated essential hypertension were divided into two subgroups according to family history: a subgroup with a parental history of premature heart attack or stroke (FV+, n = 18) and a subgroup with a family history completely negative for vascular accidents (FV-, n = 14). The two subgroups were comparable with respect to age, weight, sex distribution, blood pressure, duration of hypertension, cardiovascular risk factors, renal function, and organ damage. Baseline plasma renin activity (PRA), concentrations of aldosterone (PA), atrial natriuretic factor (ANF), and norepinephrine, and urinary electrolyte excretion were also comparable in the two subgroups. Despite these similarities, the responses to an acute saline load, measured under controlled metabolic and experimental conditions, were different in the two subgroups. In the FV+ subgroup at 60 minutes of saline load, PRA fell by 1.0 +/- 0.2 ng/ml/hr and PA concentration by 89.4 +/- 26 pg/ml and ANF concentration increased by 38 +/- 9 pg/ml, whereas in the FV- subgroup the corresponding responses were -2.3 +/- 0.3 ng/ml/hr (p less than 0.005), -190 +/- 43 pg/ml (p less than 0.05), and 80 +/- 13 pg/ml (p less than 0.005), respectively. Urinary sodium excretion was delayed in the FV+ subgroup (270 +/- 67 mu eq/min at 60 minutes) compared with the FV- subgroup (555 +/- 157 mu eq/min at 60 minutes, p less than 0.05). At 120 minutes of saline load, significant (p less than 0.005) differences in PRA and ANF concentration were still observed. In a control group of eight normal subjects the responses to a saline load were comparable to those in the FV- subgroup but greater than those in the FV+ subgroup at 60 minutes. CONCLUSIONS: These results provide evidence that the hormonal and renal adjustments to an acute salt load are impaired in hypertensive patients with a parental history of vascular accidents. We speculate that abnormalities of sodium handling may represent markers of a more rapid development of vascular injury in human hypertension.

Adult↗
PubMed1991

Salt-induced plasticity in cardiopulmonary baroreceptor reflexes in salt-resistant hypertensive patients.

To investigate the effects of salt loading on cardiopulmonary and arterial baroreceptor reflexes, 34 hypertensive patients underwent two 4-day periods with different dietary sodium intakes (70 and 370 meq/day). The patients were classified as salt-sensitive or salt-resistant depending on whether the mean arterial pressure value obtained on day 4 of high salt intake did or did not increase by 8% or more. In 22 patients cardiopulmonary and carotid baroreceptor reflexes were assessed during each dietary period by measuring the reflex responses to the application of -10 mm Hg lower body negative pressure and of +60 mm Hg increase in neck tissue pressure. Salt-resistant patients (n = 16) retained less sodium than salt-sensitive patients (n = 6) and showed a reduction in plasma norepinephrine and forearm vascular resistance during high sodium intake, whereas the salt-sensitive patients did not. During low sodium diet, no significant differences could be detected in the reflex responses to cardiopulmonary and carotid baroreceptor unloading between the two groups. High salt diet, however, potentiated the gain of cardiopulmonary baroreceptor reflex, which was expressed as the increase in plasma norepinephrine or forearm vascular resistance per millimeter of mercury decrease in pulmonary capillary wedge pressure, only in the salt-resistant hypertensive patients. In addition, the atrial natriuretic factor response to changes in pulmonary capillary wedge pressure was significantly enhanced by high salt intake only in the salt-resistant hypertensive patients. The reflex responses to carotid baroreceptor unloading were unaffected by salt loading in either group. In the remaining 12 patients, the hemodynamic effects of graded lower body negative pressure (-5, -10, -15 mm Hg) and neck tissue positive pressure (+30, +45, +60 mm Hg) were tested for both diets. Again, high salt intake significantly potentiated the cardiopulmonary baroreceptor reflex gain, expressed as the slope of the linear correlation between the changes in forearm vascular resistance (mm Hg/ml/min/100 g) and pulmonary capillary wedge pressure (mm Hg), in salt-resistant (from 3.8 +/- 0.9 to 7.2 +/- 1.0, p less than 0.05) but not in salt-sensitive patients (from 4.2 +/- 0.9 to 3.2 +/- 0.6, NS). In conclusion, the present study demonstrates that high salt diet potentiates cardiopulmonary baroreceptor reflexes and enhances atrial natriuretic factor response in salt-resistant but not in salt-sensitive hypertensive patients. The salt-induced plasticity of cardiopulmonary baroreceptor reflexes may exert a protective effect against the development of salt-induced hypertension by augmenting the reflex vasodilatory response to volume expansion.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

Failure of atrial natriuretic factor to increase with saline load in patients with dilated cardiomyopathy and mild heart failure.

To investigate whether the response of atrial natriuretic factor (ANF) to volume expansion is impaired in the early stages of dilated cardiomyopathy, the effects of saline load (SL; 0.25 ml/kg.min for 120 min) were assessed in 12 patients with dilated cardiomyopathy and asymptomatic to mildly symptomatic heart failure (HF) and in nine normal subjects (N). SL increased plasma ANF levels in N (from 14.3 +/- 2 to 19.5 +/- 3 and 26 +/- 4 pg/ml, at 60 and 120 min, respectively, P less than 0.001), but not in HF (from 42.9 +/- 9 to 45.9 +/- 9 and 43.9 +/- 8 pg/ml). Left ventricular end-diastolic volume (LVEDV) and stroke volume were increased (P less than 0.001) by SL in N but not in HF. Urinary sodium excretion (UNaV) increased in N more than in HF during SL, whereas forearm vascular resistance (FVR) did not change in N and increased in HF (P less than 0.001). In five HF patients SL was performed during ANF infusion (50 ng/kg, 5 ng/kg.min) that increased ANF levels from 37.1 +/- 10 to 146 +/- 22 pg/ml. In this group, SL raised both LVEDV (P less than 0.01) and ANF (P less than 0.05), whereas FVR did not rise. In addition, the UNaV increase and renin and aldosterone suppressions by SL were more marked than those observed in HF under control conditions. Thus, in patients with dilated cardiomyopathy and mild cardiac dysfunction, plasma ANF levels are not increased by volume expansion as observed in N. The lack of ANF response is related to the impaired cardiac adaptations. The absence of an adequate increase of ANF levels may contribute to the abnormal responses of HF patients to saline load.

Adult↗
PubMed1990

Prolonged duration of myocardial ischemia in patients with coronary heart disease and impaired cardiopulmonary baroreceptor sensitivity.

To investigate the potential contribution of cardiopulmonary reflexes in myocardial ischemia, the coronary vascular response to cardiopulmonary baroreceptor unloading and the number and the duration of spontaneous episodes of symptomatic and asymptomatic myocardial ischemia were evaluated in 23 patients with coronary heart disease. Lower-body negative pressure at -10 mm Hg, which causes selective deactivation of cardiopulmonary receptors, reduced left ventricular filling pressure in all patients, but calculated coronary vascular resistance increased in only 14 patients (from 0.846 +/- 0.1 to 1.07 +/- 0.1 mm Hg/ml/min, p less than 0.01) (group 1). In the remaining nine patients, coronary resistance did not change during cardiopulmonary receptor unloading (group 2). A 60-mm Hg increase in neck tissue pressure, which induces arterial baroreflex-mediated sympathetic activation, caused comparable coronary vasoconstriction in the two groups. Clinical characteristics of the two groups were similar, except that a lower ejection fraction was measured in group 1 (45 +/- 2% vs. 56 +/- 1%, p less than 0.01). In the 14 patients in group 1, 24-hour electrocardiographic monitoring showed 151 episodes of myocardial ischemia (average individual value, 10.8 +/- 1), 137 of which were asymptomatic, with an individual daily ischemic period of 62 +/- 6 minutes. In contrast, the nine patients in group 2 had only symptomatic episodes of myocardial ischemia, and the daily ischemic period in these patients was longer than in patients of group 1 (104 +/- 10 minutes, p less than 0.01). After a 3-day treatment with digitalis, the patients of group 2 showed 38 asymptomatic episodes of myocardial ischemia and a shorter daily ischemic period (85 +/- 6 minutes, p less than 0.01 vs. control conditions). In contrast, no change in number and duration of the ischemic episodes was detected in group 1. The effects of acute administration of digitalis (Lanatoside-C 0.02 mg/kg body wt e.v.) on the coronary vascular response to cardiopulmonary receptor unloading were assessed in a separate group of patients with ischemic heart disease. Digitalis treatment did not significantly modify the magnitude of the coronary vascular response induced by -10 mm Hg lower-body negative pressure in the patients showing in control conditions an increase of coronary vascular resistance greater than 20% of the basal value during cardiopulmonary receptor unloading. On the contrary, digitalis potentiated the coronary reflex response to -10 mm Hg lower-body negative pressure in the patients with impaired cardiopulmonary responsiveness (delta percent increase in coronary vascular resistance: 1 +/- 1% in control conditions; 23 +/- 3.9% after digitalis, p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary Angiography↗
PubMed1990

Converting enzyme inhibition prevents the effects of atrial natriuretic factor on baroreflex responses in humans.

The aim of this study was to assess the influence of atrial natriuretic factor (ANF) on arterial baroreflex chronotropic responses and to investigate whether this effect of ANF is affected by angiotensin converting enzyme inhibition (CEI). For this purpose, in 13 normal volunteers, the reflex chronotropic responses to arterial baroreceptor stimulation (phenylephrine, 25-100 micrograms i.v.) or deactivation (nitroglycerin, 25-100 micrograms i.v.) were evaluated in control conditions and during the steady-state phase of a sustained infusion of ANF (50 ng/kg/min) or placebo, before and during prolonged treatment with the converting enzyme inhibitor enalapril (20 mg p.o. for 5 days). ANF infusion, which raised plasma ANF levels from 48 +/- 19 to 1,765 +/- 203 pg/ml, was associated with a slight decrease in systemic blood pressure and no change in heart rate. In addition, it caused a significant increase of the regression slope obtained with phenylephrine (from 11.3 +/- 2 to 18.5 +/- 2 msec/mm Hg) and a significant reduction of slope of the nitroglycerin-produced regression line (from 9.3 +/- 1 to 5.6 +/- 0.6 msec/mm Hg). After sustained CEI, which raised plasma renin activity from 1.4 +/- 0.4 to 19.9 +/- 5 ng/ml/hr, ANF infusion induced an increase in plasma ANF levels and a reduction in blood pressure comparable to those observed in control conditions. During CEI, however, ANF infusion had no significant effect on the chronotropic baroreflex responses produced by phenylephrine or nitroglycerin. Chronotropic and pressor responses to cold exposure were unchanged after CEI and during ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Improvement of diastolic function after reversal of left ventricular hypertrophy induced by long-term antihypertensive treatment with tertatolol.

In 15 previously untreated hypertensive subjects with left ventricular (LV) hypertrophy who responded favorably (supine blood pressure less than or equal to 140/90 mm Hg) to antihypertensive treatment with a nonselective beta-blocking agent, tertatolol, the effects of reversal of LV hypertrophy on systolic and diastolic function were assessed. Patients underwent echocardiographic and radionuclide studies in control conditions (phase 1), after 1 month of blood pressure normalization (phase 2), after reversal of LV hypertrophy or at least a 20% reduction of LV mass compared to basal value (phase 3) and finally, after a 1-month washout (phase 4). In phase 2, blood pressure (130 +/- 2/85 +/- 1 vs 148 +/- 4/104 +/- 1 mm Hg) and heart rate (59 +/- 1 vs 76 +/- 2 beats/min) decreased (both p less than 0.01); LV mass remained unchanged. There were improvements in peak filling rate (end-diastolic volume/s) (2.4 +/- 0.1 vs 2.0 +/- 0.1), ejection fraction (65 +/- 1 vs 61 +/- 1%) and their ratio (stroke counts/s) (3.7 +/- 0.2 vs 3.2 +/- 0.1) (all p less than 0.05). In phase 3, blood pressure and heart rate were unchanged and reversal of LV hypertrophy was accompanied by a further increase in peak filling rate (2.9 +/- 0.1), ejection fraction (69 +/- 1%) and their ratio (4.1 +/- 0.1) compared to phase 2 (all p less than 0.01). Finally, in phase 4 blood pressure and heart rate returned to the basal value, but peak filling rate (2.7 +/- 0.1) and ejection fraction (65 +/- 1%), although reduced compared to phase 3, were still higher than phase 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1989

Myocardial hypertrophy and left ventricular diastolic function in hypertensive patients: an echo Doppler evaluation.

The presence and the characteristics of left ventricular diastolic dysfunction in mild to moderate systemic hypertension were evaluated in 13 normotensive subjects (Group I), in 12 hypertensive subjects without (Group II) and 28 with (Group III) LV hypertrophy who underwent two-dimensional Doppler echocardiographic study. Among Group III patients, a subset (n = 12) with a dilated left ventricle was identified. Diastolic filling parameters were impaired in Group III patients while, in Group II, they were intermediate between Groups I and III. In all Group III patients normalized peak filling rate (nPFR) correlated directly with mean velocity of circumferential fibre shortening (mVCF) (r = 0.55; P less than 0.001) and inversely with left ventricular mass index (LVM) (r = -0.60; P less than 0.001), left ventricular end-diastolic diameter (LVIDd) (r = -0.63; P less than 0.001), LV peak systolic stress (LVWST) (r = -0.64; P less than 0.01). A separate analysis showed that these correlations were also present in patients without left ventricular dilation; in the subset with left ventricular dilation nPFR correlated only with LVWST (r = -0.73; P less than 0.01), but not with LVM, mVCF, LVIDd. Thus, left ventricular hypertrophy is one of the major determinants of diastolic dysfunction in hypertensives; other factors influence nPFR values in hypertensive patients when the left ventricle dilates.

Adult↗