Effects of the angiotensin-converting enzyme inhibitor alacepril in dogs with mitral valve disease Alacepril is a relatively novel angiotensin-converting enzyme inhibitor; however, the safety, tolerance, and efficacy of alacepril in terms of cough suppression in dogs with mitral valve disease (MVD) remain unknown. The aim of this study was to investigate the safety, tolerance, and cough suppression efficacy of alacepril in dogs with MVD. This was a multi-center, prospective study. Forty-two dogs with echocardiographic or radiographic evidence of cardiac enlargement in addition to cough were enrolled. Dogs were treated with alacepril (1.0-3.0 mg/kg/day) for at least 4 weeks. One dog (2.4%) developed complications, including appetite loss, lethargy, and vomiting. Thirty-six dogs were re
The Relationship between Reactive Oxygen Species and Cardiac Fibrosis in the Dahl Salt-Sensitive Rat under ACEI Administration Enalapril maleate, the oldest and most widely distributed ACEI, and alacepril, the newest and antioxidant ACEI, were compared in the point of cardioprotective effect for Dahl salt-sensitive rat. In order to evaluate the correlation between the three factors, cardiac fibrosis and blood pressure/oxidative-stress marker (tissue TBARS), index of correlation was calculated. The results showed a significant difference in cardiac fibrosis between high-dose alacepril (30 mg/kg/day, group H) and enalapril maleate (10 mg/kg/day, group E). There was significant correlation between cardiac fibrosis and oxidative-stress marker, although there was no correlation between cardiac
Beneficial effect of alacepril, a new angiotensin-converting enzyme inhibitor on albuminuria and glycemic state: an open multicenter trial. Alacepril Study Group. Alacepril is a new angiotensin-converting enzyme (ACE) inhibitor that possesses sympatho-inhibitory action. We evaluated the effect of alacepril on blood pressure and progression of diabetic nephropathy in hypertensive type II diabetics in an open multicenter trial. Eighty-nine type II diabetics with mild hypertension were treated with 50 mg of alacepril daily and observed for 12 weeks. Blood pressure was reduced significantly at 4 weeks; this reduction continued throughout the study. Urinary excretion of albumin also was reduced significantly at 12 weeks. Glycosylated hemoglobin (HbA1c) and serum total cholesterol showed significant
Effects of acute and chronic alacepril treatment on exercise capacity and hemodynamics in patients with heart failure: a preliminary study. This study determined whether alacepril treatment improves exercise hemodynamics in patients with heart failure. Supine bicycle ergometer exercise was performed after administration of placebo and after acute and chronic (12 weeks) alacepril treatment in 4 patients with heart failure. Oxygen uptake (VO2), arterial oxygen saturation (SaO2), and mixed venous oxygen saturation (SvO2) were measured continuously using a pulse oxymeter and a fiber optic catheter. Cardiac index was calculated with Fick's equation. Acute alacepril treatment did not significantly alter the VO2 or hemodynamics. After chronic alacepril treatment, peak VO2 increased (placebo vs
Effects of angiotensin-converting enzyme inhibitor alacepril in patients with stable effort angina during chronic isosorbide dinitrate treatment. Nitrate tolerance has been reported to be reversed by certain types of angiotensin-converting enzyme (ACE) inhibitors. We examined whether alacepril, a new long-acting oral ACE inhibitor, has beneficial effects against exercise-induced angina in patients with stable effort angina after substantial isosorbide dinitrate (ISDN) treatment. Thirteen men with stable effort angina were treated with oral ISDN (80 mg/d) for >3 weeks. After this period, efficacy of single oral administration of either alacepril (50 mg) or its placebo on exercise-induced angina and electrocardiographic changes was examined by treadmill exercise test in a double-blind
Effect of antihypertensive therapy on aortic distensibility in patients with essential hypertension: comparison with trichlormethiazide, nicardipine and alacepril. To assess the effect of antihypertensive drugs on aortic distensibility, we evaluated the aortic distensibility of 33 hypertensive patients before and after antihypertensive treatment by using cine magnetic resonance imaging. Thirty three hypertensive patients were divided into three groups and treated for 12 weeks with 2-4 mg trichlormethiazide per day (n = 10), 80 mg nicardipine per day (n = 13) and 50 mg alacepril per day (n = 10). There were no significant differences in mean age and mean blood pressure among the three groups. Cine magnetic resonance was performed at ascending and descending aortic levels. Aortic area
Both a calcium antagonist and ACE inhibitor reverse hypertrophy in hypertension but a calcium antagonist also depresses contractility. The aim of this study was to compare the effects of a calcium antagonist, nicardipine SR, with an angiotensin-converting enzyme (ACE) inhibitor, alacepril, on the regression of left ventricular hypertrophy (LVH) and function. Twenty patients with LVH, aged 42-78 years, were treated with nicardipine SR or alacepril. Ten patients were treated with nicardipine SR (40-80 mg) for 21 months, and the other 10 patients were treated with alacepril (25-100 mg) for 18 months. All patients underwent echocardiography to assess left ventricular structure and function before and after the treatment. After nicardipine SR or alacepril treatment, blood pressure was decreased
Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension. We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both
Responses of plasma concentrations of A type natriuretic peptide and B type natriuretic peptide to alacepril, an angiotensin-converting enzyme inhibitor, in patients with congestive heart failure. Plasma concentrations of A type or atrial natriuretic peptide (ANP) and B type or brain natriuretic peptide (BNP) are increased in patients with congestive heart failure (CHF). To examine the haemodynamic and hormonal responses, especially of ANP and BNP, to oral administration of an angiotensin-converting enzyme (ACE) inhibitor in patients with CHF and in controls. 12 patients with CHF and 11 controls. Haemodynamic variables and plasma concentrations of ANP, BNP, and other hormones were serially measured for 24 hours after alacepril (37.5 mg) was given by mouth. Pulmonary capillary wedge
Responses of plasma concentrations of A type natriuretic peptide and B type natriuretic to alacepril, an angiotensin-converting enzyme inhibitor, in patients with congestive heart failure.
[Treatment of latent diabetic nephropathy with ACE inhibitor alacepril]. Latent diabetic nephropathy with no complication such as retinopaty and hypertension was treated with Alacepril, an ACE inhibitor. This study enrolled 10 patients with microalbuminuria ranging from 5 mg/day (5 mg/gCr) to 50 mg/day (30 mg/gCr). Histological changes due to diabetic nephropathy were confirmed by renal biopsy performed in 4 of 10 patients. All the patients were divided into 2 groups; 5 patients were given 25 mg of Alacepril for 6 months and the remaining 5 patients were employed as the control. As the results, the mean blood pressure was decreased from 92.7 +/- 9.0 mmHg to 87.3 +/- 11.3 mmHg in Alacepril group but these changes were not statistically significant. Microalbuminuria were significantly decreased
on the body after exercise and Cystic fibrosis in a relative suggestive of the individual being a carrier. 11. Heart arrhythmia, known or evident on ECG 12. Known intolerance or allergy to lidocaine 13. Already taking supplemental potassium or renin angiotensin aldosterone inhibitors or other potassium elevating agents (see list below)Angiotensin Converting Enzyme Inhibitors 1. Alacepril (not available