Drugs online research references
J Pharmacol Exp Ther. 1991 Jun;257(3):919-29.
Effects of different angiotensin-converting enzyme (ACE) inhibitors on ischemic isolated rat hearts: relationship between cardiac ACE inhibition and cardioprotection.
Grover GJ, Sleph PG, Dzwonczyk S, Wang P, Fung W, Tobias D, Cushman DW.
Department of Pharmacology, Squibb Institute for Medical Research, Princeton, New Jersey.
We determined the relationship between cardiac angiotensin-converting enzyme (ACE) inhibition and anti-ischemic efficacy of several structurally different ACE inhibitors or their prodrug esters perfused through the isolated rat heart. Seven ACE inhibitors inhibited cardiac ACE to varying degrees due to differences in uptake during perfusion through nonischemic rat hearts. Zofenopril-sulfhydryl and fosinoprilic acid were the most effective of the free inhibitors. Among the prodrugs, zofenopril and S-benzoylcaptopril, hydrolyzed rapidly by cardiac esterase, were more effective than their component ACE-inhibitors, whereas fosinopril, ramipril and enalapril were poorly active. For studies in ischemic rat hearts, vehicle or drug treatment was initiated 10 min before a 25-min period of global ischemia and during a 30-min reperfusion period. Of five unesterified ACE inhibitors studied for anti-ischemic activity, only captopril and zofenopril-sulfhydryl were found to improve postischemic contractile function and reduce cell death in the isolated rat hearts. Fosinoprilic acid, ramiprilat and enalaprilat were not cardioprotective at high perfusion concentrations, despite the fact that nearly complete inhibition of cardiac ACE was achieved with all of the compounds studied. The S-benzoyl prodrugs of zofenopril-sulfhydryl and captopril were at least as potent as their component ACE inhibitors in reducing ischemic-reperfusion damage in the same model. Neither zofenopril nor captopril, however, had any effect on coronary flow before or after ischemia. Thus, it appears that the cardioprotective effects of zofenopril and captopril are independent of cardiac ACE inhibition or, at least, that ACE inhibition alone is not sufficient. Both captopril and zofenopril are sulfhydryl-containing compounds whereas the inactive compounds are not; and, thus, this group appears to be important in mediating their cardioprotective actions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1646329&dopt=Abstract
Minerva Med. 1987 Nov 15;78(21):1601-6.
[Prolonged treatment of hypertension in diabetic patients with enalapril. 1-year follow-up]
[Article in Italian]
Lanza G, Barbera R, Travaglino F, Fontana S.
Ospedale degli Infermi, Divisione di Medicina Generale B, U.S.S.L. n. 47, Biella, Vercelli.
In view of the pharmacological and chemical reasons for using ACE-inhibitors to treat diabetic hypertension, a group of 40 outpatients were treated with Enalapril. The sample consisted of 20 outpatients, 6 males, 14 females aged 48-76 (mean age 63.75), 18 of whom had type II and 2 type I diabetes and 11 under treatment by diet and hypoglycaemic drugs or insulin. All these patients presented slight or moderate essential arterial hypertension (diastolic pressure less than 115 mmHg). For about one year 17 of the patients were given 20 mg/die Enalapril and the remaining three 10 mg/die in a single morning dose. In 16 cases no other treatment was given. In 4 a non-potassium conserving diuretic was also given. Check-ups before six months into and at the end of treatment showed: a statistically significant reduction in systolic (p less than 0.05) and diastolic (p less than 0.01) pressure. In contrast no significant change was noted in heart beat, glycaemia before or after meals, body weight, glycosylated haemoglobin or any other blood chemical parameter considered. In one case only there was a slight increase in proteinuria that was however present at the start of treatment. As far as side effects are concerned there was one case of cardiac palmus during treatment and one case of coughing that regressed totally when treatment was suspended but nothing else of significance. It should be noted that the antidiabetic treatment remained unchanged throughout the period considered in most cases and at most was subjected to minimal qualitative and quantitative adjustments.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2825079&dopt=Abstract
Ann Vasc Surg. 1994 Mar;8(2):158-65.
Suppression of intimal hyperplasia in a rabbit model of arterial balloon injury by enalaprilat but not dimethyl sulfoxide.
Law MM, Colburn MD, Hajjar GE, Gelabert HA, Quinones-Baldrich WJ, Moore WS.
Section of Vascular Surgery, UCLA School of Medicine 90024.
Intimal hyperplasia appears to result from the deposition of collagen and matrix by medial myofibroblasts, which are stimulated in response to vascular injury. We hypothesized that pharmacologic inhibitors of fibroblast proliferation would suppress the development of intimal hyperplasia. We evaluated the effect of two agents known to inhibit fibroblast proliferation in vitro: enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor, and dimethyl sulfoxide (DMSO), an organic solvent. Thirty-five New Zealand white rabbits underwent standardized balloon catheter injury of the left common carotid artery. Experimental groups received daily intramuscular injections of the following: group I (n = 15), saline solution; group II (n = 10), 0.07 mg/kg enalaprilat; and group III (n = 10), 2 ml/kg of a 25% by weight DMSO solution. Injections were started 1 day prior to injury and continued 5 days a week for 8 weeks. Carotid arteries were perfusion-fixed at 12 weeks and cross-sectioned for measurement by planimetry. Intimal hyperplasia was measured as the ratio of the absolute area of intimal hyperplasia to the normalized area enclosed by the internal elastic lamina (IH/IEL) and was expressed as a percent. Mean values for IH/IEL were as follows: group I (control), 20.6 +/- 2.3%; group II (enalaprilat), 9.5 +/- 0.7%; and group III (DMSO), 17.6 +/- 2.6%. Enalaprilat-treated animals demonstrated a statistically significant suppression of intimal hyperplasia compared with controls (p < 0.01, ANOVA, Student's t test), whereas the DMSO-treated group did not. We conclude that enalaprilat is effective in suppressing the development of intimal hyperplasia in this model of arterial injury.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8198949&dopt=Abstract
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