Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exogenous bradykinin was administered to pigs in which an experimental infarction was evoked by ischemia and reperfusion. Ischemia (45 min) was induced in a closed-chest model with a balloon catheter in the left anterior descending artery, reperfusion by deflating and removing the balloon. The pigs were treated with saline (n = 11) or bradykinin (0.1 mg/kg in 30 min) infusion (n = 10) during the last 15 min of the ischemic period and the first 15 min of reperfusion. During ischemia, heart rate increased in the saline group to 120 +/- 9% of the initial value (p less than 0.05) and in the bradykinin group to 155 +/- 13% (p less than 0.05). After reperfusion, the rate-pressure product was increased in both groups. The increase of arterial creatine kinase levels was significantly less in the bradykinin-treated group. However, the catecholamine and purine levels were increased, as was the plasma renin activity when compared with the saline group. Two weeks after the infarction, six pigs had died in each group. In three out of five surviving saline-treated pigs and one out of four surviving bradykinin-treated pigs, a sustained ventricular tachyarrhythmia was inducible after programmed electrical stimulation. In conclusion, although systemically administered bradykinin caused a temporary increase in myocardial ischemia, it did reduce the (enzymatic indices of) infarct size. Therefore, the beneficial effects, previously found for ACE-inhibitors might at least partially be related to the potentiation of endogenous bradykinin.
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PMID:Beneficial effects of bradykinin on porcine ischemic myocardium. 187 66

It was demonstrated recently that a local renin-angiotensin system (RAS) exists in the heart and coronary vessels, and the angiotensin converting enzyme inhibitors can protect the heart from ischemia. Eight patients with NYHA class II-IV subjected to valve replacement were studied in protecting the heart from global ischemia with captopril during open heart surgery. After the ascending aorta was clamped, 500-1000 ml 4 degrees C modified St. Thomas No 1 cardioplegic solution containing 0.058-0.23 mmol/L captopril was perfused into coronary arteries under pressure until the electrocardiogram showed disappearance of myocardial electroactivity. The cardioplegic perfusion was repeated every 30 minutes thereafter during cardiopulmonary bypass (CPB). All the hearts rebeat after reperfusion either spontaneously or from defibrillation without any trouble. Three patients developed an A-V dissociation which returned to sinus rhythm or atrial fibrillation after a tiny dose of dopamine or isoprenaline intravenously. All the patients weaned from the CPB easily with a stable heart rate and a reasonable MAP. None of them needed inotropic support, even those with severe heart failure before operation did not either, and all recovered uneventfully.
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PMID:Captopril as a component of cardioplegia in protecting the myocardium from global ischemia during open heart surgery. A preliminary clinical report. 187 3

The purpose of this study is to evaluate the role of superoxide dismutase (SOD) in reperfusion injury after lung transplantation in mongrel dogs. Canine left lungs were used and three groups were studied. Group I underwent complete hilar stripping (n = 6). Group II underwent complete hilar stripping and was kept in warm ischemia for 60 min. by clamping left pulmonary artery and veins (n = 6). Group III underwent the same surgery as Group II and kept in warm ischemia for 120 min (n = 6). To evaluate the function of the lung, arterial blood gas, left total pulmonary resistance (ITPR) and lung wet to dry weight ratio (W/D ratio) were measured in transient contralateral pulmonary arterial occlusion periodically for 7 days after reperfusion. Also, plasma and bronchoalveolar lavage fluid (BALF) levels of SOD like activity, angiotensin converting enzyme (ACE) activity and ceruloplasmin were measured before operation and periodically after reventilation and reperfusion. Additionally, using dialyzer and electron spin resonance (ESR) spectrometry, plasma levels of extracellular SOD (EC-SOD) activity were measured. The results obtained were as follows. 1) In Group II and III, W/D ratio, ITPR and arterial blood gas were significantly increased in comparison with Group I. 2) Though there were no significant changes in the BALF levels of SOD like activity, ACE and ceruloplasmin and in the plasma levels of ACE and ceruloplasmin, the plasma level of SOD like activity rose 3 hours after reperfusion. 3) The plasma level of EC-SOD activity rose along with that of SOD like activity without any change in intra-cellular SOD levels. The above results suggest that EC-SOD plays an important role in cyto-protection against reperfusion injury after lung transplantation.
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PMID:[Experimental studies on changes of SOD activity levels and reperfusion injury after lung transplantation]. 196 Apr 52

Over 30 per cent of coronary patients die of cardiac failure excluding the acute phase of myocardial infarction. With the exception of preexisting hypertension, there is no compensatory hypertrophy in ischemic heart disease. However, hypertrophy is a costly adaptation in terms of myocardial oxygen demand and, therefore, coronary flow. Fibrous zones are unresponsive to inotropic drugs and so the treatment of cardiac failure due to ischemic heart disease consists in limiting or preventing episodes of ischemia. Each mechanism of ischemia has an appropriate treatment: the preload is reduced by trinitrin and its derivatives and by molsidomine; the after-load by calcium antagonists and angiotensin converting enzyme inhibitors; tachycardia and hypercontractile states by betablockers. The risk of arrhythmia, aggravated by many inotropic therapies, constitutes the major danger to ischemic heart failure; amiodarone, betablockers and preventive nitrate therapy are the most effective and least dangerous antiarrhythmics. Revascularisation is effective for permanently ischemic segments or for ischemia on effort but does not improve large plaques of fibrosis which sometimes require surgical ablation or plastic procedures. But these measures are incomplete if all aspects of the disease are not taken in consideration: loss of excessive body weight, exercise rehabilitation by modern techniques, limitation of bed rest at the ultimate stage of the disease allowing patients with ischemic cardiac failure a better quality of life without aggravating the prognosis.
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PMID:[Treatment of cardiac insufficiency in ischemic heart disease]. 212 13

Eleven patients with uncomplicated mild-to-moderate hypertension (diastolic pressure 95-115 mmHg) were treated for four weeks with daily single quinapril doses of 20-40 mg. Already during the second week a significant reduction in blood pressure was observed without increase of heart rate; 27.3% of patients responded to the lower dose (diastolic blood pressure [90 mmHg], and 54.6% responded to the higher dose. Drug treatment led to reduced pressure increase in response to cold stimulation without influencing the adrenergic response both in basal conditions and after cold pressor test. The drug brought about peripheral vasodilatation as shown by increased perfusion index during Doppler ultrasound examination, and improved arterial reactivity with increased perfusion index and reduced recovery time after ischemia. The reduction of angiotensin and aldosterone plasma levels during treatment was not correlated to diminished blood pressure values, indicating that the antihypertensive effect can occur via pathways different from ACE inhibition. Tolerance was excellent as shown both by clinical and laboratory evidence.
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PMID:[Clinical-instrumental evaluation of the effects of quinapril treatment in mild-to-moderate hypertension]. 214 11

The converting enzyme not only converts angiotensin I into angiotensin II but also metabolizes bradykinin. Furthermore, the effects of ischemia on myocardial tissue damage can be modulated by converting enzyme inhibitors. It is unknown whether these effects of ACE-inhibitors are due to increased bradykinin production. In this paper we describe the effects of captopril on bradykinin production in the ischemic isolated rat heart. The reduced deleterious effects of ischemia by captopril were associated with a stimulated bradykinin production. Beneficial effects of bradykinin could be due to an improved perfusion or to an effect on cellular metabolism. Therefore, we conclude that this effect on kinins by ACE-inhibitors is of importance in modulating tissue damage during ischemia.
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PMID:The effects of bradykinin and the ischemic isolated rat heart. 216 66

From the discussion of these questions, several conclusions seem firm, whereas other issues await resolution. Patients with severe CHF should be treated with diuretics, digoxin, and an ACE inhibitor. In mild and moderate CHF, a diuretic should be combined with either digoxin or an ACE inhibitor--usually the latter. However, most of these patients would benefit from receiving all three drugs. Patients with asymptomatic left ventricular systolic dysfunction are at jeopardy for progressive deterioration. Angiotensin converting enzyme inhibitors and, possibly, direct vasodilators may prevent progression. In initiating vasodilator therapy, ACE inhibitors usually should be the agent of choice. Exceptions may be patients with ongoing ischemia in whom nitrates are an appropriate alternative and those who are poor candidates because of hypotension, renal insufficiency, or hyperkalemia.
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PMID:Should all patients with congestive heart failure and dilated cardiomyopathy be treated with vasodilators? 219 51

The effects of angiotensin converting enzyme inhibitors (ACEIs), CGS 14831 (CAS 86541-78-8) and captopril, on the mechanical function and energy metabolism were studied in isolated rat hearts using global ischemia-reperfusion model. The myocardial tissue levels of ATP, creatine phosphate (CP) and pH were determined with 31P-nuclear magnetic resonance (31P-NMR). Global ischemia was induced by cross-clamping of the inflow line for 40 min. While thiol containing ACEI, captopril, significantly inhibited the ATP depletion and pH fall produced by ischemia, non-thiol compound, CGS 14831, did not have any influence on the ATP degradation and pH fall during ischemia. Both CGS 14831 (20 micrograms/ml) and captopril (80 micrograms/ml) have little influence on the mechanical function during the ischemia-reperfusion period. L-Cysteine (44.6 micrograms/ml) inhibited the pH fall significantly during the ischemia without exerting influence on the ATP degradation. These data suggest that local renin-angiotensin-aldosterone system does not play an important role in maintenance of the myocardial mechanical function during ischemia-reperfusion. The thiol residue of captopril is not responsible for the inhibitory effect of this compound on ischemia-induced ATP degradation. Some specific effect of captopril may play a role in the protective effect.
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PMID:Effects of two angiotensin converting enzyme inhibitors on the mechanical function and energy metabolism of isolated rat hearts. A nuclear magnetic resonance study with an active form of benazeprilat and captopril. 229 44

The author studied the effect of post-ischemic delayed hypoperfusion on the recovery process of brain function after complete cerebral ischemia in a dog model in which the existence of PDH had been shown previously by the author, using nicardipine as a tool to ameliorate the PDH, the effect of the drug also having been demonstrated by the author in the previous study. Twenty-four dogs underwent 15 min complete cerebral ischemia using aortic clamping method with aorto-atrial bypass formation. EEG (for 16 h) and brain functions, awakening, cranial nerve reflexes, motor functions, behaviors and respiratory functions were evaluated using neurological deficit score (NDS) periodically (for 120 h) after ischemia. Eight dogs (1 microgram group) received nicardipine 1 microgram.kg-1.min-1 for 4 h following 10 micrograms bolus iv injection 5 min after declamping of aorta, another 8 dogs (2 micrograms group) received 10 micrograms + 2 micrograms.kg-1.min-1 nicardipine in the same manner as group 1, and the remaining 8 served as controls. In 1 microgram group the first appearance of EEG activities after ischemia was earlier than control group (41 +/- 11 vs 80 +/- 33 min), and also the appearance rate of alpha waves was higher than the controls (87.5% vs 25%) 16 h after declamping of aorta. NDS scores for awakening, behavior, and respiratory functions were better in 1 microgram than the controls between 36 and 48 h post-ischemia, but there were no significant changes in the scores between the two groups 120 h after ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of post-ischemic delayed hypoperfusion on the process of recovery of brain function]. 236 39

Captopril, an angiotensin converting enzyme inhibitor, has been shown to increase prostaglandin production by an as yet unknown mechanism, which this study was designed to explore. Isolated rat heart was perfused by the Langendorff technique for 15 minutes in the presence or absence of captopril. Ischemia was then induced for 60 minutes by terminating the coronary flow, followed by 60 minutes of reperfusion. Our results indicate that captopril stimulated prostaglandin and thromboxane production, but it inhibited malonaldehyde formation. Coronary flow and high energy phosphate compounds were increased, but lactate dehydrogenase and creatine kinase release decreased, demonstrating cardioprotective effects. Captopril also inhibited the production of hydroxyl radical in the heart during reperfusion, suggesting that stimulated prostaglandin production may be linked with the generation of free radicals via the eicosanoid system.
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PMID:Enhanced prostaglandin production in the ischemic-reperfused myocardium by captopril linked with its free radical scavenging action. 269 79


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