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)

Cor pulmonale is an important consequence of COPD. Although the incidence is not precisely known, it is seen more frequently in patients with hypoxemia, CO2 retention and severely reduced FEV1. When present, it limits peripheral oxygen delivery, increases shortness of breath, and reduces exercise endurance. It is also associated with higher mortality rates independent of other prognostic variables. Numerous factors may contribute to the development of cor pulmonale in patients with COPD, but its primary cause is chronic alveolar hypoxia resulting in pulmonary vasoconstriction, vascular remodeling and pulmonary hypertension. The physical exam, chest radiograph and ECG may be helpful in detecting the presence of cor pulmonale, but because of anatomic changes that occur in the chest, these tests are often insensitive in patients with COPD. Noninvasive diagnostic techniques utilizing Doppler echocardiography and radionuclide angiography allow for detection of RV dysfunction at an earlier stage and in most cases, preclude the need for right heart catheterization. LTO2 is the only therapy shown to improve survival in patients with COPD. However, statistical proof correlating improvements in pulmonary hemodynamics with increased survival is lacking. Bronchodilators, such as the beta 2 agonists and especially theophylline, may have beneficial effects on pulmonary hemodynamics in addition to their effect on respiratory function and are useful in COPD when RV dysfunction is present. Diuretics and phlebotomy are also useful in improving symptoms in appropriate patients. Vasodilators such as calcium channel blockers and ACE-inhibitors may improve pulmonary hemodynamics acutely, but may lower arterial PO2 by worsening ventilation-perfusion matching or blunt the improvement in pulmonary hemodynamics seen with supplemental oxygen. The long-term benefits of these agents have not been proven and their routine use in patients with cor pulmonale due to COPD cannot be recommended.
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PMID:Right ventricular dysfunction in chronic obstructive pulmonary disease. Evaluation and management. 199 28

Eleven patients with coronary artery disease and chronic heart failure were studied before and three months after the angiotensin converting enzyme inhibitor enalapril was added to their frusemide medication. The following were measured: left ventricular pressure and volume with transient occlusion of the inferior vena cava, radionuclide angiography, and hormone concentrations in plasma. As in other reported studies, the clinical condition of the patients improved and their exercise tolerance increased moderately. Addition of enalapril reduced end diastolic and systolic pressure, reduced ventricular volume, and concomitantly increased the ejection fraction. The end systolic pressure-volume relation shifted to the left as it did in a similar animal study. In the animal study unloading by a vasodilator did not induce a leftward shift, so it can be inferred that in the present study unloading combined with a decrease in the angiotensin concentration was instrumental in remodelling the heart. Though unloading was expected to have a beneficial effect on the oxygen supply/demand ratio of the heart, the patients still showed the same drop in the ejection fraction during exercise as they did before treatment with enalapril, and early diastolic filling did not improve. Normally, regression of cardiac dilatation is only found if pump function improves; the present study showed that unloading in combination with angiotensin converting enzyme inhibition reshapes the ventricle without improving intrinsic pump function.
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PMID:Influence of angiotensin converting enzyme inhibition on pump function and cardiac contractility in patients with chronic congestive heart failure. 201 21

Overall 94 patients with different patterns of pulmonary tuberculosis were examined for glutathione peroxidase (GP), glutathione reductase, glucose 6-phosphate dehydrogenase (G 6-PDH) and superoxide dismutase activity in neutrophils and lymphocytes. Chemiluminescence was used to study the capacity of neutrophils to generate free oxygen forms. Neutrophils showed functional deficiency of GP and G 6-PDH. The decrease of the oxygen-producing capacity of neutrophils, unbalance of glutathione-conjugated enzymes in lymphocytes were revealed either. The role of the alterations enumerated in the reduction of function of phagocytizing and immunocompetent cells in patients with pulmonary tuberculosis is discussed.
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PMID:[The oxidative metabolic indices of phagocytizing and immunocompetent cells in patients with pulmonary tuberculosis]. 209 92

Given the absence of curative and preventive treatment of cardiac failure, symptomatic therapy is very important. In severe "non-ambulatory" cardiac failure, symptoms depend on the patient's resting hemodynamic status. This can be improved by diuretics, digitalis and vasodilators. A combination of these three drug groups is often required. However, the respective value of each group is unknown. Their use is limited by their specific undesirable secondary effects which are particularly common and severe at this advanced stage. Their effects on survival are unknown with the exception of angiotension converting enzyme inhibitors which have been shown to be beneficial. At the ambulatory stage symptoms occur on effort. In order to improve exercise capacity, the treatment chosen should increase the patient's reserve of cardiac output, limit the increase in pulmonary pressures, respect systemic arterial pressure, decrease venous pressure, dilate the muscular arterioles and improve oxygen extraction by skeletal muscle during physical exercise. Diuretics and angiotensin converting enzyme inhibitors can fulfill these objectives. The effects of the other vasodilators are more variable, due to a vasodilatation which is often inappropriate and to tachyphylaxis related to reflex activation of neuro-hormonal mechanisms. Digitalis and some vasodilator inotropic agents can improve symptoms and effort capacity. However, doubts over possible deleterious effects on mortality have to be cleared by large scale, controlled therapeutic trials. Symptoms of cardiac failure at the ambulatory stage and the effects of treatment on these symptoms should logically be evaluated by appropriate ergometric exercise stress testing, with measurement of the patient's maximum oxygen consumption whenever possible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Symptomatic treatment of chronic cardiac insufficiency]. 212 11

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

Selected functions of alveolar macrophages obtained by bronchoalveolar lavage of 12 healthy smokers were examined before and after eight weeks' treatment with an inhaled glucocorticosteroid, budesonide (400 micrograms twice daily). After budesonide treatment spontaneous as well as opsonised zymosan triggered prostaglandin E2 (PGE2) secretion from harvested cells was reduced; no such reduction in opsonised zymosan triggered leukotriene B4 (LTB4) production was observed. Neither the capacity to phagocytose opsonised yeast particles nor the superoxide radical generation triggered by the calcium ionophore A23187, 4 beta-phorbol 12-myristate 13-acetate (PMA), or opsonised zymosan ex vivo were more than marginally affected by the glucocorticosteroid treatment in vivo. Lavage fluid concentrations of angiotensin converting enzyme (ACE), however, after treatment were twice those before treatment and concentrations of fibronectin were reduced to half. Albumin concentrations in lavage fluid were not affected by the glucocorticosteroid treatment. In separate experiments treatment of alveolar macrophages with 10(-7) or 10(-6) M budesonide overnight in vitro did not affect their superoxide radical or PGE2 generation but significantly blocked LTB4 release. These data indicate that inhaled gluco-corticosteroid treatment may affect synthesis or release (or both) of ACE and fibronectin by alveolar macrophages from healthy smokers whereas other functions of these cells, such as the generation of reactive oxygen derived products ex vivo, are only marginally affected.
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PMID:Effects of an inhaled corticosteroid, budesonide, on alveolar macrophage function in smokers. 216 59

We have studied the in vitro interactions versus some blood components of the hemoglobin niosomes whose preparation and physicochemical and oxyphoric properties have been published in a precedent paper (this journal, 1989, No. 7, p. 192). This work was devoted to the research of 1) Agglutination phenomena with ABO blood group substances, plasma, some of its components and three plasma expanders, finally main erythrocytic phenotypes. 2) Adsorption of plasma proteins by immunoelectrophoresis. 3) Effects of niosomes on blood coagulation by thromboelastography. 4) Interactions between niosomes and phagocytes by electron microscopy, chemotactic migration, oxygen consumption, superoxide generation and oxydases function. These assays allow to observe and conclude that: 1) The agglutination phenomena are almost constant except with red blood cells. The agglutinates are dissociable by shaking. The agglutination appears to be nonspecific of a niosome component but is not observed with "classical" DPPC-chol-DCP liposomes. 2) Albumin and eventually transferrin are adsorbed at the surface of niosomes but without destabilizing them. 3) The vesicules show no important effects on coagulation factors, the enhancement of clotting time appearing essentially the consequence of blood dilution. 4) Niosomes phagocytosis is important but all the measurements fail to show any cellular metabolism activation: cell oxygen consumption, oxygenated metabolites generation and oxydases activity are not enhanced whatever the "electric" charge or the niosomes/phagocytes ratio used.
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PMID:[Hemoglobin niosomes. II. In vitro interactions of plasma proteins and phagocytes]. 218 79

A single blind, placebo controlled, dose-ranging 3 month study of the effects of enalapril on cardiovascular parameters, clinical status and self-paced exercise capacity was undertaken in 12 Nigerians with chronic heart failure. Enalapril exerted only a modest reduction in blood pressure and heart rate but significantly improved functional capacity (P less than 0.01), and prolonged self-paced exercise time (P less than 0.05) compared to the placebo baseline. The pressure rate product and the double product corrected for exercise time, an index of myocardial oxygen demand, exhibited a significant and sustained reduction on enalapril treatment (P less than 0.01). Concentration of sodium in the serum was significantly increased (P less than 0.05) but concentrations of potassium and creatinine were unaltered. These results demonstrate the sustained efficacy of enalapril in black Africans with heart failure and indicate no important racial difference in the response to inhibition of angiotensin converting enzyme in congestive heart failure.
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PMID:Sustained beneficial effects of enalapril in Africans with congestive heart failure. 226 16

Aldrin toxicity was studied in the brain, liver and muscle of Rana hexadactyla. It was observed that sublethal concentration of aldrin inhibited the activities of SDH, MDH and ICDH while it elevated the activities of LDH and G-6-PDH. The increase and the decrease was progressive with the exposure period. The changes were attributed to the induced toxic effects such as oxygen distress, energy crisis and microstructural changes.
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PMID:Aldrin toxicity on amphibian neuronal, hepatic and muscular tissue oxidative enzymes. 228 77

Maximal activities of antioxidant enzymes involved in oxygen free radical metabolism in skeletal muscle and liver were investigated in 4-, 26-, and 31-mo-old male Wistar-Furth rat at rest and after a single bout of treadmill exercise. In skeletal muscle, cytosolic (Cu-Zn) and mitochondrial (Mn) superoxide dismutase (SOD) specific activities were significantly higher in the aged rats and at 31 mo reached 135 and 218%, respectively, of those at 4 mo. Resting catalase activity was doubled at 31 mo compared with that at 4 mo. Glutathione peroxidase (GPX) activity increased twofold in muscle cytosol and by 47% in mitochondria of aged rats. Glutathione S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G-6-PDH) activities in muscle were also significantly elevated. Hepatic antioxidant enzymes were altered differentially with aging. Cytosolic SOD and GST activities were decreased, whereas mitochondrial GPX, GR, and G-6-PDH activities were increased. Lipid peroxidation was greater in skeletal muscle homogenate and mitochondria but lower in liver homogenate in the aged rats. An acute exercise bout had little effect on muscle or liver antioxidant enzymes regardless of the animal's age. It is concluded that aging is accompanied with an elevation of antioxidant enzyme activities and lipid peroxidation in skeletal muscle probably due to the increased oxygen free radical production and reaction.
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PMID:Alteration of antioxidant enzymes with aging in rat skeletal muscle and liver. 233 Oct 35


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