Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the period from 1968 to 1977, in the Departments of Cardiology of the S. Camillo Hospital, a study has been made about 200 cases of Congestive Cardiomyopathy (MPC) and 100 about hypertrophic obstructive (MP0). Congestive cardiomyopathies constitute 1.5% of hospitalizations with a constant trend in the long run. In comparing these two forms, Authors have noticed some differences in the symptomatology of clinical and instrumental signs: 1) in case of MPO prevail angina, syncope, ejection systolic murmur, left ventricular overload in the ECG; 2) in case of MPC they find more frequently heart failure, embolism, diastolic gallop, cardiomegaly, A/V and intraventricular conduction disturbs. The AA. conclude, in accordance with Goodwin's classification, that there is not an uniformity of these two kinds of cardiomyopathies.
G Ital Cardiol 1979
PMID:[Epidemiological and clinical observations on 300 cases of primary myocardiopathy]. 45 5

Studies were carried out in rats on myocardial adaptation to injury produced by left coronary artery ligation. In the ischemic zone, open collaterals were present as shown by studies using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). This phenomenon may explain the inhomogeneous cardiac muscle cell alteration in the early phase of coronarogenic myocardial injury. Reperfusion, as evidenced by the influx of HRP into the damaged cells, unmasked sarcolemmal membrane injury. Cardiac muscle cell stimulation modifies the binding of macromolecules to cell components and may influence the repair processes. In the surviving myocardium, correlative enzyme histochemical and ultrastructural studies demonstrated the development of alternative metabolic pathways and morphological signs of adaptation explaining increasing resistance of such cardiac muscle cells to subsequent insult.
Basic Res Cardiol
PMID:Experimental studies on cardiac muscle cell adaptation to insult. 87 Dec 98

The behaviour of some enzymatic activities, such as monoamino oxidase (MAO), diamino oxidase (DAO), catalase, peroxidase and creatin chinase (CPK) have been studied both in blood serum and myocardial tissue of acute infarcted dogs (obtained by coronary occlusion). The most significant results are the changes of the DAO activity (--50% from the control) and peroxidase activity (+60%), 6 hours after acute ischemia. The effect of reperfusion was studied 2 hours later. A recovery of DAO activities was shown, while the peroxidase activities stayed elevated. All the enzymatic activities studied were evaluated in the serum, under the same experimental conditions. An increase of all these activities was observed until 6th hour of coronary occlusion. The reperfusion of acute ischemia, after six hours, causes a further increase of CPK and MAO activities and a decrease of catalase peroxidase and particulary evident DAO activities. The results of this experiment show that reoxygenation, under our experimental conditions, increases a further enzymatic release and in part causes a metabolic recovery of heart muscle.
G Ital Cardiol 1976
PMID:[Experimental revascularization of acute myocardial infarction. II: Activity of various oxidoreductive tissutal and serum enzymes (author's transl)]. 101 Jan 98

Myocardial ischemia followed by reperfusion results in endothelial dysfunction in cats. This dysfunction is characterized by a loss of endothelium-derived relaxing factor (EDRF) release in response to endothelium-dependent dilators. This loss of endothelium-dependent relaxation (EDR) occurs significantly at 2.5 min post-reperfusion and the dysfunction progresses until it is complete at 20 min post-reperfusion. This reduced EDR is prevented by superoxide dismutase, but not by hydroxyl radical scavengers. In contrast, neutrophil accumulation in the heart, as measured by cardiac myeloperoxidase (MPO) activity, does not reach significant levels until 3 h post-reperfusion, and significant myocardial necrosis does not occur until 4.5 h post-reperfusion. No significant changes in EDR, MPO or cardiac necrosis occurred during the 90 min of ischemia. Thus, endothelial dysfunction is an early and specific marker of reperfusion injury preceding neutrophil involvement and cardiac necrosis. Superoxide radicals appear to play a key role in the decreased EDR observed early after reperfusion.
Basic Res Cardiol 1991
PMID:Endothelial dysfunction in myocardial ischemia and reperfusion: role of oxygen-derived free radicals. 165 71

A perforated balloon catheter was used in human coronary arteries after postmortem angioplasty had been performed. The catheter used has a standard angioplasty balloon with a pattern of laser-produced holes, 25 microns in size, which generate streams of fluid under pressure. Studies of the routes by which marker substances enter diseased arterial tissue when infused by the perforated balloon after experimental angioplasty are described. A colored marker dye entered the new crevices and dissection planes created by the angioplasty, but did not extend greater than 2 cm either proximal or distal to the perfused segment. Horseradish peroxidase entered tissue not only from the lumen and adventitia as occurs with its infusion into normal tissue with the perforated balloon, but also extended from new crevices and dissection planes created by the angioplasty. Platelet aggregation, coagulation and cell proliferation, the likely causes of restenosis after angioplasty, originate in the sites of greatest tissue disruption and blood stasis. These postmortem studies suggest that active drugs are delivered to the arterial wall in a manner likely to be effective in preventing these events.
J Am Coll Cardiol 1991 May
PMID:Use of the perforated balloon catheter to infuse marker substances into diseased coronary artery walls after experimental postmortem angioplasty. 170 1

The effects of low dose human superoxide dismutase and low dose taprostene, a stable analogue of prostacyclin, were investigated separately and together in a model of myocardial ischemia (1.5 h) with reperfusion (4.5 h) in open chest, anesthetized cats. Taprostene (60 ng/kg per min), human superoxide dismutase (0.25 mg/kg per h), both agents together, or their vehicle, were infused intravenously in cats starting 0.5 h after occlusion of the left anterior descending coronary artery. Neither low dose taprostene nor low dose human superoxide dismutase exerted any endothelial or myocardial protection in this model. However, the two agents together showed a significant endothelial and myocardial protection in cats with myocardial ischemia and reperfusion. Compared with cats that were untreated or received only taprostene or human superoxide dismutase, cats receiving both agents exhibited a lower plasma creatine kinase activity at every time point observed after reperfusion, a reduced area of cardiac necrosis (7 +/- 2% vs. 21 +/- 5% area at risk, p less than 0.001), lower myeloperoxidase activity in the ischemic region (p less than 0.01) and a significant preservation of vasorelaxant responses of left anterior descending coronary rings to endothelium-dependent vasodilators, acetylcholine (p less than 0.001) and A-23187 (p less than 0.001). Taprostene appears to act additively with human superoxide dismutase to inhibit neutrophil adherence and activation and to inactivate superoxide radicals, and thus reduce cellular injury 4.5 h after reperfusion of the ischemic heart. Use of this agent may allow low doses of superoxide dismutase to be used more effectively in early myocardial ischemia.
J Am Coll Cardiol 1992 Jan
PMID:Low doses of superoxide dismutase and a stable prostacyclin analogue protect in myocardial ischemia and reperfusion. 172 34

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1991 Jun 15
PMID:Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction. 190 90

We occluded the left anterior descending coronary artery of anesthetized, open-chest dogs, for 1 or 2 h. Some hearts were reperfused for 1 h after 1 h of ischemia. We isolated mitochondria from the central ischemic zone (CIZ) and a surrounding nonischemic zone (NIZ) of the left ventricle, and assayed H2O2 production using a horseradish peroxidase-dual wavelength spectrophotometric technique. Mitochondria, studied in the absence of exogenous respiratory chain inhibitors, generated H2O2 during State 4 respiration with succinate as the substrate. NIZ mitochondria in all groups produced ca. 1.5 nmols H2O2/min/mg protein (no significant differences between groups). The State 4 O2 consumption rates of NIZ mitochondria from hearts subjected to 1 h ischemia plus reperfusion, or 2 h of ischemia (ca. 30 nmols/min/mg) were significantly higher than that of NIZ mitochondria of hearts subjected to only 1 h of ischemia (23 nmols/min/mg). Thus, the ratio between H2O2 produced and State 4 O2 consumption fell from 6.5% to 5%. Mitochondria from all CIZ samples had State 4 O2 consumption rates that were not different from corresponding NIZ values. However CIZ mitochondria of hearts subjected to 1 h ischemia without reperfusion produced less H2O2 (1.1 +/- 0.1 nmols/min/mg), and had a slightly reduced H2O2/O2 ratio (4.4 +/- 0.7%), compared with their NIZ samples (1.5 +/- 0.1 nmols/min/mg; 5.3%). Reperfusion after 1 h of ischemia abolished these regional differences. The CIZ mitochondria from hearts subjected to 2 h ischemia produced only 0.75 +/- 0.22 nmols H2O2/min/mg (2.5% of State 4 O2 consumption). These values were 50% of corresponding NIZ values, and were significantly less than for any other group or tissue region. If similar phenomena occur in conscious animals subjected to incomplete regional ischemia, especially of relatively brief duration or if accompanied by reduced intracellular defenses against oxidants such as H2O2, they suggest that mitochondria persist as H2O2 sources and so may contribute to the oxidant load and myocardial dysfunction.
Basic Res Cardiol
PMID:Hydrogen peroxide generation by mitochondria isolated from regionally ischemic and nonischemic dog myocardium. 224 65

A perforated catheter was used to deliver either horseradish peroxidase or fluoresceinated heparin under pressure to the canine arterial wall. Depth of penetration of the media by horseradish peroxidase was dependent on perfusion pressure. At 5 bar pressure for 1 min, the entire media showed a reaction product for horseradish peroxidase. Fluoresceinated heparin delivered under the same conditions could be demonstrated to traverse the entire media as well. A pressure of 5 bars caused medial necrosis at 48 h after perfusion, even when the perfusing solution was saline. (This did not differ from the effect of standard angioplasty at the same pressure.) However, heparin at 5,000 U/ml did not cause medial alteration at 48 h when delivered at the lower pressure of 500 mm Hg. It is feasible to deliver heparin over 1 min in high concentration to the arterial wall by means of this balloon catheter. This method may permit the use of commercially prepared heparin in high concentration as an antiproliferative agent to control the problem of restenosis after angioplasty.
J Am Coll Cardiol 1990 Feb
PMID:Use of a perforated balloon catheter to deliver concentrated heparin into the wall of the normal canine artery. 229 88

To evaluate the relationship between mitral valve prolapse (MVP) and autonomic nerve dysfunction, clinical and immunohistochemical studies were performed. I. Clinical study Autonomic function tests and supine bicycle exercise were performed in 60 patients with MVP, 41 under 35 years of age and 19 of 35 years and older, and the results were compared with those of 31 normal controls, 19 under 35 years of age and 12 of 35 years and older. Case with positive response on postural stress and cold pressor tests were more frequent in both MVP groups than those of controls. Plasma nor-adrenaline levels were higher in the MVP groups than in the control groups during exercise. Our clinical observation suggested that autonomic dysfunction, particularly sympathetic hyperactivity, probably is present in MVP irrespective of age. II. Immunohistochemical study In 23 mitral valves (15 of normal controls and eight of MVP), three normal tricuspid, three normal aortic and three normal pulmonic valves, immunohistochemical localizations of S-100 protein, glial fibrillary acidic protein (GFAP) and neurofilament protein (NFP) were examined to detect the distribution of all nerve endings, choline acetyltransferase (ChAT) to detect the distribution of cholinergic nerve fibers, and neuropeptide Y (NPY) and calcitonin gene related peptide (CGRP) to detect the distribution of afferent nerve fibers, using the avidin-biotin peroxidase complex (ABC) method. The distribution of adrenergic nerve fibers was examined by fluorescence with the glyoxylic acid method. In normal valves, S-100 protein was mainly demonstrated in the base and body of the valve cusp. It was very scanty in the tip, and was only found in the coaptation zone that is, the layer of the atrialis or along the boundary between the atrialis and the spongiosa in the atrioventricular valves. The distribution of S-100 protein in the prolapsed mitral valve was the same as that of the normal valve except for the lack of S-100 protein in the degenerated portion. The distribution of GFAP, NFP, ChAT, NPY, CGRP and adrenergic fluorescence were the same as that of S-100 protein in both the normal and prolapsed mitral valves. It is suggested that the above-mentioned anatomical distribution of the nerve in the mitral valve is closely related to the dysfunction of the autonomic nerve system in the condition of mitral valve prolapse, because the body of the mitral valve is rich in nerve endings and this area is most easily influenced by the mechanical stimulation due to abnormal coaptation.
J Cardiol Suppl 1989
PMID:[Innervation of the mitral valve in normal and prolapsed mitral valves]. 250 27


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