hydroxyproline/infarction

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Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography.

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Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at

[Hydroxyproline in blood and urine in myocardial infarct].

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The study of the dynamics of proteinbound blood plasma oxyproline concentration and oxyproline excretion with the urine in patients with myocardial infarction is reported. During the subacute period beginning from the 3rd to the 5th week of the disease an increase in the content of these metabolites

Hydroxyproline in myocardial infarction and angina pectoris.

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Hydroxyproline in myocardial infarction and angina pectoris.

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[Dynamics of free serum hydroxyproline in myocardial infarct].

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Urinary elimination of acid mucopolysaccharides and total hydroxyproline in myocardial infarction.

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[Urinary excretion of acid mucopolysaccharides and total hydroxyproline in myocardial infarction].

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A study on myocardial fibrosis in myocardial infarction and in idiopathic cardiomyopathy: a measurement of hydroxyproline level in plasma and in myocardium.

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Protective Effect of RA on Myocardial Infarction-Induced Cardiac Fibrosis via AT1R/p38 MAPK Pathway Signaling and Modulation of the ACE2/ACE Ratio.

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Rosmarinic acid (α-o-caffeoyl-3,4-dihydroxyphenyllactic acid, RA) is a major active constituent of Rosmarinus officinalis Linn. (rosemary) having significant anti-inflammatory, anti-apoptotic, and antioxidant effects. However, the cardioprotection of RA is still not understood. The present study was

Rate of collagen deposition during healing and ventricular remodeling after myocardial infarction in rat and dog models.

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BACKGROUND We hypothesized that the rate and amount of infarct collagen deposition during healing after myocardial infarction might influence ventricular remodeling in rat and dog models. The purpose of this study was to compare rates of infarct collagen deposition and ventricular remodeling in the

Superoxide dismutase does not cause scar thinning after myocardial infarction.

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Previous studies demonstrated that treatment with superoxide dismutase, a scavenger of superoxide anions, limits the extent of myocardial injury in a canine preparation of regional myocardial ischemia and reperfusion. Little is known, however, about the effects of superoxide dismutase on the healing

[Clinical regularities of myocardial infarction repair].

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A total of 136 patients with trans- and 200 with non-transmural myocardial infarction (MI) were examined over time for chlorine-soluble mucoprotein (MP), serum hexoses (SH), their fraction-hexoses of glycosaminoglycans (H-GAG), and hexoses of glycoproteins (H-GP), serum, plasma and urine

Panax quinquefolium saponin attenuates ventricular remodeling after acute myocardial infarction by inhibiting chop-mediated apoptosis.

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Panax quinquefolium saponin (PQS) alleviates hypoxia-reoxygenation injury of cardiomyocytes in vitro by inhibiting excessive endoplasmic reticulum stress (ERS)-related apoptosis. We hypothesized that inhibition of excessive ERS-related apoptosis contributes to cardioprotection in ventricular

Long-term oral Asperosaponin VI attenuates cardiac dysfunction, myocardial fibrosis in a rat model of chronic myocardial infarction.

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The aim of the study was to determine the effects of Asperosaponin VI (ASA VI), a triterpene saponin isolated from Dipsacus asper Wall, on chronic myocardial infarction (MI) and possible mechanisms in rats. MI was induced by permanent ligation of the left coronary artery. Twenty-four hours after MI,

Oligomeric proanthocyanidins protect myocardium by mitigating left ventricular remodeling in isoproterenol-induced postmyocardial infarction.

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Extracellular matrix (ECM) remodeling is a major pathophysiological process during post-myocardial infarction (MI). The activation, differentiation, and proliferation of cardiac fibroblasts to myofibroblasts regulate the expression of ECM proteins. The signaling by bone morphogenetic protein

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