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Query: HUMANGGP:031673 (collagen)
 124,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To develop intravital criteria of the reperative processes following myocardial infarction, clinical, biochemical and morphological parallels were traced in 62 patients dying of myocardial infarction after different periods following the onset of the disease. It was demonstrated that a set of laboratory techniques (examinations of haptoglobin, chloridesoluble mucoprotein, of heterogeneity of mucoprotein, v2-macroglobulin) helps in the evaluation of the severity of the inflammatory and macrophagel reactions in the paranecrotic zone. A useful intravital sign of the formation of a postinfarction scar is provided by the examination of collagen metabolites--oxyproline bound with collagen-like plasma protein and free serum oxyproline and urine excretion of total oxyproline. The obtained data can be used for the development of a rehabilitation programme, differentiated therapy in various groups of patients.
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PMID:[Myocardial infarct repair in the light of clinico-biochemical and morphological studies]. 6 36

Individual glyco- and mucoproteins and collagen metabolites were determined in dynamics in 297 patients with transmural, macrofocal nontransmural, and microfocal myocardial infarction. It is shown that these laboratory findings enable one to appraise the course of myocardial infarction healing. This may serve as one of the criteria for the elaboration of individualized rehabilitation programs.
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PMID:[Clinico-biochemical principles of healing of myocardial infarct]. 8 40

In 6-weeks-old, 5-months-old and 21-months-old rats myocardial infarction was induced by coronary artery ligature. After performing the ligature the animals were administered 3H-thymidine, 3H-proline or 35S-sulphate at different times. The following parameters were determined: number of DNA- and tropocollagen-synthesizing connective tissue cells at the infarction border and at the infarction site; mean silver grain density above the nuclei or cells; duration of a cycle; number of mitoses, and incorporation of radioactive sulphate at the infarction site. In addition, the labelling and mitotic indices as well as the percentage of the standard deviation from the mean values were estimated. The following results were obtained: 1. The rate of granulation tissue formation in the necrotic zone is determined by the mitotic activity of the cells. With advancing age the cell cycles are being prolonged which results in retardation of wound healing. 2. The disturbed DNA-replication in old age is not associated with a time shift in the occurrence of the mitotic and labelling peaks. 3. With advancing age the number of fibroblasts synthesizing collagen precursors decreases. There exists no age-dependence of the 3H-proline incorporation rate, of the intracellular transport, of the synthesis of collagen precursor and of the release of labelled tropocollagen. In all age-groups under study these processes last approximately 4 hours. 4. Collagen fibre formation is accompanied by an increased synthesis of acid mucopolysaccharides. In infarction callosities the content of acid mucopolysaccharides mostly is constant. 5. The proliferating endothelial cells have a pronounced metabolic activity and a markedly short generation time.
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PMID:The influence of age on the wound healing of experimental myocardial infarction in rats. 13 6

The relationship between ultrasonic attenuation and collagen content is examined in hearts from normal dogs and in hearts from dogs subjected to ischemic injury by coronary occlusion as an approach toward elucidating the physical mechanisms responsible for the attenuation of soft tissue. Increased ultrasonic attenuation is shown to correlate well with increased collagen concentration determined biochemically in regions of ischemic injury studied 2, 4, and 6 weeks following occlusion. Extrapolation of experimentally determined relationship between attenuation and collagen concentration suggests that collagen is responsible for not more than 15% of the attenuation observed in normal myocardium. These results indicate that collagen appears to be the principal determinant of the elevated attenuation detected in regions of myocardial infarction, but is apparently not the primary determinant of the attenuation of normal myocardium.
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PMID:The relationship between collagen and ultrasonic attenuation in myocardial tissue. 48 19

There is increasing evidence that the sudden, unpredicatable event initiating myocardial infarction is fissuring of an atherosclerotic plaque. The resulting haemorrhage into the arterial wall produces obstructive platelet thrombi, just as arterial haemorrhages elsewhere produce haemostatic platelet plugs. It has been suggested that such platelet aggregation depends on ADP originating in red cells which are subjected to excessive haemodynamic stress at the site of haemorrhage. The release of ADP from red cells has been demonstrated in vitro in equivalent condtions of shear stress; and other mechansims, such as activation by collagen, cannot account for the rapidity with which the platelets react. One of us (G.V.R.B.) has suggested that drugs capable of counteracting haemolysis might diminish the activating effect of erythrocytes on platelets and so inhibit their aggregation as thrombi. Thus, chlorpromazine, added to human blood at concentrations which diminish haemoylsis but do not directly affect platelet aggregation, prolonged the 'bleeding time' from small holes in artificial vessels where extravasation is terminated, as in living arterioles, by aggregated platelets. The bleeding time was also prolonged by apyrase, consistent with the conclusion that the chlorpromazine acted through decreasing plasma ADP. We show here that this occurs through the anti-haemolytic action of chlorpromazine.
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PMID:Inhibition of platelet thrombus formation by chlorpromazine acting to diminish haemolysis. 49 37

In diabetic and glucocorticoid-treated rats myocardial infarction is produced by coronary artery ligation. After the ligation was performed the animals were given 3H-thymidine or 3H-proline at different times. The following parameters were determined: number of DNA- and tropocollagen-synthesizing connective-tissue cells both at the infarction border and infarction site; mean silver-grain density above the nuclei or cells; number of mitoses. The labelling and mitotic indices as well as the standard deviation (in percent) from the mean values were calculated. The following results were obtained: 1. The retarded formation of collagen fibres in diabetic animals is caused by a reduced number of tropocollagen-synthesizing fibroblasts and by a diminished synthesizing performance of the individual cells. 2. Glucocorticoids have a pronounced inhibitory effect on granulation-tissue formation, The 3H--thymidine indices are strikingly low. The synthesis of collagen precursors in the fibroblasts is reduced. The release of tropocollagen from the connective-tissue cells is slowed down.
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PMID:The influence of diabetes mellitus and hypercorticism on the wound healing of experimental myocardial infarction in rats. 59 51

There is evidence that glucocorticoids reduce infarct size but their use in myocardial infarction remains controversial because of their potential adverse effects on healing of the infarct. To investigate the healing process, rats received either four parenteral doses of 50 mg/kg of methylprednisolone (MP) or saline 5 min, 3,6 and 24 hr after coronary occlusion and their hearts were examined by light and electron microscopy 48 hr and seven days after occlusion. At 48 hr, in five untreated rats, only 12 +/- 7% of injured myocytes showed the persistence of striations and a relatively intact sarcolemma despite loss of nuclei and hence appeared "mummified" whereas in six MP-treated rats 72 +/- 8% of myocytes exhibited this appearance (P less than 0.001). In treated rats there were fewer phagocytes than in controls. At seven days, in seven MP-rats, mummified cells were still more prominent than in five untreated rats and there were fewer phagocytes and less collagen. In conclusion, high dose of MP delays the inflammatory process and retards the disintegration of necrotic myocytes, resulting in impaired healing.
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PMID:Mummification of the infarcted myocardium by high dose corticosteroids. 61 98

Two patients who had previously experienced old myocardial infarction and who died suddenly after an attack of chest pain were examined and discussed. In both cases two of the three main coronary arteries showed severe stenosis with canalization. Ruptured atheromatous plaque was found in the unblocked coronary artery. Fibrin was already formed and surrounded the fractured intimal collagen fiber, foam cells, and cholesterin clefts, but a luminal thrombi had not yet been formed. Fresh occluding thrombi were formed at the site of the ruptured atheromatous plaque. Coronary thrombi containing abscess components such as foam cells, cholesterin clefts, and the fractured intimal collagen fiber were found in our preliminary study. These views support the supposition that this fracture between the lumen and the plaque might precede and be responsible for the formation of the thrombus and the onset of acute myocardial infarction. It was confirmed that the attack of preinfarction angina occurred at the time of the rupture of the atheromatous plaque. The rupture of the atheromatous plaque plays an important part as an initiating factor of peinfarction angina and myocardial infarction. Thus, it is necessary to examine coronary arteries by serial histopathological section method.
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PMID:Relationship between myocardial infarction and preinfarction angina: a histopathological study of coronary arteries in two sudden death cases employing serial section. 61 94

Autoradiographic studies on wound healing after experimental myocardial infarction in rats aged 6 weeks, 5 and 21 months gave the following results: 1. The interval between damage, DNA-replication and mitotic activity of the cells is age-dependent. 2. Age does not influence the capacity of the connective-tissue cells to synthesize tropocollagen. However, the number of synthesizing fibroblasts is reduced. 3. The collagen changes occuring during wound healing are not of primary, but of secondary nature; they take place if the mucopolysaccharide content is reduced. As a result, there is a decrease in the ground-substance synthesis in ageing granulation tissue. In cicatricial tissue the content of amorphous ground-substance remains greatly constant. 4. Consequently, the ageing of the collagen is governed by a biologically regulated process whose control mechanism is inherent in the cells.
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PMID:[Wound healing in old age (experimental studies on rats) (author's transl)]. 91 58

Mature male Sprague-Dawley rats were subjected to an isoproterenol-induced myocardial infarction. Animals were sacrificed on a daily basis in order to assess the temporal changes in prolyl hydroxylase activity and collagen metabolism during the acute stages of myocardial necrosis and repair. Total myocardial hydroxyproline, as an indexof collagen content, increased promptly and markedly, beginning on day 4, and remained elevated thereafter. The incorporation of (14Cl)-proline into definitive hydroxyproline of mature collagen was also increased. The activity of the enzyme prolyl hydroxylase, which regulates the rate of conversion of proline to hydroxyproline in collagen, was elevated by day 2, remained high through day4, and then declined to a relatively constant but still slightly elevated level throughout the period of repair. It is believed that changes in these parameters of collagen metabolism reflect changes in myocardial fibroblastic cell and ground substance pertinent to fundamental aspects of repair of the injuried myocardium.
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PMID:Prolyl hydroxylase and collagen metabolism after experimental mycardial infarction. 117 Jul 63


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