Advances in myocardiology最新文献_第10页

Catecholamine-induced necrosis and hypertrophy. Hemodynamic factors. 儿茶酚胺引起的坏死和肥厚。血流动力学因素。

Advances in myocardiology Pub Date : 1983-07-01 DOI: 10.1016/0022-2828(83)91141-0

K. Middleton, A. Henderson, M. Lewis

引用次数: 1

Verapamil and nifedipine limit infarct size in the dog. 维拉帕米和硝苯地平限制狗的梗死面积。

Advances in myocardiology Pub Date : 1983-07-01 DOI: 10.1016/0022-2828(83)90877-5

J. Downey, D. Hearse, S. Yoshida, M. Maxwell, D. Yellon

引用次数: 6

Morphometric analysis of calcium-tolerant myocytes isolated from the adult rat heart. 从成年大鼠心脏分离的钙耐受心肌细胞的形态计量学分析。

Advances in myocardiology Pub Date : 1983-07-01 DOI: 10.1016/0022-2828(83)91083-0

A. Slade, N. Severs, T. Powell, V. Twist, G. E. Jones

引用次数: 5

Myocardial reoxygenation damage. Can it be circumvented? 心肌再氧损伤。它能被规避吗?

Advances in myocardiology Pub Date : 1983-02-01 DOI: 10.1042/CS064030PA

S. Chappell, M. Lewis, A. Henderson

引用次数: 4

Release of purine nucleosides and oxypurines from the isolated perfused rat heart. 离体灌注大鼠心脏嘌呤核苷和氧嘌呤的释放。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_31

J W de Jong, E Harmsen, P P de Tombe, E Keijzer

引用次数: 7

Mechanisms of degradation of myofibrillar and nonmyofibrillar protein in heart. 心肌纤维蛋白和非纤维蛋白降解的机制。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_17

J M Ord, J R Wakeland, J S Crie, K Wildenthal

引用次数: 6

Adaptation of the organism during long-lasting survival with a total artificial heart. 有机体在全人工心脏长期存活期间的适应性。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_21

J Vasků, P Hanzelka, J Cerný, J Vasků, E Urbánek, M Dostál, P Guba, V Pavlícek, Z Gregor, V Krcma, H Janecková, O Sotolová, T Sládek, B Hartmannová, E Sotáková, P Wendsche, L Krcek, P Urbánek, M Gregorová

引用次数: 0

Effect of exogenous amino acids on the contractility and nitrogenous metabolism of anoxic heart. 外源氨基酸对缺氧心脏收缩力和氮代谢的影响。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_27

O I Pisarenko, E S Solomatina, I M Studneva, V E Ivanov, V I Kapelko, V N Smirnov

{"title":"Effect of exogenous amino acids on the contractility and nitrogenous metabolism of anoxic heart.","authors":"O I Pisarenko, E S Solomatina, I M Studneva, V E Ivanov, V I Kapelko, V N Smirnov","doi":"10.1007/978-1-4757-4441-5_27","DOIUrl":"https://doi.org/10.1007/978-1-4757-4441-5_27","url":null,"abstract":"The effect of exogenous glutamic acid and arginine on the contractility of isolated perfused rat heart and on the metabolism of some nitrogenous compounds was studied. Sixty-minute anoxic perfusion (95% N2 + 5% CO2) led to a fall in developed isovolumic pressure and an elevation in diastolic pressure, to an increase in the production of alanine, glutamine, and ammonia, and to a decrease in the tissue content of aspartate and glutamate. The total pool of free amino acids and taurine under these conditions remained unchanged. Subsequent 40-min reoxygenation partially restored the contractile function. Addition of 3.5 mM glutamic acid or 5 mM arginine into the perfusate before anoxia resulted in a higher level of developed pressure and a lower level of diastolic pressure during anoxia and almost complete recovery of cardiac function after subsequent reoxygenation. Both amino acids had no effect on ammonia formation by the anoxic heart but enhanced its binding in myocardial tissue via formation of glutamine and urea. It is suggested that the exogenous amino acid effect on anoxic heart is mediated by activation of substrate phosphorylation rather than the ability to bind tissue ammonia.","PeriodicalId":77831,"journal":{"name":"Advances in myocardiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17906546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

The permissive role of catecholamines in the pathogenesis of hamster cardiomyopathy. 儿茶酚胺在仓鼠心肌病发病机制中的纵容作用。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_3

G Jasmin, L Proschek

{"title":"The permissive role of catecholamines in the pathogenesis of hamster cardiomyopathy.","authors":"G Jasmin, L Proschek","doi":"10.1007/978-1-4757-4441-5_3","DOIUrl":"https://doi.org/10.1007/978-1-4757-4441-5_3","url":null,"abstract":"It was previously shown that beta-adrenergic blockers exert a protective action on the development of heart necrotic changes in cardiomyopathic hamsters. To further investigate the possible role of catecholamines in the pathogenesis of the hamster hereditary cardiomyopathy, the ventricular adrenergic nerve terminals were visualized by fluorescence histochemistry, and NE uptake and turnover were determined after i.v. injection of labeled NE. It was found that the fluorescent nerve endings strongly proliferate with the occurrence of heart necrotic changes. With healing of the myocardial lesions, the difference between control and myopathic hearts is less apparent, and NE nerve endings are literally absent in the terminal stage of the disease. There was a marked increase in NE uptake during the necrotic stage and, at the same time, a considerable rise in elimination rate constant with a maximum level at terminal state, suggesting that the NE turnover is related to the progression of the disease. In light of the present findings, it can be surmised that NE plays a permissive role in the genesis of the hamster disease by promoting the heart necrotic changes.","PeriodicalId":77831,"journal":{"name":"Advances in myocardiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17908320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Mitochondrial function in normal and hypoxic states of the myocardium. 心肌正常和缺氧状态下的线粒体功能。

Advances in myocardiology Pub Date : 1983-01-01 DOI: 10.1007/978-1-4757-4441-5_25

J R Williamson, T L Rich

{"title":"Mitochondrial function in normal and hypoxic states of the myocardium.","authors":"J R Williamson, T L Rich","doi":"10.1007/978-1-4757-4441-5_25","DOIUrl":"https://doi.org/10.1007/978-1-4757-4441-5_25","url":null,"abstract":"The relationships among isometric tension development, the oxidation-reduction states of pyridine nucleotides and cytochrome c, and the oxygenation state of myoglobin have been assessed using the arterially perfused rabbit interventricular septum under different conditions of contraction rate, perfusate [Ca2+] and pH, catecholamine stress, and hypoxia. Hypoxia was produced either by decreasing oxygen availability with maintained flow (high-flow hypoxia) or by decreasing the flow rate (ischemia). Under normoxic conditions, increased work caused a fall of the cytosolic adenine nucleotide phosphorylation potential, delta G(ATP)c, an oxidation of the pyridine nucleotides, and a reduction of cytochrome c; the opposite occurred with decreased work. Thus, the redox potential span from NADH to cytochrome c, delta Eh, varied with the energy demand such that delta Eh and delta G(ATP)c changed in the same direction. Under hypoxic conditions, all respiratory components became more reduced, and myoglobin was partially deoxygenated. The percentage change of developed tension under hypoxic conditions was approximately proportional to the percentage change of oxidized cytochrome c. When high-flow hypoxia and ischemia were compared at the same rates of oxygen delivery, the developed tension at any level of cytochrome c reduction was always lower with ischemia than with high-flow hypoxia. This difference was attributed to the low intracellular pH of ischemic tissue. Myoglobin deoxygenation was linearly related to cytochrome c reduction under all conditions of hypoxia, indicating steep oxygen gradients. The results support the concept of heterogeneous oxygenation of the tissue with mixed populations of aerobic and anaerobic mitochondria in the hypoxic state. In the full aerobic state, the control of mitochondrial respiration in situ appears similar to that of isolated mitochondria.","PeriodicalId":77831,"journal":{"name":"Advances in myocardiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17366736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7