Peculiarities of intracellular regeneration of cardiomyocytes during plastic myocardial insufficiency

2000 ◽  
Vol 130 (4) ◽  
pp. 1011-1016 ◽  
Author(s):  
L. M. Nepomnyashchikh ◽  
E. L. Lushnikova ◽  
D. E. Semenov
Keyword(s):  
Intracellular Regeneration ◽  
Myocardial Insufficiency ◽  
Plastic Myocardial Insufficiency ◽  
Regeneration Of Cardiomyocytes

Ultrastructure and Stereology of Cardiomyocytes in the Development of Regenerative and Plastic Myocardial Insufficiency during Ontogeny

2011 ◽  
Vol 151 (1) ◽  
pp. 88-94 ◽  
Author(s):  
L. M. Nepomnyashchikh ◽  
E. L. Lushnikova ◽  
N. A. Molodykh ◽  
M. G. Klinnikova ◽  
O. P. Molodykh
Keyword(s):  
Myocardial Insufficiency ◽  
Plastic Myocardial Insufficiency

The ?disappearing cardiomyocytes? phenomenon in plastic myocardial insufficiency

1984 ◽  
Vol 97 (5) ◽  
pp. 689-694 ◽  
Author(s):  
D. E. Semenov ◽  
L. A. Semenova ◽  
L. M. Nepomnyashchikh ◽  
Yu. G. Tsellarius
Keyword(s):  
Myocardial Insufficiency ◽  
Plastic Myocardial Insufficiency

Cardiotoxicity with antihypertensive drugs (literature review) Part 1. Calcium channel blockers and beta-blockers

2021 ◽  
pp. 12-19
Author(s):  
A. N. Esaulenko ◽  
A. Yu. Moiseeva ◽  
A. A. Ivannikov ◽  
I. V. Bratischev ◽  
Kh. G. Alidzhanova
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Antihypertensive Drugs ◽  
Beta Blockers ◽  
Research Literature ◽  
Channel Blockers ◽  
Distinctive Features ◽  
Experimental Pharmacology ◽  
Myocardial Insufficiency ◽  
Β Blockers

The effect of hypotensive drugs overdose on cardiovascular system is poorly studied; it should undergo clinical, experimental pharmacology and toxicology together with cardiology. There is too little information about cardiotoxicity of beta-blockers (β-blockers) and calcium channel blockers (CCB) in existing research literature. Intoxication from these groups of drugs causes similar severe hemodynamic abnormalities and myocardial insufficiency, however pathophysiological mechanisms of these abnormalities are not thoroughly studied. The review highlights how difficult it is to identify toxic level and distinctive features of clinical evidence of intoxication. Methods of diagnosis as well as β-blockers and CCB overdose treatment are discussed.

scholarly journals Myofibrillolysis and fibrosis predicts myocardial insufficiency

2019 ◽  
Vol 16 (2) ◽  
pp. 57-64
Author(s):  
Jerzy Pacholewicz ◽  
Michał Zakliczyński ◽  
Jerzy Nożyński ◽  
Paweł Nadziakiewicz ◽  
Michał Zembala ◽  
...  
Keyword(s):  
Myocardial Insufficiency

scholarly journals Elevated hepatic 11β-hydroxysteroid dehydrogenase type 1 induces insulin resistance in uremia

2014 ◽  
Vol 111 (10) ◽  
pp. 3817-3822 ◽  
Author(s):  
Ananda Chapagain ◽  
Paul W. Caton ◽  
Julius Kieswich ◽  
Petros Andrikopoulos ◽  
Nanda Nayuni ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Signaling ◽  
Hydroxysteroid Dehydrogenase ◽  
Metabolic Disturbances ◽  
Intracellular Regeneration ◽  
Rat Models ◽  
Hepatic Expression ◽  
Lipogenic Genes ◽  
Subtotal Nephrectomy

Insulin resistance and associated metabolic sequelae are common in chronic kidney disease (CKD) and are positively and independently associated with increased cardiovascular mortality. However, the pathogenesis has yet to be fully elucidated. 11β-Hydroxysteroid dehydrogenase type 1 (11βHSD1) catalyzes intracellular regeneration of active glucocorticoids, promoting insulin resistance in liver and other metabolic tissues. Using two experimental rat models of CKD (subtotal nephrectomy and adenine diet) which show early insulin resistance, we found that 11βHSD1 mRNA and protein increase in hepatic and adipose tissue, together with increased hepatic 11βHSD1 activity. This was associated with intrahepatic but not circulating glucocorticoid excess, and increased hepatic gluconeogenesis and lipogenesis. Oral administration of the 11βHSD inhibitor carbenoxolone to uremic rats for 2 wk improved glucose tolerance and insulin sensitivity, improved insulin signaling, and reduced hepatic expression of gluconeogenic and lipogenic genes. Furthermore, 11βHSD1−/− mice and rats treated with a specific 11βHSD1 inhibitor (UE2316) were protected from metabolic disturbances despite similar renal dysfunction following adenine experimental uremia. Therefore, we demonstrate that elevated hepatic 11βHSD1 is an important contributor to early insulin resistance and dyslipidemia in uremia. Specific 11βHSD1 inhibitors potentially represent a novel therapeutic approach for management of insulin resistance in patients with CKD.

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