RESUMO
There are two viewpoints concerning cardiac regeneration. One assumes that the myocardium of an adult human heart has a weak regenerative capacity. According to another, myocardium can renew at a high rate due to the presence of resident stem cells. This study was aimed to test the role of stem cells in myocardium repopulation in adult humans of different age by examining the distribution of cardiomyocytes as to their size and ploidy. Cytofluorimetry and interferometry were used to determine the dry weight, volume and ploidy of myocytes isolated from the left ventricle of the normal heart of 12 men aged 20-30 years (n = 7) and 40-50 years (n = 5). Dry weight of cardiomyocytes made up 6906 ± 182 pg (10(-12) g) aged 20-30 years and 9126 ± 263 pg in men aged 40-50 years. There were no cells with an intermediate volume between amplifying and mature myocytes. The number of candiomyocytes in the left ventricle made up (3.18 ± 0.05) x 10(9) cells in the age group 20-30 years and (2.06 ± 0.6) x 10(9) cells in the age group 40-50 years. Most of the myocyte population was represented by mononucleate cells with tetraploid nuclei (41.3%). Proportion of myocytes of different ploidy classes did not change in the interval from 20 to 50 years. Our results strongly suggest that stem cells of the heart are not involved in the regeneration of human myocardium during aging. The function of the aging heart is mostly compensated by the hypertrophy of the remaining myocytes.
Assuntos
Envelhecimento/fisiologia , Núcleo Celular/genética , Ventrículos do Coração/citologia , Miócitos Cardíacos/fisiologia , Ploidias , Regeneração/fisiologia , Adulto , Contagem de Células , Núcleo Celular/ultraestrutura , Tamanho Celular , Humanos , Masculino , Pessoa de Meia-Idade , Miocárdio/citologia , Miócitos Cardíacos/ultraestrutura , Células-Tronco/citologiaRESUMO
Contractile cardiomyocytes in various parts of the heart differ in shape, size, ploidy, and other parameters. However, it is not known whether their population is heterogeneous within each heart chamber. In this paper, dry weight and ploidy of cardiomyocytes were estimated in different parts of rat left ventricle. It was found that the dry weight of cardiomyocytes in medial part of left ventricular anterior wall is higher than in other parts of the ventricle. Cardiomyocyte ploidy is the same in different regions of the left ventricle.
Assuntos
Ventrículos do Coração/citologia , Miócitos Cardíacos/citologia , Animais , Ploidias , RatosRESUMO
Nonsteroid anti-inflammatory drug glucural (water-soluble N-methyl-D-glucosamine complex with 6-methyluracyl) improves survival of isolated rat hepatocytes stored in suspension. This effect of glucural is presumably explained by its membranotropism.
Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Citoproteção/efeitos dos fármacos , Hepatócitos/efeitos dos fármacos , Hepatócitos/fisiologia , Uracila/análogos & derivados , Animais , Sobrevivência Celular/efeitos dos fármacos , Citoproteção/fisiologia , Consumo de Oxigênio/efeitos dos fármacos , Ratos , Uracila/farmacologiaRESUMO
The goal of this study was to examine the state of hepatocyte mitochondrial respiratory chain of rats with toxic hepatitis induced by CCl(4) and ethanol. Oxygen consumption by hepatocytes and mitochondria was determined. Endogenous oxygen consumption by pathological hepatocytes was 1.3-fold higher compared with control. Rotenone resulted in 27% suppression of respiration by pathological hepatocytes whereas 2,4-dinitrophenol produced a 1.4-fold increase of respiration. States 3 and 4 of mitochondrial respiration with malate and glutamate were found to be higher as compared to control. State dinitrophenol and state 3 respirations were similar within every group of animals when being tested with malate and glutamate or succinate. Cytochrome c oxidase activity in hepatitis was 1.8-fold higher compared with control. Simvastatin administration resulted in a decrease in hepatocyte endogenous respiration in hepatitis. The presented data lead to the assumption that the increased oxygen consumption by the respiratory chain of pathological mitochondria to be linked mainly with the altered function of complex I.