ABSTRACT
The aim of this study was to estimate the values of morphological traits of myocardium in American minks. The study was conducted on 342 male mink hearts and 416 female mink hearts. Mink coat coloration resulting from mutation or crossbreeding of mutational variants with each other and sex were assumed as a source of variation. Carcass, lung and heart weights, heart height, width, depth and circumference, as well as left and right ventricular wall weights and thickness at two locations were determined. The values of 10 indices characterising the relative size of the heart were estimated. The results showed no normal distribution of the heart traits examined. The greatest average heart weight was characteristic of male mutational colour variant minks (17.40 ± 2.34 g). These hearts were heavier by more than 8 % than those of male standard colour variant minks. The hearts of male mutational colour variant minks were characterised by the greatest left and right ventricle weights (P≤0.01) compared to those of male standard colour variant minks, in which in turn the greatest left and right ventricle wall thickness was larger than that in standard colour variant minks. It was found that a greater difference calculated between mean left ventricle wall thickness and mean right ventricle wall thickness in standard colour variant minks may provide more evidence of its adaptation to a greater effort, referring thus to their evolutionary history than to the occurrence of signs of multistage myocardial hypertrophy.
El objetivo de este estudio fue estimar los valores de los rasgos morfológicos del miocardio en el visón americano. El estudio se realizó en 342 corazones de visón macho y 416 corazones de visón hembra. La coloración de la capa de visón resultante de la mutación o el cruce de variantes mutacionales entre sí, y el sexo se asumieron como una fuente de variación. Se determinaron los pesos de la canal, los pulmones y el corazón, la altura del corazón, el ancho, la profundidad y la circunferencia, así como los pesos y el grosor de las paredes de los ventrículos izquierdo y derecho en dos ubicaciones. Se estimaron los valores de 10 índices que caracterizan el tamaño relativo del corazón. Los resultados no mostraron una distribución normal de los rasgos de los corazones examinados. El mayor peso promedio del corazón fue característico de los visones de variante de color mutacional macho (17,40 ± 2,34 g). Estos corazones eran más pesados en más de un 8 % que los de los visones con variante de color estándar machos. Los corazones de los visones de variante de color mutacional macho se caracterizaron por los mayores pesos de los ventrículos izquierdo y derecho (P≤0,01) en comparación con los de los visones de color estándar machos, en los que a su vez el mayor grosor de las paredes de los ventrículos izquierdo y derecho fue mayor que el de las variantes de colores estándar. Se observó que una mayor diferencia entre los grosores medio de las paredes de los ventrículos izquierdo y derecho en las variantes de color estándar, puede proporcionar más pruebas de su adaptación a un mayor esfuerzo, refiriéndose así a su historial evolutivo, pese a la aparición de signos de hipertrofia miocárdica multietapa.
Subject(s)
Animals , Male , Female , Heart/anatomy & histology , Mink/anatomy & histology , Mink/genetics , Organ Size/genetics , Sex Characteristics , MutationABSTRACT
Aim To discuss the effects and mechanism of Ganoderma lucidum polysaccharides and metformin on myocardial structure and hemodynamics in type 2 diabetic rats.Methods High fat diet combined with intraperitoneal injection of low dose streptozotocin 30 mg· kg -1 was applied to establish rat model of type 2 diabetes mellitus .The diabetic rats were randomly into normal control group ,diabetes group , ganoderma lucid-um polysaccharides group (600 mg· kg -1 ) , metformin group ( 600 mg · kg -1 ) , combination group ( ganoder-ma lucidum polysaccharides 300 mg · kg -1 +metform-in 300 mg· kg -1 ) .After 12 weeks′treatment,the lev-els of fasting serum glucose were determined and the hemodynamic parameters (LVSP,LVEDP,dp/dtmax,-dp/dtmax ) were determined.Collagen volume fraction ( CVF ) was detected by Van Gieson . Immunohisto-chemical method and Western blot were used to detect myocardial tissue MMP-2 protein expression .Results The fasting blood glucose was significantly decreased in the combined treatment group .Combined medication could significantly improve hemodynamic parameters in diabetic rats: reduced LVEP and raised LVEDP , dp/dtmax and -dp/dtmax .CVF was significantly decreased in combination group .The expression of MMP-2 in my-ocardial tissue was significantly inhibited .Conclusions The combination of Ganoderma lucidum polysaccha-ride and metformin can significantly improve the hemo-dynamic parameters in type 2 diabetic rats, and have a preventive effect on diabetic cardiomyopathy . The mechanism may be related to the down regulation of the expression of MMP-2.
ABSTRACT
Objective To explore the effect of trimetazidine on myocardial structure injury induced by pyran adriamycin and to clarify the protective effect of trimetazidine on. the changes of myocardial structure and its mechanism.Methods 36 Wistar rats were randomly divided into control group,model group and treatment group. The rats in model group and treatment group were injected with pyran doxorubicin 2.5 mg·kg-1 (concentration 2 g·L-1 )by the caudal vein once a week.The rats in control group were injected with equivalent normal saline for 6 weeks.The rats in treatment group were intragastricly infused with trimetazidine 5.4 mg · kg · d-1 one day before making the model.The rats in control group and model group were injected with equivalent normal saline for 8 weeks.At the end of the experiment, the myocardial enzymes in serum of the rats in various groups were measured. The morphology of myocardium tissue was detected by light microscope and electron microscope. Results Compared with model group,the levels of myoglobin,troponin I and alanine transaminase (ALT)of the rats in treatment group were significantly decreased (P<0.05).Under light microscope the myocardium of the rats in model group arranged disorderly, the structure was severely damaged, emyocardial was seen, the myofilament was dissolved;the myocardium of the rats in treatment group arranged in order, the structure was nearly integrated,partial dissolution and fracture were found.Under electron microscope in model group the myocardial muscle bundle dissolved, fractured and disappeared, and the mitochondria was decreased,and the cytoplasmic matrix cavitation was seen;the cardiomyocytes sarcomeres of the rats in treatment group arranged in order,local myofilaments were reduced slightly, the surrounding mitochondria were oval and arranged in parallel between the muscle bundles.Conclusion Trimetazidine has protective effect on the cardiomyocyte injury caused by pyran adriamycin,and its mechanism may be related to decreasing the injury of mitochondria and myocytes.
ABSTRACT
Background: This study was aimed to evaluate the structural changes of the ventricular myocardium in a physiological hypertrophic heart model due to long term aerobic and anaerobic physical training and detraining. Methods: In-vivo experimental study on Wistar rats (8 weeks old), weighing 150-250 grams who were divided into 3 large groups: control group, aerobic exercise group and anaerobic exercise group. Aerobic and anaerobic training were conducted for 4 and 12 weeks. At the end of 4 and 12 weeks of exercising, half of each exercising group was sacrificed to study the morphological and histopathological changes in myocardial structure. The remaining of the groups were given a period of 4 weeks of detraining and sacrificed at the end of the 8th and 16th week. Results: Significant differences in heart weight and left ventricular wall thickness was found in the 4 weeks of aerobic and anaerobic group compared to the control group (751.0 ± 36.5 gr and 791.1 ± 15.8 gr vs 588 ± 19.4 gr ), (3.34 ± 0.12 mm and 3.19 ± 0.1 mm vs 2.80 ± 0.07 mm). An increase in heart mass weight was observed in both 12 weeks aerobic and anaerobic training group compared to the control group (1030.8 ± 82.4 gr and 1140.4 + 0.24 gr vs 871.6 ± 62.0 gr). Heart volume of the 12 weeks aerobic-anaerobic groups showed a significant increase (3.58 ± 0.31 mm and 4.04 ± 0.30 mm) compared to the control group (2.82 ± 0.14 mm). The length of cardiomyocyte was in log 10 to normalize the data. There was a significant increase in the length of the cardiac muscle cells of the 4 weeks aerobic and anaerobic group (1.09± 0.08 μm and 1.00± 0.12 μm) compared with the control group (0.73± 0.1 μm). Width of heart muscle cells in the 4 weeks aerobic-anaerobic group showed a significant increase when compared to the control group (5.38± 1.3 μm and 5.5± 2.11 μm) vs (2.74± 0.53 μm). Significant reduction in the length of cardiac muscle cells in the detrained 4 weeks aerobic group (0.94± 0.08 μm) was found when compared to the treatment group (1.09± 0.08 μm). Significant differences were found between the length of cardiac muscle cells in the 12 weeks aerobic-anaerobic groups (1.3± 0.04 μm and 1.2± 0.07 μm) compared to the control group (0.95± 0.69 μm). Significant width increments of heart muscle cells was found in the 12 weeks aerobic-anaerobic groups (7.3± 1.01 μm and 6.44± 0.08 μm) compared to the control group (4.52 ± 0.91 μm). Conclusion: Long term aerobic and anaerobic training causes an increase in both wall thickness and diameter of the left ventricular cavity, as well as slight fibrosis. The increase in wall thickness, diameter, and fibrosis diminish during detraining period.