Myocardial Degeneration

Severe degenerative myocardial disease occurred in female C3H/OUJ mice fed purified diets for 36 weeks; the diet contained 5% or 20% fat as non-hydrogenated soybean oil. Deaths of lactating females of this group (17/35 high fat diet and 7/35 low fat diet animals) were due to sudden cardiovascular collapse. Cardiomegaly with marked atrial and ventricular myocardial mineralization was seen at necropsy. Histologically. the random, myopathic foci were characterized by severe myocardial degeneration, mineralization, and fibrosis. Mural thrombosis, pulmonary arteriosclerosis, and mild myocardial inflammatory cell infiltrates were also present. Pathological changes were similar to those of dystrophic cardiac calcinosis, an incidental necropsy finding in certain mouse strains.

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Myocardial Degeneration in Myasthenia Gravis

Southern Medical Journal ◽

10.1097/00007611-196406000-00018 ◽

1964 ◽

Vol 57 (6) ◽

pp. 708-710

Author(s):

DALE GROOM ◽

EDWARD E. McKEE

Keyword(s):

Myasthenia Gravis ◽

Myocardial Degeneration

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DISSOCIATION OF FACTORS INFLUENCING MYOCARDIAL DEGENERATION AND GENERALIZED CARDIOCIRCULATORY FAILURE

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1969.tb16742.x ◽

1969 ◽

Vol 156 (1 Experimental) ◽

pp. 396-420 ◽

Cited By ~ 24

Author(s):

E. Bajusz ◽

F. Homburger ◽

J. R. Baker ◽

P. Bogdonoff

Keyword(s):

Factors Influencing ◽

Myocardial Degeneration

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Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine

Baghdad Science Journal ◽

10.21123/bsj.2019.16.3(suppl.).0719 ◽

2019 ◽

Vol 16 (3(Suppl.)) ◽

pp. 0719

Author(s):

Hadeel Kamil Khaleel

Keyword(s):

Pulmonary Congestion ◽

Male Mice ◽

Histological Changes ◽

Cardiac Atrophy ◽

Vascular Congestion ◽

Myocardial Degeneration ◽

Liver And Kidney ◽

Tissue Changes ◽

Myocardial Fibers ◽

Hepatocyte Necrosis

The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.

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Suspected avocado (Persea americana) poisoning in goats

Journal of the South African Veterinary Association ◽

10.4102/jsava.v62i4.1788 ◽

1991 ◽

Vol 62 (4) ◽

pp. 186-188 ◽

Cited By ~ 10

Author(s):

P. Stadler ◽

I. B.J. Van Rensburg ◽

T. W. Naudé

Keyword(s):

Clinical Findings ◽

Persea Americana ◽

Lung Oedema ◽

Histopathological Findings ◽

Myocardial Degeneration ◽

Severe Lung

A herd of 15 Cameroon goats was suspected of having" been poisoned by eating leaves of the Fuerte variety of avocado pear (Persea americana). Two of the affected goats were examined clinically, while necropsies were carried out on 3 of the 4 that had died. The most significant clinical findings were tachycardia, hyperpnoea and evidence of lung oedema. At necropsy severe lung oedema, hydrothorax and hydropericardium were present. Severe myocardial degeneration, necrosis and fibrosis were the major histopathological findings.

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Myocardial Degeneration in Chronic Solvent Abuse

Medicine Science and the Law ◽

10.1177/002580248802800308 ◽

1988 ◽

Vol 28 (3) ◽

pp. 217-218 ◽

Cited By ~ 5

Author(s):

Susan M. Claydon

Keyword(s):

Heart Failure ◽

Acute Heart Failure ◽

Histological Examination ◽

Myocardial Degeneration ◽

Solvent Abuse

Chronic solvent abuse is leading to increasing reports of death from cardiac related causes. This case involves a 21-year-old man who died of acute heart failure. Histological examination of his heart showed extensive chronic damage of the myocardium. He had regularly and frequently abused solvents for five years.

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Prevention of myosin-induced autoimmune myocarditis in mice by anti-L3T4 monoclonal antibody

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y02-159 ◽

2003 ◽

Vol 81 (2) ◽

pp. 84-88 ◽

Cited By ~ 7

Author(s):

Hai-Tao Yuan ◽

Yu-Hua Liao ◽

Zhaohui Wang ◽

Ji-Hua Dong ◽

Lin-Sheng Cao ◽

...

Keyword(s):

Monoclonal Antibody ◽

Immune Tolerance ◽

Light Microscope ◽

Myocardial Injury ◽

Inflammatory Cells ◽

Treated Group ◽

Cardiac Myosin ◽

Pathological Changes ◽

Autoimmune Myocarditis ◽

Myocardial Degeneration

This study was aimed at studying the effect of the induction of immune tolerance to swine cardiac myosin from anti-L3T4 monoclonal antibody injection and whether the immune tolerance could protect mice with myosin-induced myocarditis from myocardial injury. Twenty-four Balb/c mice were divided into two groups at random. All of the mice were immunized with swine cardiac myosin on the 1st day, 14th, 28th, 42nd, and 52nd day. Immune tolerance was induced by triplicate injections of 400 μg anti-L3T4 McAb on the 0 day (intravenous), 1st day, and 2nd day (intraperitoneal) in McAb-treated group. In the saline-treated group, saline of the same volume as anti-L3T4 monoclonal antibody was used as a control. The sera and hearts biopsies of all mice were collected on the 58th day. The anti-cardiac myosin antibody was examined with ELISA, and pathological changes of heart were observed by light microscope. It was shown that mice immunized with swine cardiac myosin could produce anti-myosin antibody and the anti-cardiac myosin antibody was positive in most of the saline-treated group but negative in the McAb-treated group. Morphologically, myocardial degeneration, necrosis, and infiltration of inflammatory cells were found in the saline-treated group but not in the McAb-treated group. In conclusion, this study indicated that the immune tolerance to cardiac myosin was induced by the anti-L3T4 monoclonal antibody, and accordingly myocardial injury could be prevented by induction of immune tolerance.Key words: anti-L3T4 monoclonal antibody, myosin, immune tolerance, myocarditis.

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