Clinical Pathology
Mahsa Hasanzadeh-Moghadam; Mohammad Hassan Khadem-Ansari; Gholam Hossein Farjah; Yousef Rasmi
Volume 9, Issue 2 , June 2018, , Pages 129-135
Abstract
Myocardial infarction is commonly considered as a leading cause of cardiovascular disease taking the lives of seven million people annually. Liver dysfunction is associated with cardiac diseases. The profile of abnormal liver functions in heart failure is not clearly defined. This study was designed ...
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Myocardial infarction is commonly considered as a leading cause of cardiovascular disease taking the lives of seven million people annually. Liver dysfunction is associated with cardiac diseases. The profile of abnormal liver functions in heart failure is not clearly defined. This study was designed to investigate the protective effects of betaine on liver injury after myocardial infarction induced by isoprenaline in rats. Forty-eight male rats were divided into four groups: the control group received normal diet and the experimental groups received 50, 150, and 250 mg kg-1 body weight of betaine daily through gastric gavages for 60 days. All of experimental and control groups experienced myocardial infarction, induced by subcutaneous injection of 100 mg kg-1 isoprenaline in two consecutive doses )8:00 AM to 8:00 PM). Liver enzymes including aspartate transaminase (AST) and alanine transaminase (ALT) were significantly reduced in the groups treated with betaine, compared with the control group. The total antioxidant capacity in the experimental groups, treated with betaine, showed a significant increase, compared with the control group. In the control group, severe lesions were created in the liver tissue, while degenerative changes of liver tissue significantly reduced in groups treated with different doses of betaine, showing the repair of liver tissue. Betaine decreased apoptosis in the experimental groups in comparison with the control group. Betaine showed a protective effect against biochemical and histological changes in liver tissue caused by the induction of myocardial infarction via isoprenaline injection.
Pathology
Masoumeh Moradi-Arzeloo; Amir Abbas Farshid; Esmaeal Tamaddonfard; Siamak Asri-Rezaei
Volume 7, Issue 1 , March 2016, , Pages 47-54
Abstract
In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. ...
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In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. Rats were given intraperitoneal injections of histidine (40 mg kg-1) and vitamin C (40 mg kg-1) alone and combined daily for 21 days. Propranolol (10 mg kg-1) was orally administered daily for 10 days (from day 11 to day 21). Myocardial infarction was induced by subcutaneous injections of 150 mg kg-1 of isoproterenol at an interval of 24 hr on days 20 and 21. Blood and tissue samples were taken for histopathological and biochemical evaluations following electrocardiography recording on day 21. Isoproterenol elevated ST segment, increased heart weight, heart rate, serum activities of aspartate transaminase, lactate dehydrogenase, creatine kinase-MB and heart tissue content of malondialdehyde, and decreased R wave amplitude and superoxide dismutase and catalase activities of heart tissue. Necrosis, edema and inflammatory cells infiltration were observed in myocardial tissue sections. Our results indicated that histidine and vitamin C alone, and especially in combination prevent isoproterenol-induced cardiotoxicity and have similar protective effects with propranolol. Cardioprotective effects of histidine and vitamin C may be associated with their ability to reduce free radical-induced toxic effects.
