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sucrose/infarction

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BACKGROUND Protectin (CD59) is a recently discovered inhibitor of the complement membrane attack complex (MAC). In the present study we investigated expression of protectin in human heart and examined the relationship between MAC deposition and protectin in myocardial infarction. METHODS Myocardial
Depression is diagnosed in 15-30% of patients following myocardial infarction (MI) and this may also be observed in the rat. We measured the effects of the antidepressant sertraline on behavioural and biochemical events following MI in a rat model. Following surgery, MI rats and sham controls were
OBJECTIVE The aim of study is to investigate the changes of structure and function of heart in diabetic rat after myocardial infarction, and to study the expression of the GLUT4 and the effects of trimetazidine on the ventricular remodeling. METHODS Type 2 diabetes rat was made by feeding with a
BACKGROUND Circulating immune complexes (CIC) are frequently found in postinfarction patients. The constituents of these CIC are mostly unknown. OBJECTIVE The objective of the current study was to assess whether CIC containing alimentary proteins and antibodies against these proteins are implicated
In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after

Changes in sarcolemmal proteins in subacute myocardial infarction in the dog.

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Previous studies have shown degradation of cardiac structural proteins and disruption of the sarcolemma as a result of acute myocardial infarction. However, there is no evidence to date on changes in sarcolemmal membrane proteins induced by experimental subacute myocardial infarction. We studied
OBJECTIVE Major depressive disorder occurs in 15%-30% of patients who have had a myocardial infarction (MI), but the neurobiological mechanisms involved are not well understood. Previously, we found early intracellular signalling changes in the limbic system after acute MI in rats. The aim of the
BACKGROUND Corticotrophin releasing hormone (CRH) is believed to mediate stress-induced behaviors, implying a broader, integrative role for the hormone in the psychological stress response, and studies on CRH in physical stress are few. This study was undertaken to investigate whether CRH plays an
BACKGROUND There is an increased incidence of major depressive disorder (MDD) in individuals after myocardial infarction (MI), but the pathophysiological processes mediating this association are unclear. Our previous study demonstrated an increase in pro-apoptotic pathways in the myocardium and
High-fat or high-carbohydrate food consumption contributes to changes in myocardial tolerance to ischemia. However, with respect to experimental models, most studies used diets with very high doses of cholesterol, saturated fatty acids, or fructose. In our study, we fed rats a high-fat diet based on
Prediabetes is an important risk factor for Type 2 diabetes and cardiovascular complications, such as myocardial infarction. However, few studies explore female sex in this context. Here, we aim to investigate the effects of high-fat high-sucrose diet on cardiac parameters and sensitivity to
Impotence commonly occurs after events such as acute myocardial infarction, coronary bypass, head trauma, and cerebral bleeding, including subarachnoid hemorrhage. We hypothesize that the hypoxia accompanying these events could damage the blood-testis barrier (BTB) and so cause testicular
To evaluate lysosomal involvement in myocardial infarction, coronary artery thrombosis was induced by ligation in 16 dogs. Biopsies of infarcted and normal left ventricles were studied by ultrastructural cytochemistry and subcellular fractionation (0.25 M sucrose) from 30 min to 96 hrs post injury.
Increased lipid peroxidation and reduced glutathione levels in liver of rats fed high sucrose high fat (HSHF) diet were normalized by concomitant administration of (+)-catechin hydrate. Plasma non-enzymatic antioxidants viz. alpha-tocopherol, ascorbic acid and total thiols decrease were also
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