Toshinobu Horie

Immunohistochemical localization of endothelin in human vascular endothelial cells

The cellular localization of endothelin (ET), a novel vasoconstrictor peptide, was studied in human vascular tissues by immunohistochemistry. Distinct and diffuse staining for ET-like immunoreactivity was demonstrated in the cytoplasm of vascular endothelial cells, but not in smooth muscle cells or adventitial fibroblasts. The specificity was confirmed by the negative results following immunoabsorption. These findings suggest that human vascular endothelial cells function as an endocrine and/or paracrine cells for ET secretion.

Chronic effects of metoprolol on myocardial β-adrenergic receptors in doxorubicin-induced cardiac damage in rats.

This study was designed to clarity whether chronic administration of metoprolol had any influence on cardiac β-adrenergic receptors (BAR) in doxoruhicin (DOX)-induced cardiac damage. DOX was injected through the tail vein into rats 13 mg kg week. n 22 for 5 weeks. One week after the final injection. the rats were randomly divided into two groups. M (with metoprolol. 10 mg kg day subcutaneously s.c.: n 11) and D (without metoprolol: n – 10) After 3-week infusion. plasma norepinephrine (NE) levels and BAR density 11* liodocyanopindolol (ICYP) binding on crude membranes] were measured. Left and right ventricular end-diastolic pressure (LVEDP. RVEDP) and myocardial NE levels were also measured, and the results were compared with those from an age-matched control group (C. n - 11). Decreased BAR density and increased plasma NE levels were evident in group D. indicating dowmregulation. In group M. BAR density and plasma NE levels were similar to those in group C. The myocardial NE levels, were decreased in group D, but were higher in group M than in group D. The LVEDP and RVEDP Were increased in group D, but were almost normal in group M. These results suggest that metoprolol is a promising drug for treatment of DOX-induced cardiac damage.

Relationship between myocardial infarction and preinfarction angina: a histopathological study of coronary arteries in two sudden death cases employing serial section.

Two patients who had previously experienced old myocardial infarction and who died suddenly after an attack of chest pain were examined and discussed. In both cases two of the three main coronary arteries showed severe stenosis with canalization. Ruptured atheromatous plaque was found in the unblocked coronary artery. Fibrin was already formed and surrounded the fractured intimal collagen fiber, foam cells, and cholesterin clefts, but a luminal thrombi had not yet been formed. Fresh occluding thrombi were formed at the site of the ruptured atheromatous plaque. Coronary thrombi containing abscess components such as foam cells, cholesterin clefts, and the fractured intimal collagen fiber were found in our preliminary study. These views support the supposition that this fracture between the lumen and the plaque might precede and be responsible for the formation of the thrombus and the onset of acute myocardial infarction. It was confirmed that the attack of preinfarction angina occurred at the time of the rupture of the atheromatous plaque. The rupture of the atheromatous plaque plays an important part as an initiating factor of peinfarction angina and myocardial infarction. Thus, it is necessary to examine coronary arteries by serial histopathological section method.