| Budget Amount *help |
¥24,000,000 (Direct Cost: ¥24,000,000)
Fiscal Year 1985: ¥8,500,000 (Direct Cost: ¥8,500,000)
Fiscal Year 1984: ¥15,500,000 (Direct Cost: ¥15,500,000)
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| Research Abstract |
To investigate whether disseminative coronary embolization with microspheres elicits the chronic heart failure, we observed serial changes in hemodynamics, coronary circulation, histology and <beta> -receptor density after the coronary embolization with microspheres of 15- m ( ) in dogs. Immediately after the coronary embolization, a marked myocardial ischemia was elicited; lactate production, a decrease in fractional shortening and patchy ischemia (succinic dehydrogenase staining) were observed with an increase in coronary blood flow. A week after embolization, however, the resting coronary blood flow recovered to the control with absense of myocardial necrosis, but coronary flow reserve was significantly decreased. Histological examination indicated a delayed recovery from myocardial ischemia. Up to 5 hours, the patchy ischemia of 100-200 um( ), severe intracellular edema and a decrease in glycogen granules were observed. After a week, microscopic view demonstrated the apparently nor
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mal myocardium except a few myocytolytic lesions. Glycogen granules were markedly increased and mitochondriosis and rough endoplasmic reticulum were also observed, indicating compensatory metabolic hyperfunction. Hemodynamic studies 24 hours after microsphere embolization revealed a marked cardiac dysfunction; mean aortic pressure and dP/dt were markedly decreased, whereas the time constant of isovolumic left ventricular pressure decay (T) was increased. These hemodynamic changes were almost recovered after a week except for the diastolic function. Cardiac response to isoproterenol were preserved in both acute and chronic phases. Myocardial norepinephrine content was preserved 24 hours but it was significantly decreased a week after the microsphere embolization. In contrast, <beta> -adrenergic density was increased in the chronic phase. Therefore, the apparently normal systolic function despite the depletion of myocardial norepinephrine may be compensated by an increase in <beta> -adrenoceptor density. These results indicate that the prolonged myocardial ischemia elicits the prestage of chronic heart failure; q depletion of myocardial norepinephrine and impairement of diastlic function. Less
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