Fundamental study of occurence mechanism and therapy for myocardial lesions with the mitral insufficiency.
Grant-in-Aid for Scientific Research (B)
|Allocation Type||Single-year Grants|
Applied veterinary science
|Research Institution||Tokyo University of Agriculture and Technology|
YAMANE Yoshihisa Tokyo University of Agriculture and Technology, Faculty of Agriculture, Professor, 農学部, 教授 (50262225)
SUZUKI Kaoru Tokyo University of Agriculture and Technology, Faculty of Agriculture, Assistan, 農学部, 助手 (90226499)
MARUO Kouzi Tokyo University of Agriculture and Technology, Faculty of Agriculture, Associat, 農学部, 助教授 (40124276)
NOISHIKI Yasuharu Yokohama City University School of Medicine, First Department of Surgery, Lectur, 医学部, 講師 (60033263)
|Project Period (FY)
1995 – 1996
Completed(Fiscal Year 1996)
|Budget Amount *help
¥6,800,000 (Direct Cost : ¥6,800,000)
Fiscal Year 1996 : ¥1,100,000 (Direct Cost : ¥1,100,000)
Fiscal Year 1995 : ¥5,700,000 (Direct Cost : ¥5,700,000)
|Keywords||dog / mitral insufficiency / myocardial fibrosis / platelet aggregation / microembolus / activated clotting time / 家兎|
Recently, acquired heart disease of companion animals is increasing in aged animals, especially the mitral valve disease is a social problem in clients. The mitral valve disease, that is myxomatous degeneration of mitral valve is seen in aged dogs. Myxomatous degeneration effects primarily the chordae tendinea and leaflets, and the chordae elongate and may eventually rupture leading to acute worsening of the mitral regurgitation. The mitral leaflets thicken and become redundant with billowing into the left atrium. Degeneration and abnormal collagen synthesis occur in the central zona fibrosa area of the cusps near the chordal insertions. In one view, the myocardium in the mitral valve disease dogs is most commonly thrown into the fibrosis. It had been described that the etiology of the myocardial fibrosis may be peripheral arterial microembolization or idiopathic. But, the etiology was uncertainly.
The purpose of this study is to clear up of the occurence mechanism and to establish of t
he therapy for myocardial lesions with the mitral insufficiency.
If the myocardial fibrosis was caused by the coronary arterial microembolus in the mitral valve disease, alterations in platelet function is suggested, and activated platelets might relate to peripheral microembolization in heart muscle. In order to evaluate relationship between fibrosis and microembolus in myocardium, following research was operated. To bigin with, platelet aggregation in dogs with heart disease was mesured using ADP (adenosin 5'-diphosphate) as stimulator, and was compared with in dogs without heart disease.
New evaluation method called EPS (Enhancement of Platelet Sensitivity) was compared with usual Max aggregation rate method. Against our expectations, ADP induced lower level of platelet aggregation in many dogs with heart disease. This results indicates that, in heart diseasies such as mitral regurgitation and aortic valve stenosis, platelets unrelentingly suffer from stimulation with regurgitation and turbulent flow, and due to this stimulation lifespan of platelets was shorten and platelets showed lower aggregation.
Nextly, we done the experimentally study the same as above-mentioned in the mitral valve diseases. But, the results completely was similar to it.
Furthermore, the same data was obtained in the dogs with mitral regurgitation which ws prepared experimentaly.
Finally, We refered the canine myocardium with the fibrosis pathomorphologically.The result, fibrosis of the myocardium not be caused by microembolus in peripheral coronary arteries. It was found that they were myocardial fibrosis of the circumvascular/interstitial rather than displacemental fibrosis or fibrosis due to microembolus. Less
Research Output (4results)