Fundamental study of occurence mechanism and therapy for myocardial lesions with the mitral insufficiency.

近年来，老年动物获得性心脏病的发病率呈上升趋势，尤其是二尖瓣病变更是困扰患者的一个社会问题。二尖瓣病，即二尖瓣粘液瘤样变性，见于老年犬。粘液瘤样变性主要影响肌腱索和瓣叶，而肌索延长并可能最终破裂，导致二尖瓣返流的急性恶化。二尖瓣小叶变厚，变得多余，并涌入左心房。退变和胶原合成异常发生在靠近脊索附着点的牙尖中央纤维带区域。在一种观点中，二尖瓣病变犬的心肌最常被抛入纤维化。心肌纤维化的病因有外周动脉微栓塞术或特发性。但其病因尚不清楚，本研究的目的是明确…的发生机制，建立t-DNA的发病机制二尖瓣病变合并二尖瓣关闭不全时应多加治疗。如果心肌纤维化是由二尖瓣病变的冠状动脉微栓子引起的，则提示血小板功能的改变，而活化的血小板可能与心肌外周微栓塞术有关。为了评价心肌纤维化与微栓子的关系，进行了以下研究。以ADP(5‘-二磷酸腺苷)为刺激剂，以Bigin为指标，测定了心脏病犬的血小板聚集率，并与非心脏病犬进行了比较，并与常用的最大聚集率法进行了比较。与我们的预期相反，ADP在许多心脏病狗身上诱导了较低水平的血小板聚集。这一结果表明，在二尖瓣关闭不全和主动脉瓣狭窄等心脏疾病中，血小板持续受到返流和湍流的刺激，从而缩短了血小板的寿命，降低了血小板的聚集性。此外，在制备的二尖瓣返流犬中也获得了同样的数据。最后，我们从病理形态上参照了有纤维化的犬心肌。结果表明，心肌纤维化不是由周围冠状动脉微栓子引起的。发现为血管周围/间质的心肌纤维化，而不是移位性纤维化或微栓性纤维化。较少

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 … More 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