CLINICAL APPLICATION OF END SYSTOLIC P-V RELATIONS

本研究的统一假设是，长期MR患者的反流体积进行性增加刺激交感神经系统（SNS）的激活，作为维持有效前输出、动脉压和组织灌注的代偿机制。这种代偿机制影响β - AR反应性降低，导致左室收缩功能障碍。因此，二尖瓣手术治疗将在一定程度上恢复左室收缩功能，SNS活动减弱，β - AR反应恢复。5例患者的初步研究表明，反流量与腺苷酸环化酶活性（r=0.86）和收缩功能（r=0.75）之间存在关系。同样，相关血浆去甲肾上腺素水平和腺苷酸环化酶活性与收缩功能保持一致（r=0.91和0.65）。因此，初步数据支持这一假设。

The unifying hypothesis of this investigation is that the progressive increase in regurgitant volume in patients with long-term MR stimulates activation of the sympathetic nervous system (SNS) as a compensatory mechanism to maintain effective forward output, arterial pressure, and tissue perfusion. This compensatory mechanism affects a decrease in beta AR responsiveness resulting in LV contractile dysfunction. It follows, therefore, that treatment with mitral valve surgery will restore LV contractile function to the extent that SNS activity is diminished and beta AR responsiveness is restored. Preliminary studies in five patients have demonstrated a relationship between regurgitant volume and adenylyl cyclase activity (r=0.86) and contractile function (r=0.75). Similarly, correlatal plasma norepinephrine levels and adenylyl cyclase activity reserved with contractile function (r=0.91 & 0.65). Thus, preliminary data support the hypothesis.