CLINICAL APPLICATION OF END SYSTOLIC P-V RELATIONS

这项调查的统一假设是， 接受长期MR刺激的患者中的耐受量增加 交感神经系统（SNS）的激活作为补偿 维持有效前向输出、动脉压和 组织灌注这种代偿机制会影响β AR反应性导致LV收缩功能障碍。因此， 因此，二尖瓣手术治疗将恢复LV 收缩功能，SNS活动减少， β AR反应性恢复。在5名患者中进行的初步研究 已经证明了免疫体积和腺苷酸之间的关系 环化酶活性（r=0.86）和收缩功能（r=0.75）。 同样地， 孕妇血浆去甲肾上腺素水平和腺苷酸环化酶活性 保留收缩功能（r= 0.91&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.