Kruzliak Peter, Pechanova Olga, Kara Tomas
Institute of Normal and Pathological Physiology and Centre of Excellence for Regulatory Role of Nitric Oxide in Civilization Diseases, Slovak Academy of Sciences, Bratislava, Slovak Republic,
Heart Fail Rev. 2014 May;19(3):383-90. doi: 10.1007/s10741-013-9397-4.
Nitric oxide (NO) is often used to treat heart failure accompanied with pulmonary edema. According to present knowledge, however, NO donors are contraindicated when systolic blood pressure is less than 90 mmHg. Based on recent findings and our own clinical experience, we formulated a hypothesis about the new breakthrough complex lifesaving effects of NO donors in patients with cardiac arrest and cardiopulmonary resuscitation therapy. It includes a direct hemodynamic effect of NO donors mediated through vasodilation of coronary arteries in cooperation with improvement of cardiac function and cardiac output through reversible inhibition of mitochondrial complex I and mitochondrial NO synthase, followed by reduction in reactive oxygen species and correction of myocardial stunning. Simultaneously, an increase in vascular sensitivity to sympathetic stimulation could lead to an increase in diastolic blood pressure. Confirmation of this hypothesis in clinical practice would mean a milestone in the treatment for cardiac arrest and cardiopulmonary resuscitation.
一氧化氮（NO）常用于治疗伴有肺水肿的心力衰竭。然而，根据目前的认知，当收缩压低于90 mmHg时，禁忌使用NO供体。基于最近的研究发现以及我们自己的临床经验，我们提出了一个关于NO供体在心脏骤停和心肺复苏治疗患者中具有新的突破性综合救生作用的假设。它包括NO供体通过冠状动脉血管舒张介导的直接血流动力学效应，同时通过可逆性抑制线粒体复合物I和线粒体NO合酶来改善心脏功能和心输出量，随后减少活性氧并纠正心肌顿抑。同时，血管对交感神经刺激的敏感性增加可能导致舒张压升高。在临床实践中证实这一假设将意味着心脏骤停和心肺复苏治疗的一个里程碑。
