Division of Neonatology, Mt Sinai Medical Center, Miami Beach, FL 33140, United States.
Resuscitation. 2011 Jun;82(6):767-75. doi: 10.1016/j.resuscitation.2011.02.012. Epub 2011 Mar 10.
Cardiac arrest (CA) and resuscitation are models of whole body ischemia reperfusion injury. Interventions performed prior to (pre-treatment) or after (post-treatment) can result in cardioprotection. Myocardial stunning, characterized by microcirculatory and contractile dysfunction after CA, is an important component of the post-cardiac arrest syndrome. Periodic acceleration (pGz), produced by the cyclical motion of the supine body headward to footward, increases microcirculatory blood flow to vital organs and elicits production of endothelial derived cytoprotective factors in normal animals. We tested the hypothesis that application of pGz 30 min after return of circulation from CA, as a delayed post-treatment strategy, would improve regional microcirculatory blood flow to vital organs and functional indices of myocardial stunning in pigs.
8 min of unsupported VF followed by cardiopulmonary resuscitation and defibrillation was carried out in twenty anesthetized and paralyzed male swine who were randomized to delayed post-treatment with pGz (dPost) or none (CONT). pGz was begun 30 min after return of circulation along with conventional mechanical ventilation. Hemodynamics, echocardiogram, and regional blood flows were measured as well as biochemical index of cardiac tissue injury.
All animals had spontaneous return of circulation after cardiopulmonary resuscitation (CPR) and defibrillation. dPost animals had less myocardial stunning and greater regional blood flows to the heart, brain, kidneys, ileum and stomach than CONT. Post-treatment with pGz blunted the increase in Troponin I produced by CA and resuscitation, and, induced a greater rise in endothelial derived nitric oxide synthase (eNOS) and its phosphorylation (p-eNOS).
Delayed post-treatment with pGz as a therapeutic strategy, protects against early myocardial stunning in VF cardiac arrest by improving microcirculatory blood flow to the heart and also protects other vital organs by this mechanism.
心脏骤停（CA）和复苏是全身缺血再灌注损伤的模型。在（预处理）之前或之后（后处理）进行的干预可导致心脏保护。CA 后以微循环和收缩功能障碍为特征的心肌顿抑是心脏骤停后综合征的重要组成部分。周期性加速（pGz），由仰卧位头部向脚的周期性运动产生，增加重要器官的微循环血流，并在正常动物中引起内皮衍生的细胞保护因子的产生。我们检验了这样一个假设，即在 CA 后循环恢复 30 分钟后应用 pGz（延迟后处理策略）可改善重要器官的区域微循环血流和猪的心肌顿抑的功能指标。
在 20 只麻醉和麻痹的雄性猪中进行 8 分钟无支持的 VF，然后进行心肺复苏和除颤，随机分为延迟后处理 pGz（dPost）或无处理（CONT）。在循环恢复后 30 分钟开始 pGz，并同时进行常规机械通气。测量血流动力学、超声心动图和区域血流以及心脏组织损伤的生化指标。
所有动物在心肺复苏（CPR）和除颤后均自发恢复循环。dPost 动物的心肌顿抑程度较轻，心脏、大脑、肾脏、回肠和胃的区域血流较多。CPR 后应用 pGz 可减轻 CA 和复苏引起的肌钙蛋白 I 升高，并诱导内皮衍生型一氧化氮合酶（eNOS）及其磷酸化（p-eNOS）的更大升高。
作为治疗策略的延迟后处理 pGz 通过改善心脏的微循环血流来保护 VF 心脏骤停后的早期心肌顿抑，并通过这种机制保护其他重要器官。
