Wang Meng, Verhaegh Rabea, Tsagakis Konstantinos, Brencher Lisa, Zwanziger Denise, Jakob Heinz G, Groot Herbert de, Dohle Daniel-Sebastian
Department of Thoracic and Cardiovascular Surgery, West German Heart Center Essen, University Hospital, Duisburg-Essen University, Essen, Germany.
Department of Cardiac Surgery, Sun Yat-Sen University, Sun Yat-Sen Memorial Hospital, Guangzhou, China.
Thorac Cardiovasc Surg. 2018 Jan;66(1):99-108. doi: 10.1055/s-0037-1603935. Epub 2017 Jun 27.
Acute mesenteric ischemia following cardiovascular surgery is a rare but fatal complication. We established a new rat model for hemodynamic monitoring during mesenteric ischemia/reperfusion (I/R) and evaluated the impact of mesenteric I/R on hemodynamics and remote organ injury.
Mesenteric I/R was induced in male Wistar rats by superior mesenteric artery occlusion for 90 minutes, followed by 120 minutes of reperfusion. Before I/R, ventilation and hemodynamic monitoring including mean arterial blood pressure (MAP) and cardiac output (CO) were established. During reperfusion Geloplasma (I/R + Geloplasma, = 6) and Ringer's solution (I/R + Ringer, = 6) were titrated according to CO and compared with I/R without volume resuscitation (I/R only, = 6) and a sham group (sham, = 6). Blood samples were regularly taken for serum marker measurements. After reperfusion organs were harvested for histology studies.
After acute mesenteric I/R, MAP and CO decreased ( < 0.01) while systemic and pulmonary vascular resistance increased ( < 0.01) continuously in the I/R group. Volume substitution according to CO initially stabilized hemodynamic parameters, but CO declined independently in the late stage. Compared with the I/R + Ringer group, the I/R + Geloplasma group required less volume for resuscitation ( < 0.01), experienced less metabolic acidosis. I/R groups had more organ injuries, more neutrophils sequestration, and higher creatine phosphokinase-MB levels than sham group.
A new model for CO monitoring after mesenteric I/R injury demonstrated severe hypovolemic shock during reperfusion followed by remote myocardial and lung injury. Far less colloid volume is needed for hemodynamic stabilization after I/R compared with crystalloid volume.
心血管手术后发生的急性肠系膜缺血是一种罕见但致命的并发症。我们建立了一种用于肠系膜缺血/再灌注（I/R）期间血流动力学监测的新型大鼠模型，并评估了肠系膜I/R对血流动力学和远处器官损伤的影响。
通过肠系膜上动脉闭塞90分钟，然后再灌注120分钟，在雄性Wistar大鼠中诱导肠系膜I/R。在I/R之前，建立通气和血流动力学监测，包括平均动脉血压（MAP）和心输出量（CO）。在再灌注期间，根据CO滴定明胶（I/R +明胶，n = 6）和林格氏液（I/R +林格氏液，n = 6），并与未进行容量复苏的I/R组（仅I/R，n = 6）和假手术组（假手术，n = 6）进行比较。定期采集血样进行血清标志物测量。再灌注后收获器官进行组织学研究。
急性肠系膜I/R后，I/R组的MAP和CO降低（P < 0.01），而全身和肺血管阻力持续增加（P < 0.01）。根据CO进行容量替代最初可稳定血流动力学参数，但后期CO独立下降。与I/R +林格氏液组相比，I/R +明胶组复苏所需的容量更少（P < 0.01），代谢性酸中毒较轻。I/R组比假手术组有更多的器官损伤、更多的中性粒细胞滞留和更高的肌酸磷酸激酶-MB水平。
肠系膜I/R损伤后CO监测的新模型显示，再灌注期间出现严重的低血容量性休克，随后出现远处心肌和肺损伤。与晶体液相比，I/R后血流动力学稳定所需的胶体液量要少得多。
