Zakaria El Rasheid, Hurt Ryan T, Matheson Paul J, Garrison R Neal
Department of Surgery, University of Louisville, Louisville, KY, USA.
Am J Surg. 2003 Nov;186(5):443-8. doi: 10.1016/j.amjsurg.2003.07.006.
After resuscitation from hemorrhagic shock, intestinal microvessels constrict leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. Our recent studies have demonstrated that topical and continuous exposure of the gut microvasculature to a clinical solution (Delflex; Fresenius Medical Care), as a technique of direct peritoneal resuscitation (DPR), reverses the postresuscitation vasoconstriction and hypoperfusion to a sustained dilation and hyperperfusion. We hypothesize that initiation of DPR simultaneously with resuscitation from hemorrhagic shock enhance organ blood flow to all tissues surrounding the peritoneal cavity as well as distant organs.
Male Sprague-Dawley rats were anesthetized, intubated and cannulated for monitoring of hemodynamics and for withdrawal of blood. Rats were hemorrhaged to 50% of mean blood pressure for 60 minutes prior to resuscitation with shed blood plus 2 volumes of saline. Animals were randomized for intraperitoneal therapy with 30 mL saline (group 1, n = 9), or Delflex (group 2, n = 9). Whole organ blood flow was measured by colorimetric microsphere technique with phantom organ at baseline, after completion of resuscitation, and at 120 minutes postresuscitation. Replenishment of the dwelling intraperitoneal saline or Delflex was performed in (group 3, n = 8), and (group 4, n = 8), respectively at 90 minutes postresuscitation, and a single whole organ blood flow was performed at 120 minutes postresuscitation.
Direct peritoneal resuscitation caused a significant increase in blood flow to the jejunum (35%), ileum (33%), spleen (48%), and pancreas (57%), whereas a marked increase in blood flow was detected in the lung (111%), psoas major muscle (115%), and diaphragm (132%), as compared with the saline treated animals in group 1. At 120 minutes postresuscitation, organ blood flow returned to the prehemorrhagic shock baseline level in all organs irrespective of peritoneal therapy. Replenishment of the intraperitoneal solution in group 3 and 4, enhanced blood flow to the liver, kidneys, and diaphragm.
Direct peritoneal resuscitation enhanced blood flow to organs incited in the pathogenesis of multiple organ failure that follows hemorrhagic shock.
失血性休克复苏后,肠微血管收缩导致血流受损。尽管恢复并维持了中心血流动力学,但这种情况仍会发生。我们最近的研究表明,作为直接腹膜复苏(DPR)技术,将肠道微血管局部并持续暴露于一种临床溶液(Delflex;费森尤斯医疗集团),可将复苏后的血管收缩和灌注不足转变为持续的血管扩张和高灌注。我们假设,在失血性休克复苏的同时启动DPR可增强流向腹膜腔周围所有组织以及远处器官的器官血流。
雄性Sprague-Dawley大鼠麻醉后插管,用于监测血流动力学和采血。大鼠在复苏前以失血量达到平均血压的50%并持续60分钟,然后用自体失血加两倍体积的生理盐水进行复苏。动物被随机分为两组,分别接受30 mL生理盐水的腹腔内治疗(第1组,n = 9)或Delflex治疗(第2组,n = 9)。在基线、复苏完成后以及复苏后120分钟,采用比色微球技术并使用模拟器官测量全器官血流。分别在复苏后90分钟,对第3组(n = 8)和第4组(n = 8)补充腹腔内生理盐水或Delflex,并在复苏后120分钟进行一次全器官血流测量。
与第1组接受生理盐水治疗的动物相比,直接腹膜复苏使空肠血流显著增加(35%)、回肠血流增加(33%)、脾脏血流增加(48%)、胰腺血流增加(57%),而肺血流(111%)、腰大肌血流(115%)和膈肌血流(132%)显著增加。在复苏后120分钟,无论腹膜治疗情况如何,所有器官的器官血流均恢复到出血性休克前的基线水平。第3组和第4组补充腹腔内溶液后,肝脏、肾脏和膈肌的血流增加。
直接腹膜复苏可增强流向在失血性休克后继发多器官功能衰竭发病机制中受累器官的血流。