Douzinas Emmanuel E, Pitaridis Marinos T, Patsouris Efstratios, Kollias Spyridon, Boursinos Vasilios, Karmpaliotis Dimitrios I, Gratsias Yiannis, Evangelou Evangelos, Papalois Apostolos, Konstantinidou Anastasia E, Roussos Charis
Departmentof Critical Care, University of Athens medical School, Greece.
Crit Care Med. 2003 Aug;31(8):2183-9. doi: 10.1097/01.CCM.0000080488.30157.D8.
The circulatory shock following intestinal ischemia-reperfusion injury has been attributed to hypovolemia. The purpose of the current study is to clarify the pathophysiology of this type of shock and to test the hypothesis that hypoxemic compared with normoxemic reperfusion improves hemodynamics.
Randomized animal study.
Medical school laboratory.
Twenty-one pigs.
Pigs were subjected to 120 mins of intestinal ischemia by clamping the superior mesenteric artery. Upon declamping, the animals were randomized into two groups: a group that received hypoxemic reperfusion (HR group, n = 8) with a PaO2 = 30-35 and a control group reperfused with PaO2 = 100 mm Hg (control group, n = 13).
Measurements included mean arterial pressure, cardiac index, pulmonary artery occlusion pressure, and requirements for fluids and epinephrine. Biopsies from the terminal ileal mucosa were taken for malondialdehyde measurements at baseline, at 120 mins of ischemia, and at 30 and 60 mins of reperfusion. A piece of left ventricle was obtained after 120 mins of reperfusion for histologic studies. Five of 13 animals of the control group died in intractable shock; no animal of the HR group died (p =.11). The decrease in the mean arterial pressure during reperfusion was more pronounced in the control group (p <.008) despite the larger doses of epinephrine administered, compared with the HR group (p <.02). During reperfusion, both groups exhibited a decrease in cardiac index; this was more pronounced in the control group (p =.0007). Pulmonary artery occlusion pressure increased during reperfusion in both groups and was more pronounced in the control group (p =.04 at 60 mins). Although mixed venous blood oxygen saturation of the control animals was higher at 30 mins of reperfusion (p =.005), it declined after 60 mins and became lower than that of HR animals at the end of reperfusion (p <.02). The myocardial histopathologic injury score was higher in the control group (2.0 +/- 0.69 and 3.4 +/- 0.89 for the HR and control groups, respectively; p <.03). The concentrations of intestinal mucosa malondialdehyde were significantly higher in the control group at 60 mins of reperfusion (p <.03).
Acute myocardial ischemia and left heart failure significantly contribute to the circulatory shock that follows intestinal ischemia/reperfusion injury and are attenuated by hypoxemic reperfusion.
肠缺血再灌注损伤后的循环性休克一直被认为是由于血容量不足所致。本研究的目的是阐明这类休克的病理生理学机制,并验证与常氧再灌注相比,低氧再灌注可改善血流动力学这一假说。
随机动物研究。
医学院实验室。
21头猪。
通过钳夹肠系膜上动脉使猪经历120分钟的肠缺血。松开钳夹后,将动物随机分为两组:一组接受低氧再灌注(HR组,n = 8),动脉血氧分压(PaO2)维持在30 - 35;另一组为对照组,再灌注时PaO2维持在100 mmHg(对照组,n = 13)。
测量指标包括平均动脉压、心脏指数、肺动脉闭塞压以及液体和肾上腺素的需求量。在基线、缺血120分钟时以及再灌注30分钟和60分钟时,取回肠末端黏膜组织活检以测量丙二醛含量。再灌注120分钟后取左心室组织进行组织学研究。对照组13只动物中有5只因顽固性休克死亡;HR组无动物死亡(p = 0.11)。与HR组相比,尽管给予了更大剂量的肾上腺素,但对照组在再灌注期间平均动脉压的下降更为明显(p < 0.008)(p < 0.02)。再灌注期间,两组的心脏指数均下降;对照组下降更为明显(p = 0.0007)。两组在再灌注期间肺动脉闭塞压均升高,对照组更为明显(60分钟时p = 0.04)。虽然对照组动物在再灌注30分钟时混合静脉血氧饱和度较高(p = 0.005),但60分钟后下降,且在再灌注结束时低于HR组动物(p < 0.02)。对照组心肌组织病理学损伤评分更高(HR组和对照组分别为2.0 ± 0.69和3.4 ± 0.89;p < 0.03)。再灌注60分钟时,对照组肠黏膜丙二醛浓度显著更高(p < 0.03)。
急性心肌缺血和左心衰竭在肠缺血/再灌注损伤后的循环性休克中起重要作用,低氧再灌注可减轻这种损伤。