Frässdorf Jan, Luther Bernd, Müllenheim Jost, Otto Florian, Preckel Benedikt, Schlack Wolfgang, Thämer Volker
Department of Anesthesiology, University Hospital of Düsseldorf, Düsseldorf, Germany.
J Cardiothorac Vasc Anesth. 2006 Apr;20(2):187-95. doi: 10.1053/j.jvca.2005.11.001. Epub 2006 Feb 21.
The influences of groin incision, duration of ischemia, and the effects of prostaglandin E1 (PGE1) on ischemia-reperfusion (I/R) injury of the hind limb in rabbits were evaluated.
A prospective study.
Laboratory.
In 64 rabbits, bilateral hind limb ischemia was induced by occlusion of the abdominal aorta. Volume changes, neuromuscular function of the hind limb, and creatine kinase (CK) release were measured as variables of tissue injury.
Eight rabbits served as untreated controls (CON). In 2 groups (each n = 14), 3 hours of ischemia were followed by 3 hours of reperfusion (I/R). In 2 different groups (each n = 14), 45 minutes of ischemia were followed by 2 hours of reperfusion. To determine effects of PGE1, 1 I/R group of each ischemia duration was treated intravenously with 80 ng/kg/min of PGE1 starting 30 minutes after the onset of ischemia (I/R-PGE1). To determine effects of groin incision on edema formation, volume changes were determined in the "operated" right (CON-R, 3h-R, 3h-PGE1-R and 45 min-R, 45 min-PGE1-R) or in the "nonoperated" left hind limb (CON-L, 3h-L, 3h-PGE1-L and 45 min-L, 45 min-PGE1-L), representing a subgroup analysis.
Volume changes after I/R occurred only in operated legs after ischemia (3h-R: 2.3 +/- 0.3 mL, p < 0.0001 v CON-R and 3h-L; 45 min-R: 0.8 +/- 0.2 mL, p < 0.01 v 45 min-L). PGE1 reduced edema formation in the operated legs (3h-PGE1-R: 1.0 +/- 0.4 mL, p < 0.0001 v 3h-R; 45 min-PGE1-R: 0.5 +/- 0.3 mL, p = 1.0 v 45 min-R). Groin incision without I/R had no effect on edema formation (CON-R: -0.13 +/- 0.17 mL of baseline). The increase of CK release from 616 +/- 584 U/L in controls to 5,921 +/- 2,156 U/L after 3 hours of ischemia (p < 0.001) was attenuated by treatment with PGE1 (3,732 +/- 2,653, p < 0.05 v I/R). Forty-five minutes of ischemia did not lead to cellular damage as measured by CK release (I/R: 606 +/- 364 U/L). Recovery of neuromuscular function was not affected by PGE1.
Development of edema during I/R depends on groin incision of the hind limb and on the duration of ischemia. The I/R injury is attenuated by PGE1 treatment, in terms of reduced edema formation and CK release, but not in terms of neuromuscular function.
评估腹股沟切口、缺血持续时间以及前列腺素E1(PGE1)对兔后肢缺血再灌注(I/R)损伤的影响。
前瞻性研究。
实验室。
64只兔,通过阻断腹主动脉诱导双侧后肢缺血。测量体积变化、后肢神经肌肉功能以及肌酸激酶(CK)释放,作为组织损伤的变量。
8只兔作为未治疗对照(CON)。2组(每组n = 14),缺血3小时后再灌注3小时(I/R)。2个不同组(每组n = 14),缺血45分钟后再灌注2小时。为确定PGE1的作用,每个缺血持续时间的1个I/R组在缺血开始30分钟后静脉注射80 ng/kg/min的PGE1(I/R-PGE1)。为确定腹股沟切口对水肿形成的影响,在“手术侧”右后肢(CON-R、3h-R、3h-PGE1-R和45 min-R、45 min-PGE1-R)或“非手术侧”左后肢(CON-L、3h-L、3h-PGE1-L和45 min-L、45 min-PGE1-L)测量体积变化,这代表一项亚组分析。
I/R后的体积变化仅发生在缺血后的手术侧肢体(3小时组右侧:2.3±0.3 mL,与CON-R和3小时组左侧相比,p < 0.0001;45分钟组右侧:0.8±0.2 mL,与45分钟组左侧相比,p < 0.01)。PGE1减少了手术侧肢体的水肿形成(3小时组右侧PGE1:1.0±0.4 mL,与3小时组右侧相比,p < 0.0001;45分钟组右侧PGE1:0.5±0.3 mL,与45分钟组右侧相比,p = 1.0)。无I/R的腹股沟切口对水肿形成无影响(CON-R:相对于基线为-0.13±0.17 mL)。缺血3小时后,CK释放从对照组的616±584 U/L增加到5921±2156 U/L(p < 0.001),PGE1治疗使其减弱(3732±2653,与I/R组相比,p < 0.05)。45分钟的缺血未导致CK释放所测量的细胞损伤(I/R组:606±364 U/L)。神经肌肉功能的恢复不受PGE1影响。
I/R期间水肿的形成取决于后肢的腹股沟切口和缺血持续时间。PGE1治疗可减轻I/R损伤,表现为水肿形成和CK释放减少,但对神经肌肉功能无影响。