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小容量复苏可恢复大鼠胰腺出血引起的微循环障碍。

Small-volume resuscitation restores hemorrhage-induced microcirculatory disorders in rat pancreas.

作者信息

Vollmar M D, Preissler G, Menger M D

机构信息

Institute for Clinical and Experimental Surgery, University of Saarland, Germany.

出版信息

Crit Care Med. 1996 Mar;24(3):445-50. doi: 10.1097/00003246-199603000-00014.

Abstract

OBJECTIVES

Pancreatic hypoxia/ischemia, as a consequence of shock-induced microcirculatory failure, is considered a causative factor in the initiation and/or progression of pancreatic tissue injury. The aim of this study was to compare the effects of "small volume resuscitation" with conventional isovolemic colloid and hypervolemic crystalloid resuscitation on pancreatic microcirculation after hemorrhagic shock.

DESIGN

Randomized, controlled intervention trial.

SETTING

University laboratory.

SUBJECTS

Twenty-three male Sprague-Dawley rats anesthetized with á-chloralose mechanically and ventilated.

INTERVENTIONS

Rats subjected to 1 hr of hemorrhagic shock (mean arterial pressure of 40 mm Hg) were resuscitated with lactated Ringer's solution (four-fold shed volume/20 mins), 10% hydroxyethyl starch (shed volume/5 mins), or 7.2% sodium chloride-10% hydroxyethyl starch (10% shed volume/2 mins).

MEASUREMENTS AND MAIN RESULTS

The microcirculation of pancreatic acinar tissue was studied by means of intravital fluorescence microscopy and laser Doppler flowmetry. At 1 hr after resuscitation, mean arterial pressure, pancreatic capillary erythrocyte velocity, and erythrocyte flux were found to be significantly increased when compared with those values in the shock state. However, mean arterial pressure, pancreatic capillary erythrocyte velocity, and erythrocyte flux did not completely return to preshock values, regardless of the type of fluid used for resuscitation. At 15 mins and 1 hr after resuscitation, shock-induced capillary perfusion failure (reduction of functional capillary density) was restored to 91% to 94% of baseline values in all groups. Pancreatic capillary narrowing, indicating microvascular endothelial cell swelling, was abolished by resuscitation with both isotonic hydroxyethyl starch and hypertonic hydroxyethyl starch (p<.05 vs. lactated Ringer's solution).

CONCLUSIONS

Despite replacement of only 10% of actual blood loss, small-volume resuscitation with hypertonic hydroxyethyl starch is as effective as the ten-fold volume of isotonic hydroxyethyl starch and, due to prevention of microvascular endothelial cell swelling, superior to the 40-fold volume of isotonic lactated Ringer's solution in regard to restoration of the shock-induced microcirculatory disturbances of rat pancreatic acinar tissue.

摘要

目的

胰腺缺氧/缺血作为休克诱导的微循环衰竭的后果,被认为是胰腺组织损伤起始和/或进展的一个致病因素。本研究的目的是比较“小容量复苏”与传统等容胶体和高容晶体复苏对失血性休克后胰腺微循环的影响。

设计

随机对照干预试验。

地点

大学实验室。

对象

23只雄性Sprague-Dawley大鼠,用α-氯醛糖机械麻醉并进行机械通气。

干预措施

经历1小时失血性休克(平均动脉压40mmHg)的大鼠用乳酸林格氏液(失血量的4倍/20分钟)、10%羟乙基淀粉(失血量/5分钟)或7.2%氯化钠-10%羟乙基淀粉(失血量的10%/2分钟)进行复苏。

测量和主要结果

通过活体荧光显微镜和激光多普勒血流仪研究胰腺腺泡组织的微循环。复苏后1小时,与休克状态下的值相比,平均动脉压、胰腺毛细血管红细胞速度和红细胞通量显著增加。然而,无论用于复苏的液体类型如何,平均动脉压、胰腺毛细血管红细胞速度和红细胞通量并未完全恢复到休克前的值。复苏后15分钟和1小时,休克诱导的毛细血管灌注衰竭(功能性毛细血管密度降低)在所有组中恢复到基线值的91%至94%。等渗羟乙基淀粉和高渗羟乙基淀粉复苏均消除了表明微血管内皮细胞肿胀的胰腺毛细血管狭窄(与乳酸林格氏液相比,p<0.05)。

结论

尽管仅补充了实际失血量的10%,高渗羟乙基淀粉小容量复苏与等渗羟乙基淀粉10倍容量的复苏效果相同,并且由于预防了微血管内皮细胞肿胀,在恢复大鼠胰腺腺泡组织休克诱导的微循环紊乱方面优于等渗乳酸林格氏液40倍容量的复苏。

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