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低氧血症和低血容量对肠绒毛微循环的协同有害影响*。

Synergistic deleterious effect of hypoxemia and hypovolemia on microcirculation in intestinal villi*.

机构信息

1Laboratoire de Microcirculation, Energétique, Inflammation, Insuffisance Circulatoire Aigue, Université Paris VII-XI-XIII, Paris, France. 2Service d'Anesthésie-Réanimation Chirurgicale, Hôpital de Bicêtre, Université Paris-Sud, Hôpitaux universitaires Paris-Sud, Assistance Publique-Hôpitaux de Paris, Le Kremlin Bicêtre, France. 3BakerIDI Heart and Diabetes Institute, Monash University, Melbourne, Australia. 4Service d'Anatomie pathologique, Groupe hospitalier Paris-Seine-Saint Denis, Hopital Jean Verdier, AP-HP, Bondy, France. 5France et Universite Paris 13, Sorbonne Paris Cite, UFR SMBH, Bobigny, France.

出版信息

Crit Care Med. 2013 Nov;41(11):e376-84. doi: 10.1097/CCM.0b013e318292388d.

Abstract

OBJECTIVE

To investigate the effect of hypoxemia, hemorrhagic shock, and the association of both of these on intestinal microcirculation (microcirculatory perfusion and leukocytes-endothelium interactions in postcapillary venules), as it can be encountered in hemorrhagic shock following trauma.

DESIGN

Prospective controlled experimental study.

SETTING

University research laboratory.

SUBJECTS

Forty-eight anesthetized and mechanically ventilated Balb/c mice.

INTERVENTION

Mice were randomly assigned to hypoxemia group in which we decreased inspired oxygen fraction during 60 minutes to reach a PaO2 of 40 mm Hg, hemorrhagic shock group in which animals were exsanguinated to a mean arterial pressure level of 40 mm Hg during 30 minutes, hypoxemia-hemorrhagic shock group in which PaO2 was decreased to 40 mm Hg during 60 minutes with exsanguination from the 30th to the 60th minute to a mean arterial pressure level of 40 mm Hg; or control group.

MEASUREMENTS AND MAIN RESULTS

Hypoxemia decreased RBCs velocity in intestinal villi but did not alter the fraction of perfused villi. Hypoxemia also triggered leukocytes adhesion to the venular endothelium. Hemorrhagic shock not only decreased RBCs velocity in villi but also slightly altered the fraction of perfused villi (94% ± 2% in hemorrhagic shock group vs 100% ± 0% in control group, p < 0.005). Furthermore, hemorrhagic shock triggered leukocytes adhesion to the venular endothelium to the same extent as hypoxemia. When hypoxemia was associated to hemorrhagic shock, it decreased villous RBCs velocity in an additive manner and the fraction of perfused villi dropped in a synergistic manner (69% ± 3% in hypoxemia-hemorrhagic shock group vs 94 ± 2 in hemorrhagic shock group, p < 0.005). The association of hypoxemia and hemorrhagic shock did not further amplify leukocytes adhesion to intestinal venules compared with either hypoxemia or hemorrhagic shock alone.

CONCLUSIONS

During hemorrhagic shock, the occurrence of hypoxemia considerably alters villous intestinal perfusion as it decreases the fraction of perfused villi in a synergistic manner, thereby increasing the risk of villous ischemia. The association of hypoxemia and hemorrhagic shock did not amplify leukocytes adhesion to the endothelium further than either hemorrhagic shock or hypoxemia alone did. As hypoxemia frequently occurs simultaneously with hemorrhagic shock in traumatic conditions, it can worsen gut ischemia leading to the exacerbation of multiple organ failure syndrome.

摘要

目的

研究低氧血症、失血性休克以及两者同时存在时对肠道微循环(后微静脉中毛细血管灌注和白细胞-内皮细胞相互作用)的影响,因为这在创伤后失血性休克中可能会遇到。

设计

前瞻性对照实验研究。

地点

大学研究实验室。

对象

48 只麻醉并机械通气的 Balb/c 小鼠。

干预

小鼠随机分为低氧血症组,在 60 分钟内降低吸入氧分数,使 PaO2 达到 40mmHg;失血性休克组,在 30 分钟内将动物放血至平均动脉压水平 40mmHg;低氧血症-失血性休克组,在 60 分钟内将 PaO2 降低至 40mmHg,从第 30 分钟到第 60 分钟放血至平均动脉压水平 40mmHg;或对照组。

测量和主要结果

低氧血症降低了肠绒毛中 RBCs 的速度,但并未改变灌注绒毛的比例。低氧血症还触发了白细胞与静脉内皮的黏附。失血性休克不仅降低了绒毛中 RBCs 的速度,还略微改变了灌注绒毛的比例(失血性休克组为 94%±2%,对照组为 100%±0%,p<0.005)。此外,失血性休克触发白细胞与静脉内皮的黏附与低氧血症程度相同。当低氧血症与失血性休克同时存在时,它以累加的方式降低了绒毛中 RBCs 的速度,并且以协同的方式降低了灌注绒毛的比例(低氧血症-失血性休克组为 69%±3%,失血性休克组为 94±2%,p<0.005)。与低氧血症或失血性休克单独作用相比,低氧血症和失血性休克的联合作用并没有进一步放大白细胞对肠道静脉的黏附。

结论

在失血性休克期间,低氧血症的发生会协同地显著改变绒毛肠道灌注,降低灌注绒毛的比例,从而增加绒毛缺血的风险。低氧血症和失血性休克的联合作用并没有比单独的失血性休克或低氧血症更能放大白细胞与内皮的黏附。由于低氧血症在创伤条件下经常与失血性休克同时发生,它可能会加重肠道缺血,导致多器官衰竭综合征的恶化。

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