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脓毒症期间精氨酸的肠道吸收减少。

Reduced intestinal absorption of arginine during sepsis.

作者信息

Gardiner K R, Gardiner R E, Barbul A

机构信息

Department of Surgery, Sinai Hospital, Baltimore, MD 21215, USA.

出版信息

Crit Care Med. 1995 Jul;23(7):1227-32. doi: 10.1097/00003246-199507000-00012.

Abstract

OBJECTIVE

To investigate the effect of sepsis on the intestinal absorption of arginine.

DESIGN

Controlled, nonintervention study.

SETTING

Surgical research laboratories of Sinai Hospital of Baltimore.

SUBJECTS

Male Sprague-Dawley rats.

INTERVENTIONS

Experimental sepsis induced by cecal ligation and puncture or intraperitoneal injection of lipopolysaccharide.

MEASUREMENTS AND MAIN RESULTS

Sepsis assessed by peritoneal and blood cultures. Intestinal absorption estimated by measuring the transfer of 3H-arginine by everted jejunal sacs prepared from septic and control animals (n = 6 per group) at multiple time points after the induction of sepsis (6, 12, 24, 48, and 72 hrs after cecal ligation and puncture; 6 and 12 hrs after intraperitoneal injection of lipopolysaccharide). Induction of peritonitis in the rat by cecal ligation and puncture significantly reduced the in vitro uptake of arginine by everted jejunal sacs at 12, 24, and 48 hrs after laparotomy. Arginine transfer by everted jejunal sacs was also significantly reduced in rats as early as 6 hrs after intraperitoneal injection of endotoxin (endotoxin 273 +/- 14; saline 377 +/- 14 nmol/sac/hr). Data are expressed as mean +/- SEM. Recovery from sepsis was associated with normalization of arginine transfer by intestinal sacs.

CONCLUSIONS

Experimental sepsis, induced by either cecal ligation and puncture or intraperitoneal injection of lipopolysaccharide, resulted in impaired intestinal amino acid uptake. Impaired intestinal arginine absorption may explain the lack of benefit of enteral, compared with parenteral, arginine therapy on survival from a septic insult.

摘要

目的

研究脓毒症对精氨酸肠道吸收的影响。

设计

对照、非干预性研究。

地点

巴尔的摩西奈医院外科研究实验室。

对象

雄性斯普拉格 - 道利大鼠。

干预措施

通过盲肠结扎和穿刺或腹腔注射脂多糖诱导实验性脓毒症。

测量指标及主要结果

通过腹膜和血培养评估脓毒症。通过测量由脓毒症大鼠和对照大鼠(每组n = 6)制备的外翻空肠囊在脓毒症诱导后的多个时间点(盲肠结扎和穿刺后6、12、24、48和72小时;腹腔注射脂多糖后6和12小时)对3H - 精氨酸的转运来估计肠道吸收。盲肠结扎和穿刺诱导大鼠腹膜炎后,剖腹术后12、24和48小时外翻空肠囊对精氨酸的体外摄取显著降低。腹腔注射内毒素后6小时,大鼠外翻空肠囊的精氨酸转运也显著降低(内毒素组273±14;生理盐水组377±14 nmol/囊/小时)。数据以平均值±标准误表示。脓毒症恢复与肠道囊精氨酸转运正常化相关。

结论

通过盲肠结扎和穿刺或腹腔注射脂多糖诱导的实验性脓毒症导致肠道氨基酸摄取受损。与肠外精氨酸治疗相比,肠道精氨酸吸收受损可能解释了肠内精氨酸治疗对脓毒症损伤存活无益处的原因。

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