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三磷酸腺苷-氯化镁(ATP-MgCl2)可在创伤失血性休克后早期恢复肠道吸收能力。

ATP-MgCl2 restores gut absorptive capacity early after trauma-hemorrhagic shock.

作者信息

Singh G, Chaudry K I, Chaudry I H

机构信息

Department of Surgery, Michigan State University, East Lansing 48824.

出版信息

Am J Physiol. 1993 May;264(5 Pt 2):R977-83. doi: 10.1152/ajpregu.1993.264.5.R977.

DOI:10.1152/ajpregu.1993.264.5.R977
PMID:8498607
Abstract

The aim of this study was to determine whether ATP-MgCl2 as an adjunct to resuscitation has any beneficial effect on the depressed gut absorptive capacity (GAC) after hemorrhage and, if so, whether alterations in whole blood viscosity (WBV) are, in part, responsible for those effects. Rats were anesthetized, a laparotomy was performed (i.e., trauma induced), and blood vessels were cannulated. The animals then underwent fixed pressure (40 mmHg) hemorrhage, followed by resuscitation with lactated Ringer solution. One group received 50 mumol/kg ATP-MgCl2 and another received saline during resuscitation. At 2 and 4 h after the end of hemorrhage, a 1-h D-xylose absorption test was performed. Viscosity determinations were made at corresponding time points in another set of rats subjected to sham hemorrhage, acute hemodilution, or hemorrhage and resuscitation. Results show that xylose absorption is depressed after hemorrhage and resuscitation and that ATP-MgCl2 restored it to normal. D-Xylose absorption was inhibited by glucose, indicating a facilitated transport process. Furthermore, WBV was reduced by the administration of ATP-MgCl2. Thus ATP-MgCl2 improves GAC early after hemorrhage and resuscitation, possibly by reducing WBV, and may be a useful adjunct to resuscitation, allowing for early enteral nutrition.

摘要

本研究的目的是确定作为复苏辅助手段的ATP - MgCl₂对出血后降低的肠道吸收能力(GAC)是否有任何有益作用,以及如果有作用,全血粘度(WBV)的改变是否部分地导致了这些作用。将大鼠麻醉,进行剖腹手术(即诱导创伤),并插入血管插管。然后动物接受固定压力(40 mmHg)出血,随后用乳酸林格溶液进行复苏。一组在复苏期间接受50 μmol/kg ATP - MgCl₂,另一组接受生理盐水。在出血结束后2小时和4小时,进行1小时的D - 木糖吸收试验。在另一组接受假出血、急性血液稀释或出血及复苏的大鼠的相应时间点测定粘度。结果表明,出血和复苏后木糖吸收降低,而ATP - MgCl₂将其恢复至正常。葡萄糖抑制D - 木糖吸收,表明存在易化转运过程。此外,给予ATP - MgCl₂可降低WBV。因此,ATP - MgCl₂可能通过降低WBV在出血和复苏后早期改善GAC,并且可能是复苏的有用辅助手段,从而允许早期肠内营养。

相似文献

1
ATP-MgCl2 restores gut absorptive capacity early after trauma-hemorrhagic shock.三磷酸腺苷-氯化镁(ATP-MgCl2)可在创伤失血性休克后早期恢复肠道吸收能力。
Am J Physiol. 1993 May;264(5 Pt 2):R977-83. doi: 10.1152/ajpregu.1993.264.5.R977.
2
Restoration of gut absorptive capacity following trauma-hemorrhagic shock by the adjuvant use of heparan sulfate.通过辅助使用硫酸乙酰肝素恢复创伤性失血性休克后的肠道吸收能力。
J Trauma. 1993 May;34(5):645-51; discussion 651-2. doi: 10.1097/00005373-199305000-00006.
3
Depressed gut absorptive capacity early after trauma-hemorrhagic shock. Restoration with diltiazem treatment.创伤失血性休克后早期肠道吸收能力下降。地尔硫䓬治疗可恢复该能力。
Ann Surg. 1991 Dec;214(6):712-8. doi: 10.1097/00000658-199112000-00011.
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Differential effects of ATP-MgCl2 on portal and hepatic arterial blood flow after hemorrhage and resuscitation.出血和复苏后ATP-MgCl2对门静脉和肝动脉血流的不同影响。
Am J Physiol. 1992 Dec;263(6 Pt 1):G895-900. doi: 10.1152/ajpgi.1992.263.6.G895.
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ATP-MgCl2 restores depressed endothelial cell function after hemorrhagic shock and resuscitation.
Am J Physiol. 1995 Apr;268(4 Pt 2):H1390-6. doi: 10.1152/ajpheart.1995.268.4.H1390.
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Diltiazem reduces whole blood viscosity following trauma-hemorrhagic shock and resuscitation.地尔硫䓬可降低创伤失血性休克及复苏后的全血黏度。
Circ Shock. 1993 Mar;39(3):231-6.
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ATP-MgCl2 restores the depressed cardiac output following trauma and severe hemorrhage even in the absence of blood resuscitation.即使在没有进行血液复苏的情况下,ATP-氯化镁也能恢复创伤和严重出血后降低的心输出量。
Circ Shock. 1992 Apr;36(4):277-83.
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Administration of ATP-MgCl2 after trauma-hemorrhage and resuscitation restores the depressed cardiac performance.创伤性出血和复苏后给予三磷酸腺苷-氯化镁可恢复降低的心脏功能。
J Surg Res. 1997 Apr;69(1):159-65. doi: 10.1006/jsre.1997.5065.
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Administration of ATP-MgCl2 following hemorrhage and resuscitation increases hepatic phosphoenolpyruvate carboxykinase and decreases pyruvate kinase activities.出血和复苏后给予三磷酸腺苷-氯化镁可增加肝脏磷酸烯醇式丙酮酸羧激酶活性,并降低丙酮酸激酶活性。
Biochim Biophys Acta. 1997 Oct 20;1336(3):549-56. doi: 10.1016/s0304-4165(97)00069-x.
10
ATP-MgCl2 treatment after trauma-hemorrhage/resuscitation increases hepatocyte P2-purinoceptor binding capacity.
Am J Physiol. 1994 Jun;266(6 Pt 2):R1810-5. doi: 10.1152/ajpregu.1994.266.6.R1810.

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