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多巴酚丁胺对猪远端结肠缺血的影响。

The effect of dobutamine on distal colon ischaemia in the pig.

作者信息

Björck M, Bergqvist D, Haglund U

机构信息

Department of Surgery, Lasarettet, Skellefteå, Sweden.

出版信息

Intensive Care Med. 1998 Feb;24(2):178-84. doi: 10.1007/s001340050542.

Abstract

OBJECTIVE

To test the hypotheses that dobutamine increases intestinal blood flow, it reduces mucosal acidosis and it prevents mucosal injury in an experimental porcine model of distal colonic ischaemia. And the hypothesis that mannitol prevents reperfusion injury.

DESIGN

Randomised animal experiment.

SETTING

University Hospital, Department of Experimental Research.

MATERIALS

Twenty-four pigs.

INTERVENTIONS

Twenty-one pigs were subjected to 7 h of controlled non-occlusive intestinal ischaemia of the distal colon, consisting of an occlusion of the inferior mesenteric artery (IMA) and a constriction of the superior mesenteric artery (SMA). At 3.5 h six pigs were treated with dobutamine, six with mannitol (0.18 g/kgBW), six with dobutamine and mannitol and three served as controls. Three non-ischaemic pigs were treated with dobutamine.

MEASUREMENTS AND RESULTS

All animals were haemodynamically stable throughout the experiment. There was no difference in any variable between the animals treated with mannitol and those not treated. The ischaemic dobutamine-treated animals increased their cardiac output (CO) by 14% compared to baseline and by 59% compared to controls. The median final dosage of dobutamine was 13.2 micrograms/kg per min (range 8.6-25.8). The blood flow in the restricted SMA, the intramucosal pH of the colonic mucosa (pHi) and the degree of histological mucosal injury were identical in animals treated with dobutamine and controls. The pH gap (pHa-pHi) correlated well (r = 0.97) with the PCO2 gap (aPCO2-intestinal PCO2). The non-ischaemic animals treated with dobutamine increased CO by 37% and blood flow of the SMA by 16%.

CONCLUSIONS

Dobutamine increased CO but did not ameliorate or deteriorate colonic ischaemia in this experimental model. The PCO2 gap correlated well with the pH gap.

摘要

目的

验证以下假说,即多巴酚丁胺可增加肠道血流量、减轻黏膜酸中毒并预防远端结肠缺血的实验性猪模型中的黏膜损伤。以及甘露醇可预防再灌注损伤这一假说。

设计

随机动物实验。

地点

大学医院实验研究部。

材料

24头猪。

干预措施

21头猪接受7小时的远端结肠控制性非闭塞性肠缺血,包括肠系膜下动脉(IMA)闭塞和肠系膜上动脉(SMA)缩窄。在3.5小时时,6头猪用多巴酚丁胺治疗,6头用甘露醇(0.18 g/kg体重)治疗,6头用多巴酚丁胺和甘露醇治疗,3头作为对照。3头非缺血猪用多巴酚丁胺治疗。

测量与结果

所有动物在整个实验过程中血流动力学稳定。用甘露醇治疗的动物与未治疗的动物在任何变量上均无差异。缺血性多巴酚丁胺治疗的动物与基线相比心输出量(CO)增加了14%,与对照组相比增加了59%。多巴酚丁胺的最终中位剂量为每分钟13.2微克/千克(范围8.6 - 25.8)。用多巴酚丁胺治疗的动物与对照组相比,受限SMA中的血流量、结肠黏膜的黏膜内pH值(pHi)以及组织学黏膜损伤程度相同。pH差值(pHa - pHi)与PCO2差值(动脉血PCO2 - 肠道PCO2)相关性良好(r = 0.97)。用多巴酚丁胺治疗的非缺血动物CO增加了37%,SMA血流量增加了16%。

结论

在该实验模型中,多巴酚丁胺增加了CO,但未改善或加重结肠缺血。PCO2差值与pH差值相关性良好。

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