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[肠道缺血中的高乳酸血症。II. 实验原理]

[Hyperlactacidemia in intestinal ischemia. II. Experimental principles].

作者信息

Nutz V, Sommer J H, Schultze-Petzold J

出版信息

Langenbecks Arch Chir. 1987;370(2):69-78. doi: 10.1007/BF01254085.

Abstract

Looking for an early laboratory parameter in diagnosis of acute bowel ischemia, we caused an acute ischemia of the rabbit bowel by clamping the superior mesenteric artery. The blood tests showed a significant increase of lactate during 80 min of ischemia. This lactate excess continued nearly 40 min after revascularization of the bowel, but disappeared nearly completely after 90 min. Neither the laparotomy without clamping the superior mesenteric artery, nor the experimental clamping of the a. femoralis communis led to a lactacidemia. The lactacidemia in our experiments is compared with clinical observations in acute bowel diseases and vascular surgery with clamping of the aorta. The reasons of the specific high lactate excess of bowel ischemia are discussed. The fast increase of the lactate following mesenteric vascular occlusion and the rapid normalisation of lactate after recovery demonstrate a sensitive method in the diagnosis and controlling the treatment of acute bowel diseases with an insufficient blood supply.

摘要

为了寻找急性肠缺血诊断的早期实验室指标,我们通过夹闭肠系膜上动脉造成兔肠急性缺血。血液检测显示,在缺血80分钟期间乳酸显著增加。肠再灌注后,这种乳酸过量持续了近40分钟,但90分钟后几乎完全消失。未夹闭肠系膜上动脉的剖腹手术以及股总动脉的实验性夹闭均未导致乳酸血症。我们将实验中的乳酸血症与急性肠道疾病和主动脉夹闭的血管手术中的临床观察结果进行了比较。讨论了肠缺血时特定高乳酸过量的原因。肠系膜血管闭塞后乳酸的快速增加以及恢复后乳酸的快速正常化证明了一种用于诊断和控制血液供应不足的急性肠道疾病治疗的敏感方法。

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