Fujimoto K, Price V H, Granger D N, Specian R, Bergstedt S, Tso P
Department of Physiology, Louisiana State University Medical Center, Shreveport 71130.
Am J Physiol. 1991 Apr;260(4 Pt 1):G595-602. doi: 10.1152/ajpgi.1991.260.4.G595.
The purpose of this study was to assess intestinal function after ischemia-reperfusion (I/R). In two groups of intestinal lymph fistula rats (experimental), the superior mesenteric artery (SMA) was isolated and occluded for 10 min. In the remaining two groups (controls), the SMA was isolated but not occluded. Twenty-four or forty-eight hours after I/R, a lipid test meal containing radioactive triolein was infused at 3 ml/h for 8 h. Radioactive lipid in lymph, lumen, intestinal wall, portal and systemic blood, epididymal fat pads, and liver was determined. Lymph radioactive lipid output was markedly depressed in the 24-h experimental rats compared with the other three groups, and this deficiency was restored 48 h after I/R. This reduction in lipid output in lymph appeared to be the result of an increased portal transport of the infused radioactive lipid rather than a deficiency of digestion or absorption of infused triolein. We have further validated the markedly increased portal transport of radioactive lipid after I/R by using Triton WR-1339, which blocks peripheral metabolism of hepatic very low-density lipoproteins (VLDL). When Triton WR-1339 was introduced in 24 experimental and control animals, the experimental rats accumulated significantly more radioactive lipid (12-14% of infused lipid) than the control animals (2-3% of infused lipid), indicating a marked increase in portal transport of radioactive lipid, which was taken up by the liver and then resecreted into circulation as VLDL. Thus intestinal lipid absorption is sensitive to the deleterious effects of ischemia followed by reperfusion, and therefore it may be used as a functional assessment of the small intestine after I/R-induced injuries.
本研究的目的是评估缺血再灌注（I/R）后的肠道功能。在两组肠道淋巴瘘大鼠（实验组）中，分离肠系膜上动脉（SMA）并阻断10分钟。在其余两组（对照组）中，分离SMA但不阻断。I/R后24或48小时，以3 ml/h的速度输注含放射性三油酸甘油酯的脂质试验餐，持续8小时。测定淋巴、肠腔、肠壁、门静脉和全身血液、附睾脂肪垫及肝脏中的放射性脂质。与其他三组相比，24小时实验组大鼠的淋巴放射性脂质输出明显降低，这种不足在I/R后48小时恢复。淋巴中脂质输出的减少似乎是由于输注的放射性脂质门静脉转运增加，而非输注的三油酸甘油酯消化或吸收不足所致。我们通过使用Triton WR-1339进一步验证了I/R后放射性脂质门静脉转运的显著增加，Triton WR-1339可阻断肝脏极低密度脂蛋白（VLDL）的外周代谢。当在24只实验动物和对照动物中引入Triton WR-1339时，实验大鼠积累的放射性脂质（占输注脂质的12 - 14%）明显多于对照动物（占输注脂质的2 - 3%），表明放射性脂质门静脉转运显著增加，该脂质被肝脏摄取，然后作为VLDL重新分泌入循环。因此，肠道脂质吸收对缺血再灌注的有害作用敏感，因此可作为I/R诱导损伤后小肠功能评估的指标。
