Ojteg G, Bayati A, Källskog O, Wolgast M
Acta Physiol Scand. 1987 Mar;129(3):295-304. doi: 10.1111/j.1748-1716.1987.tb08072.x.
The macromolecular permeability of renal capillaries and the intravascular red cell aggregation resulting from 45 min of warm ischaemia were investigated. The effects of the xanthine oxidase inhibitor Allopurinol on these factors and also on the post-ischaemic nephron function were also studied. Following ischaemia there was a more than 10-fold increase in the transport from plasma to renal hilar lymph both of plasma proteins and of two isomers of lactate dehydrogenase (LDH)-the nearly neutral LDH-M4 and the negatively charged LDH-H4. The ischaemia also resulted in massive intravascular red cell aggregation, especially in the renal medulla. Through reduction of plasma xanthine oxidase activity from 13.1 +/- 1.1 microU microliter-1 (mean +/- SEM) to essentially zero by Allopurinol, the capillary leakiness was substantially diminished with almost complete normalization after 120 min. At the same time the relative volume of trapped red cells was reduced; in the inner stripe of the outer medulla, for example, it decreased from 11.3 +/- 1.7% in untreated animals to 4.0 +/- 1.1% after treatment with 20 mg of Allopurinol given intravenously 3 h before the ischaemia. Oral feeding with 4 mg of Allopurinol day-1 for one week gave essentially the same result. The net driving force for filtration after treatment with this drug was thus 19 mmHg, as against 26 mmHg in the normal kidney and the resulting SNGFR was half the normal. The total filtration rate was proportionally more reduced to less than 1/3 of the normal. Tubular obstruction was still present but was not as severe as in untreated kidneys (Karlberg et al., 1982b) where the tubular fluid flow and thereby the filtration are essentially zero. It is suggested that oxygen free radicals increased the macromolecular permeability and the adhesiveness of white blood cells and that these two factors combined underlie the aggregation of red blood cells in the medullary vasa recta with consequent persistence of medullary ischaemia.
研究了肾毛细血管的大分子通透性以及45分钟热缺血导致的血管内红细胞聚集情况。还研究了黄嘌呤氧化酶抑制剂别嘌呤醇对这些因素以及缺血后肾单位功能的影响。缺血后，血浆蛋白和乳酸脱氢酶（LDH）的两种异构体——近乎中性的LDH-M4和带负电荷的LDH-H4，从血浆向肾门淋巴的转运增加了10倍以上。缺血还导致大量血管内红细胞聚集，尤其是在肾髓质。通过别嘌呤醇将血浆黄嘌呤氧化酶活性从13.1±1.1微单位/微升（平均值±标准误）降至基本为零，毛细血管渗漏明显减少，120分钟后几乎完全恢复正常。与此同时，被困红细胞的相对体积减少；例如，在髓质外带的内条纹中，它从未经治疗的动物中的11.3±1.7%降至缺血前3小时静脉注射20毫克别嘌呤醇治疗后的4.0±1.1%。每天口服4毫克别嘌呤醇，持续一周，结果基本相同。用这种药物治疗后，滤过的净驱动力为19毫米汞柱，而正常肾脏中为26毫米汞柱，由此产生的单肾肾小球滤过率（SNGFR）是正常的一半。总滤过率按比例降低得更多，不到正常的1/3。肾小管阻塞仍然存在，但不如未治疗的肾脏严重（卡尔伯格等人，1982b），在未治疗的肾脏中，肾小管液流动以及由此产生的滤过基本为零。有人认为，氧自由基增加了大分子通透性和白细胞的黏附性，这两个因素共同导致了髓质直小血管中红细胞的聚集，从而导致髓质缺血持续存在。
