RENAL CAPILLARY-PERMEABILITY AND INTRAVASCULAR RED-CELL AGGREGATION AFTER ISCHEMIA .1. EFFECTS OF XANTHINE-OXIDASE ACTIVITY
RENAL CAPILLARY-PERMEABILITY AND INTRAVASCULAR RED-CELL AGGREGATION AFTER ISCHEMIA .1. EFFECTS OF XANTHINE-OXIDASE ACTIVITY
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DOI：
10.1111/j.1748-1716.1987.tb08072.x
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发表时间：
1987-03-01
期刊：
影响因子：
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通讯作者：
WOLGAST, M
中科院分区：
文献类型：
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作者：
OJTEG, G;BAYATI, A;WOLGAST, M
本文观察了热缺血45分钟后肾毛细血管大分子通透性和血管内红细胞聚集的变化。还研究了黄嘌呤氧化酶抑制剂别嘌呤醇对这些因子以及对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-近中性LDH-M4和带负电荷的LDH-H4从血浆向肾门淋巴液的转运增加了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。通过将血浆黄嘌呤氧化酶活性从13.1 ± 1.1 μU μ1 - 1（平均值± SEM）至基本为零时，毛细血管渗漏显著减少，120 min后几乎完全恢复正常。同时，捕获红细胞的相对体积减少;例如，在外髓的内条中，缺血前3小时静脉注射20 mg别嘌呤醇后，它从未治疗动物的11.3 ± 1.7%下降到4.0 ± 1.1%。每天口服4 mg别嘌呤醇，持续1周，结果基本相同。因此，用这种药物治疗后过滤的净驱动力为19 mmHg，而正常肾脏为26 mmHg，所得SNGFR为正常值的一半。总滤过率按比例降低至正常值的1/3以下。肾小管阻塞仍然存在，但不像未治疗的肾那样严重（Karlberget等人，1982 b），其中管状流体流动以及由此的过滤基本上为零。这表明，氧自由基增加了大分子的渗透性和白色血细胞，这两个因素相结合的基础上聚集的红细胞在髓直血管随之持续的髓质缺血。
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‐M4and 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 μU μ1‐1(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‐1for 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 (Karlberget 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.