Renal capillary permeability and intravascular red cell aggregation after ischaemia. I. Effects of XXXX oxidase activity.

@entity3624 @entity26 @entity880 @entity6554 @entity208
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 @entity3624 oxidase inhibitor @entity208 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 @entity880 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 @entity3624 oxidase activity from 13.1 +/- 1.1 microU microliter-1 (mean +/- SEM) to essentially zero by @entity208 , 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 @entity208 given intravenously 3 h before the ischaemia. Oral feeding with 4 mg of @entity208 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. @entity6554 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 @entity26 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.
