Effects of Free Radical Scavengers on Renal Circulation after Ischaemia in the Rabbit

Abstract

The intrarenal erythrocyte distribution, total renal blood flow and renal vascular resistance were studied before and during recirculation after 60 min of warm ischaemia in three groups of rabbits. One group was pretreated with superoxide dismutase, another with catalase and the third group was not pretreated at all. In non-pretreated ischaemic kidneys there was a significant trapping of labelled erythrocytes in the outer stripe of the medulla. This trapping was not seen in non-ischaemic control kidneys and was completely prevented by pretreatment with either superoxide dismutase or catalase. In non-pretreated ischaemic kidneys there was a transient increase in total renal blood flow during the first 5 min of recirculation, after which it returned to preischaemic values. After pretreatment with catalase the postischaemic increase in blood flow was more pronounced but again the blood flow returned to preischaemic values within 30 min. Pretreatment with superoxide dismutase resulted in a rapid postischaemic increase in blood flow which remained high throughout the 30 min period studied. The renal vascular resistance decreased initially during recirculation after ischaemia in both pretreated and non-pretreated kidneys. In the latter it returned to pre-ischaemic values within 10 min whereas a slower increase was observed after catalase pretreatment. After pretreatment with superoxide dismutase the resistance remained low during the 30 min recorded.

Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.

“…If the mitochondria are damaged in the ischemic state and are reoxygenated, a greater amount of oxygen would be reduced outside the electron transport chain, thereby generating more superoxide and hydroxy radicals (2). Therefore, another plausible explanation for the result that benidipine prevented the lipid peroxidation is that benidipine reduced Ca overload which could lead to mitochondrial damage; and therefore, the leak of free radicals from the mitochondria was prevented during the reperfusion.…”

“…On the other hand, there have been some reports that the pro duction of oxygen free radicals is involved in the development of ischemic renal failure (2)(3)(4).…”

Ischemia/Reperfusion-Induced Pancreatitis

“…The pathogenesis of ischemia/reperfusion injury has been investigated intensively in many organs, including skeletal muscle, brain, heart, kidney, liver, stomach, intestine, and skin [1, 2, 3, 4, 5, 6, 7, 8]. Ischemia-induced tissue damage not only becomes more apparent, but is also markedly enhanced as a result of recirculation of oxygenated blood into the ischemic tissue during reperfusion.…”

Post-Ischaemic Administration of Hyperosmolar Mannitol Enhances Erythrocyte Trapping in Outer Medullary Vasculature in the Rat Kidney

“…The potential mechanisms by which mannitol may exert this protective action include vasodilation [2], re duced cell swelling [5,6] and wash-out of intratubular casts [3], Mannitol also has a scav enger effect on reactive oxygen metabolites (ROM), which might prevent reoxygenation cell injury [7],…”