Effects of free radical scavengers on renal circulation after ischaemia in the rabbit.

@article{Hansson1983EffectsOF,
  title={Effects of free radical scavengers on renal circulation after ischaemia in the rabbit.},
  author={R Hansson and Olof Jonsson and Sven Lundstam and Silas Pettersson and Tore Scherst{\'e}n and Johan Waldenstr{\"o}m},
  journal={Clinical science},
  year={1983},
  volume={65 6},
  pages={
          605-10
        }
}
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… 
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Prevention of ischaemic acute renal failure with superoxide dismutase and sucrose.
TLDR
Superoxide dismutase (20 mg) given just before primary ischaemia and in the early recirculation phase was found to ameliorate the red cell aggregation in the renal medulla, in particular, in the inner stripe of the outer zone the volume of trapped red cells decreased, thus allowing improved restoration of medullary blood flow.
Mechanism of erythrocyte trapping in ischaemic acute renal failure.
TLDR
It is believed that oxygen-derived free radicals generated in the early recirculation phase contribute to the increase in macromolecular permeability, since the scavenger bovine superoxide dismutase and allopurinol, a xanthine oxidase inhibitor, were found to prevent this unfavourable chain of events.
ESR-measurement of oxygen radicals in vivo after renal ischaemia in the rabbit. Effects of pre-treatment with superoxide dismutase and heparin.
The effects of intracellular and extracellular superoxide dismutase and heparin administration on oxygen radical formation after ischaemia in the rabbit kidney were studied. Radicals were measured…
Effects of radical scavengers and antioxidant on ischemic acute renal failure in rabbits.
TLDR
The results suggest that radical scavengers may exert a protective effect against ischemia acute renal failure by other actions rather than ROS scavenging, and support involvement of ROS in IARF in rabbits.
Preservation of cortical microcirculation after kidney ischemia-reperfusion: Value of an iron chelator
TLDR
It is shown that 60 minutes of normothermic ischemia is followed by a significant reduction in cortical microcirculatory flow (no-reflow phenomenon).
Oxygen free radicals in ischemic acute renal failure in the rat.
TLDR
The oxygen free radical scavengers SOD and DMTU, and allopurinol, which inhibits free radical generation, protected renal function after ischemia, and restoration of oxygen supply to ischemic kidney results in the production of oxygen free radicals, which causes renal injury by lipid peroxidation.
Renal capillary permeability and intravascular red cell aggregation after ischaemia. I. Effects of xanthine oxidase activity.
TLDR
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.
Role of iron in postischemic renal injury in the rat.
To determine whether iron participates in free radical-mediated postischemic renal injury and lipid peroxidation, we examined the effects of removal of endogenous iron or provision of exogenous iron…
The long-term outcome of post-ischaemic acute renal failure in the rat. I. A functional study after treatment with SOD and sucrose.
TLDR
The long-term outcome in rat kidneys subjected to 45 min of warm ischaemia with no treatment and after administration of SOD and SOD combined with 2 ml of a 12% sucrose solution was studied by the micropuncture technique and it would seem that two-thirds of the nephrons had undergone complete degeneration.
Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.
TLDR
The results suggest that lipid peroxidation and Ca-overload play causative roles in the pathogenesis of acute isChemic renal failure and that benidipine protects the ischemic kidney by inhibiting these deteriorating consequences.
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