MECHANISM OF ERYTHROCYTE TRAPPING IN ISCHEMIC ACUTE-RENAL-FAILURE

Forty-five minutes of warm ischaemia and 20 min of recirculation in the rat kidney was found to result in (1) a massive transient extravasation of plasma upon recirculation and (2) an increase in plasma-lymph transport of proteins during the first hours after onset of circulation. This was accompanied by trapping of erythrocytes, as determined with 51Cr-labelled erythrocytes, in the capillaries, mainly in the inner stripe of the outer medulla. At scanning electron microscopy of vibratome sections, the trapping appeared as aggregates of polygonally shaped erythrocytes. It is concluded that 45 min of ischaemia and 20 min of recirculation results in an increase in the permeability of the renal capillaries. This increase leads to extravasation of capillary plasma with consequent local haemoconcentration, causing an increase in vascular resistance and in capillary hydrostatic pressure. This elevated pressure will, in turn, lead to perpetuating extravasation of plasma, further haemoconcentration and so on, eventually resulting in dense packing of polygonal erythrocytes, obstructing the blood flow. 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.