Renal accumulation of ammonia: the cause of post-ischaemic functional loss and the "blue line".
The "blue line", a dark discoloration at the corticomedullary junction, is a constant finding after a significant period of renal ischaemia. In this study, it has been shown to be caused by packing of all of the peritubular capillaries at the corticomedullary junction with red blood cells. Five rats and 10 dogs were alkalinised by replacing their drinking water with 2% sodium bicarbonate for 2 weeks pre-operatively, in order to inhibit the glutaminase enzyme system and thereby decrease ammonia accumulation during ischaemia. Five rats and 6 dogs were used as unprotected controls. All animals were subjected to 60 min warm ischaemia. Renal function was significantly protected in the alkalinised rats (P less than 0.002) and dogs (P less than 0.001), with the serum creatinine rising to a maximum of 0.21 +/- 0.03 mmol/l in the alkalinised rats and 0.18 +/- 0.04 mmol/l in the alkalinised dogs. There was no "blue line" in the alkalinised animals. It is suggested that the "blue line" plays a central role in post-ischaemic renal failure. Prevention of ammonia formation by alkalinisation protects against ischaemic renal damage and the formation of the "blue line".
D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D004285:Dogs; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism; D007672:Kidney Cortex / Q000473:pathology; D007679:Kidney Medulla / Q000473:pathology; D051381:Rats; D017693:Sodium Bicarbonate
D001639:Bicarbonates; D000641:Ammonia; D017693:Sodium Bicarbonate; D003404:Creatinine