Haemodynamic consequences of experimental papillary necrosis in the rat.
Experimental renal papillary necrosis induced by 2-bromoethylamine hydrobromide (BEA) results in hypertension in the rat. The haemodynamics of this increase in blood pressure were investigated with radiolabelled microspheres, thus enabling individual organ blood flows to be evaluated. Total peripheral resistance was raised in BEA-treated rats (3.6 +/- 0.3 mmHg ml-1 min X 100 g) compared with control rats (2.87 +/- SEM 0.2, P less than 0.05) whilst cardiac index remained similar (39.9 +/- 3.6 vs 39.2 +/- 3.1 ml min-1 100 g-1). Heart and brain from BEA rats demonstrated a significant rise in vascular resistance with a normal blood flow. In the kidneys vascular resistance increased still further and here there was a reduction in renal blood flow despite an increase in kidney size. These findings are compatible with a loss of renomedullary vasodepressor mechanisms acting directly or indirectly on the resistance vessels.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004195:Disease Models, Animal; D005021:Ethylamines; D005260:Female; D006439:Hemodynamics; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology*; D007681:Kidney Papillary Necrosis / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow; D014655:Vascular Resistance
D005021:Ethylamines; C004504:2-bromoethylamine