Systemic hemodynamics in nephrotoxic acute renal failure.
Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated (microsphere method) in awake rats, 3, 6, and 24 h after induction of acute renal failure by mercuric chloride (HgCl2; 4.7 mg/kg body weight). 3 h after injection of HgCl2, CO and RBF decreased to 77 and 72% of respective control values of 32.0 +/- 2.4 and 4.65 +/- 0.44 ml/min/100 g. Renal vascular resistance (RVR) and total peripheral resistance (TPR) were significantly increased compared to control at this time. Similar results were observed 6 h after administration of HgCl2. Volume expansion with plasma (2% of body weight) restored CO, RBF, TPR, and RVR to normal 3 h after injection of HgCl2. Despite significantly elevated blood urea nitrogen 24h after injection of HgCl2 (103.7 mg%), all hemodynamic parameters were within control range. Plasma volume was normal 3 h after HgCl2 but was significantly elevated compared to control 24 h after HgCl2 (4.73 vs. 3.92 ml/100 g, p less than 0.01). These findings indicate that factors other than preferential renal vasoconstriction may be involved in the transient renal ischemia of HgCl2-induced acute renal failure.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000503:physiopathology*; D000818:Animals; D002302:Cardiac Output; D002712:Chlorides / Q000009:adverse effects; D006439:Hemodynamics; D007668:Kidney / Q000098:blood supply; D008297:Male; D008628:Mercury / Q000009:adverse effects; D010953:Plasma Volume; D051381:Rats; D012039:Regional Blood Flow; D014655:Vascular Resistance
D002712:Chlorides; D008628:Mercury