Renal haemodynamics in mercuric chloride-poisoned dogs.
Intrarenal haemodynamics and glomerular dynamics have been investigated in dogs with mercuric chloride-induced acute renal failure. The early phase (12 and 24 hr after the intravenous injection of 2 mg/kg HgCl2) is characterized by some decrease in renal bloodflow, due to afferent (preglomerular) vasoconstriction, while in the later phase (48 and 72 hr after poisoning a pronounced increase in RBF due to efferent (postglomerular) vasodilatation supervenes. Urinary volumes amounts to normal in the early phase, followed by oligo-anuria in the 48 and 72 hr groups. Extraction ratio of inulin, i.e. the filtration fraction and, consequently, glomerular filtration rate show a progessive decline and trend towards zero in the 72 hr group. The pronounced decrease in glomerular capillary pressure is due to both absolute and relative increase and decrease in afferent and efferent resistances, repectively. The progressive fall in effective filtration pressure is brought about by the decrease of glomerular capillary pressure, combined with increased colloid osmotic pressure due to haemoconcentration. Total and segmental intrarenal vascular resistances are reduced by hyperosmotic mannitol infusions resulting in renal hyperaemia. Glomerular filtration rate is, however, not influenced by mannitol and effective filtration pressure remains unaltered. Osmotic diuresis ensues in the early phase but urinary output is not restored in the late, i.e. oligo-anuric, phase.
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000503:physiopathology; D000818:Animals; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000098:blood supply* / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D008630:Mercury Poisoning / Q000503:physiopathology*; D009336:Necrosis; D014554:Urination; D014655:Vascular Resistance / Q000187:drug effects
D008353:Mannitol