Role of No in the Regulation of Systemic and Renal Hemodynamics Following Hemorrhagic Shock in the Rate
Abstract
The systemic and renal hemodynamic responses to NO inhibit ion with L-NAME were compared in both normotensive, normovolemic rats and in rats following acute hemorrhagic hypotension. Mean arterial blood pressure (MAP) increased in normovolemic as well as in hemorrhaged, hypotensive rats. Systemic vascular resistance (SVR) also increased in both groups but the increase was greater in normotensive rats (104 +/- 11%) than hypotensive rats (64 +/- 14%). Renal vascular resistance (RVR) also increased more in normotensive rats (189 +/- 20%) than hypotensive rats (102 +/- 19%) (p < 0.05). GFR was markedly reduced by L-NAME in normovolemic rats (from 3.0 +/- 0.1 to 2.1 +/- 0.1 ml/min/300g) > In striking contrats GFR but increased in hemorrhaged rats following L-NAME (from 1.8 +/- 0.2 to 2.5 +/- 0.2 ml/min/300g. In summary, the L-NAME-induced increase in vascular resistance is markedly reduced following hemorrhage suggesting that NO production or availability is reduced. However, NO production continues in the hemorrhaged rat and contributes substantially to the hypotension and functional renal insufficiency associated with acute severe volume depletion.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 30, 1994
- Accession Number
- ADA360367
Entities
People
- Anthony Thompson
- C. R. Valeri
- W. Lieberthal
Organizations
- Boston University