Decreased blood volume does not contribute to impaired hemodynamic counterregulation to hemorrhagic shock in acute alcohol intoxicated rodents
Abstract
Acute alcohol intoxication (AAI) accentuates hypotension (HT) and impairs blood pressure recovery during fluid resuscitation following hemorrhage (HEM). We hypothesized that AAI may decrease blood volume (BV) and thus contribute to the greater HT in response to a given blood loss. The aim of this study was to determine whether AAI decreases BV. Chronically‐catheterized, adult male Sprague‐Dawley rats (250‐300g) received a primed‐constant (2.5g/kg + 300mg/kg/h) 15h intragastric infusion of alcohol, dextrose (DEX), or no infusion (NI). AAI resulted in a marked increase in urine output 1 hr and 2h into the infusion as compared to DEX‐infused and NI controls, (72% and 84% respectively; p<0.050) and a significant decrease in urine osmolarity (OSM) (58%, p<0.050). At the completion of the 15h infusion, there were no differences in urine output or OSM among the groups. AAI produced a significant (4%; p<0.05) increase in plasma OSM 2h into the infusion, which normalized at 15h of alcohol infusion. BV (10%) was not significantly different between groups. These results show that AAI produces early stimulation of urine output associated with increased plasma OSM. We hypothesize that this results in increased vasopressin release which increases water reabsorption, preserving BV. These findings suggest that the greater HT following HEM is not the result of decreased BV. Supported by DOD PR‐054196 and NIAAA‐AA7577.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2009
- Source ID
- 10.1096/fasebj.23.1_supplement.lb87
Entities
People
- Annie Mcgraw Whitaker
- Patricia E. Molina
Organizations
- LSU Health Sciences Center New Orleans
- United States Department of Defense