Early stimulation of vasopressin release maintains circulating blood volume in alcohol intoxicated rodents
Abstract
Acute alcohol intoxication (AAI) decreases mean arterial blood pressure (MABP), results in greater hypotension during hemorrhagic shock (HS), and impairs MABP recovery during fluid resuscitation from HS. The underlying mechanisms have been identified to include attenuation of neuroendocrine activation without alteration of pressor response. Whether AAI decreases blood volume, lowering tolerance to blood loss was not known. Chronically‐catheterized, adult male Sprague‐Dawley rats (250–300g) received a primed‐constant (2.5g/kg + 0.3g/kg/h) 15h intragastric infusion of alcohol or isocaloric/isovolumic dextrose (DEX). AAI resulted in an early and transient significant increase in urine output, decreased urine osmolality, and increased plasma osmolality. This was associated with a significant increase (43%; p<0.05) in circulating arginine vasopressin (AVP) 1h into the infusion. Blood volume and hematocrit were not different between the AAI and DEX groups at completion of the 15h infusion. These results suggest that AAI stimulates diuresis leading to increased plasma osmolality, which in turn stimulates AVP release decreasing urine output and restoring plasma osmolality. We conclude that decreased blood volume does not contribute to the impaired hemodynamic stability observed in AAI+HS. Supported by DOD PR‐054196 and NIAAA‐AA7577.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2010
- Source ID
- 10.1096/fasebj.24.1_supplement.794.10
Entities
People
- Annie M. Whitaker
- Patricia E. Molina
Organizations
- LSU Health Sciences Center New Orleans
- National Institute on Alcohol Abuse and Alcoholism
- United States Department of Defense