Abstract
Centrally released arginine vasopressin (AVP) has been reported to increase the water permeability of brain capillaries under normal and pathological conditions. In present experiment, we divided cold-injured brain into cortical and deep structure, and studied the effect of central administration of V1 receptor antagonist (5 ng, 50 ng, and 500 ng per rat) on vasogenic brain edema. Cold injury induced significant increases in brain water and tissue sodium content of bilateral cortical structures, but no changes in bilateral deep structures. Intraventricular administration of Vi receptor antagonist (50 ng) significantly reduced this accumulation of water and sodium in cortical structures without any change in plasma osmolality. A large quantity of this antagonist (500 ng) showed no changes in brain water content of bilateral cortical structures. It is suggested that this antagonist has an optimal concentration of this antagonist for inhibiting vasogenic brain edema.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
