Biomaterial Database

[The effect of arginine vasopressin receptor antagonist on the rat cold-injured brain]. 1993

M Kagawa, and S Nagao

Department of Neurological Surgery, Kagawa Medical School.

Centrally released arginine vasopressin (AVP) has been reported to increase the water permeability of brain capillaries under both normal and pathological conditions. It is not known, however, whether AVP regulates the permeability of brain capillaries via a V1 receptor or a V2 receptor. In the present experiments, we attempted to suppress cold-induced brain edema with V1 or V2 receptor antagonists. Adult rats were intraventricularly administered with 5 ng, 50 ng, or 500 ng of V1 receptor antagonist, or 50 ng or 500 ng of V2 receptor antagonist. Ten minutes after administration, a cold injury was induced in the left hemisphere of the brain by applying a freezing probe, which had been cooled by liquid nitrogen, to the left parietal skull for 20 seconds. Brain water and tissue sodium content were then measured 24 hours after the cold-injury. In experiment 1, the brain water content had significantly increased in both the injured and non-injured hemispheres. The administration of 50 ng of V1 receptor antagonist resulted in a significant reduction in the brain water content of the bilateral hemispheres. Administration of 50 ng of V2 receptor antagonist produced a significant reduction in the brain water content of the non-injured hemisphere only. A 500 ng administration of both antagonists did not change the brain water content of the bilateral hemispheres. In experiment 2, we divided the cold injured brain into cortical and deep structures and observed the effect of the V1 receptor antagonist. Cold-injury induced significant increases in brain water and the tissue sodium content of the bilateral cortical structures, but no changes in bilateral deep structures.(ABSTRACT TRUNCATED AT 250 WORDS)

UI	MeSH Term	Description	Entries
D008297	Male		Males
D001929	Brain Edema	Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)	Brain Swelling,Cerebral Edema,Cytotoxic Brain Edema,Intracranial Edema,Vasogenic Cerebral Edema,Cerebral Edema, Cytotoxic,Cerebral Edema, Vasogenic,Cytotoxic Cerebral Edema,Vasogenic Brain Edema,Brain Edema, Cytotoxic,Brain Edema, Vasogenic,Brain Swellings,Cerebral Edemas, Vasogenic,Edema, Brain,Edema, Cerebral,Edema, Cytotoxic Brain,Edema, Cytotoxic Cerebral,Edema, Intracranial,Edema, Vasogenic Brain,Edema, Vasogenic Cerebral,Swelling, Brain
D001930	Brain Injuries	Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.	Brain Lacerations,Acute Brain Injuries,Brain Injuries, Acute,Brain Injuries, Focal,Focal Brain Injuries,Injuries, Acute Brain,Injuries, Brain,Acute Brain Injury,Brain Injury,Brain Injury, Acute,Brain Injury, Focal,Brain Laceration,Focal Brain Injury,Injuries, Focal Brain,Injury, Acute Brain,Injury, Brain,Injury, Focal Brain,Laceration, Brain,Lacerations, Brain
D003080	Cold Temperature	An absence of warmth or heat or a temperature notably below an accustomed norm.	Cold,Cold Temperatures,Temperature, Cold,Temperatures, Cold
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D001127	Arginine Vasopressin	The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.	Argipressin,Vasopressin, Arginine,Arg-Vasopressin,Argipressin Tannate,Arg Vasopressin
D017207	Rats, Sprague-Dawley	A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.	Holtzman Rat,Rats, Holtzman,Sprague-Dawley Rat,Rats, Sprague Dawley,Holtzman Rats,Rat, Holtzman,Rat, Sprague-Dawley,Sprague Dawley Rat,Sprague Dawley Rats,Sprague-Dawley Rats
D051381	Rats	The common name for the genus Rattus.	Rattus,Rats, Laboratory,Rats, Norway,Rattus norvegicus,Laboratory Rat,Laboratory Rats,Norway Rat,Norway Rats,Rat,Rat, Laboratory,Rat, Norway,norvegicus, Rattus
D065092	Antidiuretic Hormone Receptor Antagonists	Endogenous compounds and drugs that inhibit or block the activity of ANTIDUIRETIC HORMONE RECEPTORS.	Antidiuretic Hormone Antagonist,Antidiuretic Hormone Receptor Antagonist,Vasopressin Antagonist,Vasopressin Receptor Antagonist,Antidiuretic Hormone Antagonists,Vasopressin Antagonists,Vasopressin Receptor Antagonists,Antagonist, Antidiuretic Hormone,Antagonist, Vasopressin,Antagonist, Vasopressin Receptor,Antagonists, Antidiuretic Hormone,Antagonists, Vasopressin,Antagonists, Vasopressin Receptor,Hormone Antagonist, Antidiuretic,Hormone Antagonists, Antidiuretic,Receptor Antagonist, Vasopressin,Receptor Antagonists, Vasopressin