Brain Water Accumulation after the Central Administration of Vasopressin

Abstract

The intraventricular administration of vasopressin or DDAVP (desmopressin acetate) increased the brain water content from 78.2% to 79.2-79.5%. This was achieved without an accompanying water load. The applied water load alone did not increase the water content of the brain. There was no significant difference in the water content of the brain between animals treated with intraventricular vasopressin and intravenous water load and animals receiving only intraventricular vasopressin. The water content of the olfactory bulbs of the control animals was 3.8% higher than that of the hemispheres. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% subsequent to the intraventricular administration of DDAVP. Measurement of the brain electrolyte content was not conclusive as to the mechanism of water permeability changes. The possible mechanism is discussed. Although no tissue or cerebrospinal fluid concentrations of vasopressin enabling comparison with clinical pathological conditions have been measured, it is suggested that increased secretion of vasopressin into the cerebrospinal fluid in conditions such as subarachnoid hemorrhage or intracranial hypertension of various origins might play a role in edema formation.

Bumetanide Inhibition of the Blood-Brain Barrier Na-K-Cl Cotransporter Reduces Edema Formation in the Rat Middle Cerebral Artery Occlusion Model of Stroke

“…There is good evidence, however, that hypoxia and the peptides vasopressin and endothelin, all factors present during ischemia, stimulate activity of the BBB cotransporter. We have found that vasopressin, which is centrally released during ischemia (Dóczi 1993;Landgraf 1992;Ostrowski et al, 1992;Sorensen et al, 1985) and promotes edema formation (Dickinson and Betz, 1992;Dóczi, 1993;Dóczi et al, 1982Dóczi et al, , 1984Hertz et al, 2000;Rosenberg et al, 1990), is also a potent stimulator of the brain microvascular Na-K-Cl cotransporter (O'Donnell et al, 1995a), as is endothelin, which is also released during ischemia (Barone et al, 1994;Kawai et al, 1996bKawai et al, , 1997Spatz et al, 1997). We have shown that vasopressin stimulates the brain endothelial cotransporter by a V1 vasopressin receptor in a manner involving elevation of intracellular [Ca 2+ ] (O'Donnell et al, 1999).…”

The physiological and pathophysiological functions of renal and extrarenal vasopressin V2 receptors

“…While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% (32).…”

“…In another study (32), intraventricular administration of desmopressin in rats increased the brain water content from 78.2% to 79.2-79.5%. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% (32).…”

Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

“…10 The hormone arginine vasopressin (AVP) was identified as a potential mediator of astrocytic cell swelling and subsequent fulminating edematous changes following cerebral injury. [11][12][13][14][15][16][17] It is thought that centrally-released AVP orchestrates the development of brain edema by inducing water and ionic movement. 18,19 Increased AVP levels activate the V1a receptor (V1aR), facilitate water transport across astrocytic cell membranes, and are associated with brain edema formation.…”