Involvement of Vasopressin in Brain Edema Formation: Further Evidence Obtained from the Brattleboro Diabetes Insipidus Rat with Experimental Subarachnoid Hemorrhage

Abstract

Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

“…Our results are well in agreement with other experimental studies showing that AVP is involved in the pathophysiology of acute brain damage, for example, after subarachnoid or intracerebral hemorrhage (Doczi et al, 1984;Rosenberg et al, 1992), cortical focal lesions (Reeder et al, 1986;Bemana and Nagao, 1999), traumatic brain injury (Armstead, 2001), global cerebral ischemia (Liu et al, 1991(Liu et al, , 1996Ikeda et al, 1997), and permanent focal cerebral ischemia (Dickinson and Betz, 1992;Shuaib et al, 2002). The amount of AVP mRNA and of AVP protein increase after experimental cerebral ischemia (Liu, 1992;Liu et al, 2000) and levels of AVP are elevated in the CSF of stroke patients (Barreca et al, 2001).…”

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).…”

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.…”