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Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy

Departments of ¹Anesthesiology and Critical Care Medicine, ²Neurology, and ³Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland

Submitted 27 June 2005 ; accepted in final form 1 December 2005

Neurohumoral responses have been implicated in the pathogenesis of ischemia-evoked cerebral edema. In a well-characterized animal model of ischemic stroke, the present study was undertaken to 1) study the profile of plasma arginine-vasopressin (AVP), and 2) determine whether osmotherapy with mannitol and various concentrations of hypertonic saline (HS) solutions influence plasma AVP levels. Halothane-anesthetized adult male Wistar rats were subjected to 2 h of middle cerebral artery occlusion with the intraluminal filament technique. Plasma AVP levels (means ± SD) were significantly elevated at 24 h (42 ± 21 pg/ml), 48 h (50 ± 28 pg/ml), and 72 h (110 ± 47 pg/ml), and returned to baseline at 96 h (22 ± 15 pg/ml) following middle cerebral artery occlusion compared with sham-operated controls (14 ± 7 pg/ml). Plasma AVP levels at 72 h were significantly attenuated with 7.5% HS (37 ± 8 pg/ml; 360 ± 11 osmol/l) compared with 0.9% saline (73 ± 6; 292 ± 6 osmol/l), 3% HS (66 ± 8 pg/ml; 303 ± 12 osmol/l), or mannitol (74 ± 9 pg/ml; 313 ± 14 osmol/l) treatment. HS (7.5%) significantly attenuated water content in the ipsilateral and contralateral hemispheres compared with surgical shams, 0.9% saline, 3% HS, and mannitol treatments. Peak plasma AVP levels were not associated with direct histopathological injury to the anterior hypothalamus. Attenuation of brain water content with 7.5% HS treatment coincides with attenuated serum AVP levels, and we speculate that this may represent one additional mechanism by which osmotherapy attenuates edema associated with ischemic stroke.

mannitol; hypertonic saline; ischemic stroke

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