AJP - Heart and Circulatory Physiology, Vol 270, Issue 4 1272-H1278, Copyright © 1996 by American Physiological Society

ARTICLES

Influence of brain injury on vasopressin-induced pial artery vasodilation: role of superoxide anion

W. M. Armstead
Department of Anesthesia, University of Pennsylvania, Philadelphia, USA.

The present study was designed to investigate the effect of fluid percussion brain injury (FPI) on vasopressin-induced pial artery vasodilation and the role of superoxide anion generation in those observed effects. In the piglet, it was observed previously the FPI produces pial artery constriction associated with free radical generation. Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. FPI of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Vasopressin in physiological and pharmacological concentrations (10 and 1,000 microU/ml) produced vasodilation that was reversed to constriction after FPI (15 +/- 1 vs. -8 +/- 1 and 25 +/- 1 vs. 13 +/- 1% for 10 and 1,000 microU/ml before and after injury, respectively). Vasopressin-induced dilation was associated with increased cerebrospinal fluid guanosine 3', 5'-cyclic monophosphate, and these biochemical changes were blunted by FPI (407 +/- 12 and 720 +/- 28 vs. 4 and 272 +/- 5 fmol/ml for control and 10 microU/ml before and after injury, respectively). In contrast, polyethylene glycol superoxide dismutase (PEG-SOD) and catalase pretreatment 30 min before FPI partially restored vasopressin-induced pial artery dilation (14 +/- 1 vs. 3 +/- 1 and 22 +/- 1 vs. 2 +/- 4% for 10 and 1,000 microU/ml before and after FPI, respectively). Similarly, biochemical changes associated with vasopressin dilation were also partially restored by PEG-SOD and catalase after FPI. These data show that vasopressin is reversed from a dilator to a vasoconstrictor after FPI and suggests the superoxide anion generation contributes to the alteration of vasopressin cerebrovascular effects after injury and that such altered vasopressin cerebrovascular effects contribute to pial vasoconstriction after FPI.

This article has been cited by other articles:

				W. M. Armstead Vasopressin-Induced Protein Kinase C-Dependent Superoxide Generation Contributes to ATP-Sensitive Potassium Channel but Not Calcium-Sensitive Potassium Channel Function Impairment After Brain Injury Stroke, June 1, 2001; 32(6): 1408 - 1414. [Abstract] [Full Text] [PDF]

				W. M. Armstead Role of endothelin-1 in age-dependent cerebrovascular hypotensive responses after brain injury Am J Physiol Heart Circ Physiol, November 1, 1999; 277(5): H1884 - H1894. [Abstract] [Full Text] [PDF]

				A. Venteicher and W. M. Armstead Vasopressin contributes to dynorphin modulation of hypoxic cerebrovasodilation Am J Physiol Heart Circ Physiol, December 1, 1998; 275(6): H2072 - H2079. [Abstract] [Full Text] [PDF]

				W. M. Armstead ATP-dependent K+ channel activation reduces loss of opioid dilation after brain injury Am J Physiol Heart Circ Physiol, May 1, 1998; 274(5): H1674 - H1683. [Abstract] [Full Text] [PDF]

				T. Kasemsri and W. M. Armstead Endothelin impairs ATP-sensitive K+ channel function after brain injury Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2639 - H2647. [Abstract] [Full Text] [PDF]

				W. M. Armstead Brain Injury Impairs ATP-Sensitive K+ Channel Function in Piglet Cerebral Arteries Stroke, November 1, 1997; 28(11): 2273 - 2280. [Abstract] [Full Text]