(Stroke. 1995;26:874-877.)
© 1995 American Heart Association, Inc.
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Presented in part at the Society of Cerebral Blood Flow and Metabolism meeting in Sendai, Japan, May 22-28, 1993.
From Neurology (G.R.) and Research Services (E.E.), Veterans Affairs Medical Center, and the Departments of Neurology and Physiology (G.R.), University of New Mexico School of Medicine, Albuquerque.
Correspondence to Gary A. Rosenberg, MD, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM 87131.
Background and Purpose Atrial natriuretic peptide (ANP) and arginine vasopressin regulate brain water and electrolytes. Treatment with ANP at the onset of a hemorrhagic injury reduces edema. Clinically, however, hemorrhagic masses form too rapidly for preventive treatment. Therefore, we measured the effect of ANP on brain edema after the hemorrhagic mass was formed.
Methods Adult rats had hemorrhagic lesions produced by the intracerebral injection of 0.4 U bacterial collagenase. Four hours later, an infusion of ANP (120 or 700 ng/kg per 20 hours) was begun into the peritoneum using an implanted miniosmotic pump. Twenty-four hours after the injury, brain water and electrolyte values were measured. The mechanism of ANP action was explored in other groups of rats that either had osmolality increased with mannitol or were injected with the cyclic GMP analogue, 8-bromo-cGMP.
Results Atrial natriuretic peptide given after a 4-hour delay significantly reduced brain water and sodium 24 hours after the injury (P<.05). However, neither mannitol nor 8-bromo-cGMP affected brain edema.
Conclusions Delayed administration of ANP reduces brain edema secondary to a hemorrhagic mass. Because it is effective after the mass has formed, ANP may be useful in treatment of edema secondary to intracranial bleeding.
Key Words: atrial natriuretic peptide brain edema intracerebral hemorrhage rats
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