Faculty Collaboration Database

Possible cellular mechanism for cerebral vasospasm after experimental subarachnoid hemorrhage in the dog. J Clin Invest 1987 Sep;80(3):875-80

Date

09/01/1987

Pubmed ID

2957393

Pubmed Central ID

PMC442315

DOI

10.1172/JCI113146

Scopus ID

2-s2.0-0023473459 (requires institutional sign-in at Scopus site)   109 Citations

Abstract

This study was undertaken to examine some of the cellular ionic mechanisms responsible for the cerebral vasospasm that occurs as a consequence of subarachnoid hemorrhage (SAH). After cisternal injection of autologous blood we documented spasm of the basilar artery upon angiography from 4 to 7 d postictus in six dogs. When these basilar arteries were isolated we observed marked membrane depolarization and enhanced electrical spike activity compared with controls. The slope of the membrane potential vs log [K]0 curve was significantly reduced in arteries exposed to SAH. Further analysis supported the concept that such altered muscle cell properties resulted from reduction in resting K+ conductance (gk). Exposure of arteries in vitro to nicorandil (10(-9)-10(-7)M) (a drug which acts by increasing gk) hyperpolarized the muscle cells and increased internal diameter. Infusion of nicorandil (3-5 micrograms/kg per min) to intact, anesthetized animals reversed, by 50%, the reduction in basilar artery diameter after experimental SAH.

Author List

Harder DR, Dernbach P, Waters A

MESH terms used to index this publication - Major topics in bold

Action Potentials
Animals
Biomechanical Phenomena
Cerebral Angiography
Dogs
Homeostasis
Ischemic Attack, Transient
Membrane Potentials
Niacinamide
Nicorandil
Osmolar Concentration
Potassium
Subarachnoid Hemorrhage