Effects of singlet oxygen scavengers on laser/dye impaired
endothelium dependent responses of brain arterioles.
Rosenblum, William I., Guy H. Nelson.
Department of Pathology (Neuropathology), Virginia Commonwealth
University - Medical College of Virginia
APStracts 2:0394H, 1995.
This study investigates the possible role of singlet oxygen in
accounting for the inhibitory effect of laser/dye injury on
endothelium dependent dilations. The combination of Helium Neon
(HeNe) laser (20 second exposure) and intravascular Evans blue
impairs endothelium dependent dilation of mouse pial arterioles by
acetylcholine (ACh), bradykinin (BK) and calcium ionophore A-23187.
These each have a different endothelium derived mediator (EDRFACh,
EDRFBK , EDRFionophore). In this study diameters at a craniotomy site
were monitored in vivo with an image splitter - television
microscope. The laser/dye injury as usual abolished the responses 10
and 30 minutes after injury, with recovery, complete or partial at 60
minutes. Dilations by sodium nitroprusside, an endothelium
independent dilator, were not affected by laser/dye. When the singlet
oxygen scavengers l-histidine (10-3M) and l-tryptophan (10-2) were
added to the suffusate over the site the responses to ACh at 10 and
30 minutes were relatively intact, the response to BK was partly
protected at 10 minutes only, and the response to ionophore was still
totally impaired at 10 and 30 minutes. Lysine, a non-scavenging amino
acid, had no protective effects with any dilator. We postulate that a
heat induced injury initiates a chain of events resulting in
prolonged singlet oxygen generation by the endothelial cell (not by
the dye). We postulate further, that destruction of EDRFACh by
singlet oxygen is responsible for laser/dye inhibition of ACh and
that generation of the radical must continue for at least 30 minutes.
On the other hand, the heat injury itself is probably responsible for
the elimination of the response to ionophore. Heat plus singlet
oxygen generated by heat damaged tissue may initially impair the
response to BK but by 30 minutes only the effects of some other
factor, presumably heat injury, account for the impaired response to
BK.
Received 13 July 1995; accepted in final form 28 August 1995.
APS Manuscript Number H649-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.