Nitric oxide synthase inhibition reverses arteriolar
hyporesponsiveness to endothelin-1 in septic rats.
Hollenberg, Steven M., Mark J. Piotrowski, Joseph E. Parrillo.
Sections of Cardiology and Critical Care Medicine, Rush
-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612
APStracts 3:0378R, 1996.
Persistent vasodilation refractory to vasopressor agents is the
hemodynamic abnormality characteristic of septic shock. Induction of
nitric oxide synthase (NOS) by sepsis-induced cytokines has been
hypothesized to play a pathogenetic role in this refractory
vasodilation. To evaluate the mechanism of vasodilation in sepsis, we
used in vivo videomicroscopy to measure responses of resistance
arterioles (15-20 microns) to topical suffusion of the potent
vasoconstrictor, endothelin-1, in rat cremaster muscle. Rats made
septic by cecal ligation and puncture were compared to controls that
underwent sham ligation. Responses to topically suffused endothelin
were assessed in septic and control rats before and after superfusion
of the muscle with the NOS inhibitor NG-methyl-L-arginine (L-NMMA).
Received 3 June 1996; accepted in final form 17 October 1996.
APS Manuscript Number R313-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996