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J Thorac Cardiovasc Surg 1995;110:157-164
© 1995 Mosby, Inc.
GENERAL THORACIC SURGERY |
Boston Mass. Durham N.C.
This work was supported by National Institutes of Health grant DK 34854 (Harvard Digestive Disease Center). J.S. is a Pew scholar in the Biomedical Sciences and the recipient of a Clinical Investigator Development award from the National Institutes of Health (HL02582).
Received for publication May 26, 1994. Accepted for publication Nov. 1, 1994. Address for reprints: David J. Sugarbaker, MD, Division of Thoracic Surgery, Brigham & Women's Hospital, 75 Francis St., Boston, MA 02115.
Abstract
The role of nitric oxide in human esophageal smooth muscle was examined. Immunostaining for constitutive nitric oxide synthase labeled nerve fibers and bundles within longitudinal and circular smooth muscle layers of resected tissue samples. Strips of circular muscle mounted in organ baths exhibited spontaneous contractions and active tone. When exposed to 5-second trains of electric field stimulation at 20 Hz, most strips exhibited intrastimulus "on" and poststimulus "off" contractions. Exposure to a 0.1µmol/L (or greater) concentration of atropine converted "on" contractions to "on" relaxations and reduced "off" contractions by 63%. Exposure to NG-nitro-L-arginine resulted in concentration-dependent enhancement of "on" contractions and abolition of "off" contractions. Excess L-arginine enhanced the reversal of these effects. Sodium nitroprusside inhibited both spontaneous and evoked contractions. These results suggest that nitric oxide synthesis is a mediator of neural inhibition of human esophageal circular smooth muscle and is necessary for the occurrence of "off" contractions. (J THORACCARDIOVASCSURG1995;110:157-64)
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