Objective: Current evidence suggests that the neurotransmitter Nitric Oxide (NO) plays a crucial role in the genesis of aboral propagative of esophageal peristalses during swallowing. However, direct evidence in this regard is lacking at present. The objective of this study was to measure changes in the level of NO within the intermuscular interstices of esophagus during normal propagative as well as abnormal esophageal peristalsis in North American opossums (Didelphis virginiana).
Methods:Five adult opossums of either sex were included in the study. All had normal esophageal motility as documented by water perfused esophageal manometry. A Calibrated, carbon fiber NO selective microelectrodes (ISNOP30/ISNOP100, WPI, Inc.) was placed within the smooth muscle portion of the esophageal wall and changes in NO levels were measured as pico-amperes (pA) with Apollo-4000 NO meter (WPI, Inc.). NO dynamics in response to reflexive deglutition were assessed during normal propagative peristalsis as well as abnormal esophageal contractions induced by intravenous (IV) administration of neural nitric oxide synthase inhibitor [L-NAME], and banding the gastro-esophageal junction (GEJ) for 4-weeks.
Results:During normal propagative esophageal peristalsis a mean change of 2158.8 [±715.9] pA was recorded by the NO meter. IV administration of L-NAME and chronic banding of GEJ induced high velocity near simultaneous, achalasia like esophageal contractions. A significantly smaller change in the levels of NO was detected within esophageal wall in these situations as compared to normal propagative peristalsis (331.9 [±188.1]pA, p
Session: Podium Presentation
Program Number: S021