Levels of nitric oxide synthase and cholecystokinin mRNA in the upper gastrointestinal tract of rats following experimental spinal cord injury

Abstract

In addition to the loss of motor and sensory function, SCI causes immediate changes to gastrointestinal (GI) tract physiology and reflex function. Reflex control of the stomach is dominated by vago‐vagal circuits which remain anatomically intact following SCI. Our previous reports indicate that SCI a) reduces gastric motility, tone, and emptying; b) diminishes vagal afferent sensitivity to GI peptides such as cholecystokinin (CCK); and c) diminishes mesenteric blood flow.The mechanisms, interrelationships, and temporal patterning of post‐SCI gastroparesis remain poorly defined. We tested the hypothesis that acute SCI induces GI inflammation and a resulting reduction of CCK mRNA expression.We used qRT‐PCR to quantify the levels of CCK, iNOS, and nNOS in the GI tract, 1 week post‐SCI. Our data show a significant increase in CCK and iNOS in the duodenum; nNOS shows an upward non‐significant trend. Jejunal expression of CCK is reduced while both iNOS and nNOS levels show a non‐significant upregulation. Our data are similar to experimental ischemia‐reperfusion of the GI tract, in which the superior mesenteric artery (SMA) occlusion causes a dramatic inflammatory response within the GI tract. We conclude that our model of SCI represents a continuum of GI ischemia and that the increase in inflammatory mediators may play a role in decreasing the sensitivity of the gastric vagal afferents.Grant Funding Source: NINDS 49177