Selective inhibition of nitric oxide synthase causes increased muscle thickness in rat esophagus

Achalasia is a primary motor dysfunction of esophagus which can be created experimentally by nitric oxide synthase (NOS) inhibition. Although several theories have been suggested, mechanism of increased esophageal muscle thickness in achalasia is still unclear. An experimental study was performed to evaluate the esophageal muscle thickness after selective inhibition of NOS in rats.

Wistar albino rats (n=18) weighing 150-200g of both sexes were included in the study. After anesthetization with ketamine hydrochloride, esophageal body and distal esophagus were sampled in control group (CG, n=6). In sham group (SG, n=6), intraperitoneal saline (1ml) injection was performed for 21days. l-NAME (l-nitroarginin metyl ester, selective inhibitor of NOS) group (LNAMEG, n=6) received 100mg/kg/d l-NAME intraperitoneally for 21days. The esophageal body and distal esophagus were removed for histopathological analysis in each group. All samples were evaluated for total and circular muscle thickness with hemotoxylene-eosine (HE) staining.

None of the samples showed pathologic finding in esophageal mucosa. There was no difference between CG and SG for total and circular muscle thickness in esophageal body and distal esophagus. LNAMEG had higher median levels of both total and circular muscle thickness than CG and SG in esophageal body (P<0.05). However, in distal esophageal segments, only total muscle thickness was statistically higher in LNAMEG than CG and SG (P<0.05).

Selective inhibition of NOS causes increased total smooth muscle thickness in esophageal body and distal esophagus. However, this effect could not detected in circular muscle in the distal esophagus. We suggest that NOS inhbition not only increases esophageal peristalsis but also causes muscle hypertrophy in esophagus.