Effects of anti-hypertensive drugs on esophageal body contraction

AIM:To clarify the effects of anti-hypertensive drugs on esophageal contraction and determine their possi-ble relationship with gastro-esophageal reflux disease.METHODS:Thirteen healthy male volunteers were enrolled. Esophageal body peristaltic contractions and lower esophageal sphincter (LES) pressure were measured using high resolution manometry. All subjects were randomly examined on four separate occasions following administrations of nifedipine,losartan,and atenolol,as well as without any drug administration.RESULTS:Peristaltic contractions by the esophageal body were separated into three segments by two troughs. The peak peristaltic pressures in the mid and lower segments of the esophageal body under atenolol administration were signifi cantly higher than those without medication in a supine position. On the other hand,peristaltic pressures under nifedipine administration were lower than those observed without drug ad-ministration. Losartan did not change esophageal body peristalsis. Atenolol elevated LES pressure and slowed peristaltic wave transition,while the effects of nifedip-ine were the opposite. CONCLUSION:Among the anti-hypertensive drugs tested,atenolol enhanced esophageal motor activity,which was in contrast to nifedipine.

Extracellular matrix gene expression in human trabecular meshwork cells following mechanical fluid flow stimulation

AIM: To investigate changes in extracellular matrix(ECM) gene expression in human trabecular meshwork(HTM) cells in response to mechanical fluid flow stimulation.METHODS: HTM cells were grown on a glass plate coated with 0.02% type Ⅰ collagen(COL) and exposed to shear stress(0, 0.2, 1.0 dyne/cm;) for 12 h.Changes in genes related to the ECM were evaluated by real-time reverse transcriptase-polymerase chain reaction.Phosphorylation of Smad2 protein was investigated by Western blotting.RESULTS: After mechanical stimulation, COL type 4 alpha 2, COL type 6 alpha 1, and fibronectin-1 mRNA were significantly higher than the static control(P<0.05, <0.05, and <0.01, respectively).The metalloproteinase-2 and plasminogen activator inhibitor-1 mRNA were significantly higher than the static control(P<0.05 and <0.01, respectively), while the differences in the tissue inhibitors of metalloproteinases-2 mRNA were not significant.The phosphorylation of Smad2 levels was significantly higher compared to the static control cells.CONCLUSION: Changes in the expressions of genes associated ECM metabolism result in HTM cells after mechanical stimulation.The mechanical stimulation of the aqueous humor to the trabecular meshwork may promote ECM turnover and contribute to intraocular pressure homeostasis.

Techniques for Avoiding Saccular Extended Obstruction at the Anastomotic Site of Functional End-to-End Anastomosis

Saccular extended obstruction is generated when the anastomotic site of functional end-to-end anastomosis is extended saccularly and blocked by intestinal contents. This is a specific complication of functional end-to-end anastomosis. Saccular extended obstruction of the anastomotic site of func-tional end-to-end anastomosis causes postoperative intestinal obstruction. Saccular extended obstruction places a heavy burden on patients because surgery is necessary for treatment of intestinal obstruction due to saccular extended obstruction. However, saccular extended obstruction is not a commonly recognized complication. The greatest factor contributing to the development of saccular extended obstruction is an acute angle between the portions of the intestinal tract oral and aboral to the anastomotic site. When this angle approaches obtuse angle, preferably close to a straight line, stagnation of the intestinal contents does not occur at the anastomotic site of functional end-to-end anastomosis and saccular extended obstruction is avoided. For making the angle of anastomotic intestinal tracts obtuse or straight, it may be effective that the entry hole of stapling suture instrument creating the anastomotic stoma is closed perpendicular to the intestinal axis.