Fibrosis of gastric cardia after endoscopic sclerosis. Mechanism for control of experimental reflux?
Endoscopic sclerosis of the gastric cardia (ESGC) prevents experimental gastroesophageal reflux (GER) without changes in lower esophageal sphincter (LES) pressure and length. This study was performed to define the histologic appearance of the esophagus and stomach one year after ESGC. Four dogs were studied one year after ESGC with morrhuate sodium; ESGC had been performed at six sites, 1-3 cm distal to the esophagogastric junction. All animals had stable weight and eating habits at sacrifice. Light microscopy of the cardia and LES included morphometry of wall thickness (mm) and assessment of fibrosis (- to ). The esophagus had minimal changes; the gastric cardia had focal fibrosis, maximal on the greater curve, without any change difference in wall thickness. ESGC results in fibrosis of the gastric cardia, without significant changes in the esophagus. These changes prevent GER, possibly by preventing the initiation of a reflux event.
Carvalho
P J
PJ
Department of Surgery, University of Illinois, Cook County Hospital, Chicago 60612.
Donahue
P E
PE
Miidla
I
I
Davis
P E
PE
Shen
Y J
YJ
Bombeck
C T
CT
Nyhus
L M
LM
D000818:Animals; D002299:Cardia / Q000473:pathology*; D004285:Dogs; D004943:Esophagogastric Junction / Q000503:physiopathology; D004947:Esophagus / Q000473:pathology*; D005355:Fibrosis / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000473:pathology / Q000517:prevention & control*; D005773:Gastroscopy; D011312:Pressure; D012598:Sclerosis / Q000473:pathology; D015911:Sclerotherapy / Q000379:methods