vasoactive-intestinal-peptide and Esophagitis

Topics: Animals; Atropine; Cats; Dogs; Esophageal and Gastric Varices; Esophageal Diseases; Esophageal Neoplasms; Esophagitis; Esophagogastric Junction; Esophagoscopy; Esophagus; Gastroesophageal Reflux; Hexamethonium Compounds; Humans; Opossums; Papio; Peristalsis; Rats; Swine; Vasoactive Intestinal Peptide

We aim to investigate the effects of different electroacupuncture (EA) frequencies at ST-36 on esophageal motility, and to compare the effect of EA on serum gastrin (GAS), motilin (MTL), and vasoactive intestinal peptide (VIP). Thirty-two cats were divided into four equal groups. All animals underwent a Heller myotomy. After esophagitis developed two frequencies (2/15 Hz or 2/100 Hz) of EA were delivered into ST-36 (LEA group [low EA], HEA group [high EA]). Animals submitted to EA on a non-point region (EANP) were used as controls (LEANP group, HEANP group), respectively. Esophageal motility was continuously monitored. The lower esophageal sphincter pressure (LESP) decreased significantly after myotomy. The LESP decreased in both LEA and LEANP cats, and in LEA cats the pressure decrease was greater. The LESP increased in the HEA group, which was higher than that in the HEANP group (P < 0.05). High-frequency EA significantly increased the peak amplitude in esophageal peristalsis. There was a decrease in serum GAS and MTL in LEA cats compared with LEANP cats (both P < 0.01). GAS and MTL were higher in the HEA group than in the HEANP group (both P < 0.01). Serum VIP decreased in the HEA group (P < 0.05), while it increased in the LEA group (P < 0.05), compared with EANP groups, respectively. EA with a high frequency at ST-36 enhances LESP as well as esophageal motility, while EA with a low frequency decreases LESP. The effect of EA is acupoint-specific, and this effect appears to be mediated through GAS, MTL and VIP.

Topics: Animals; Cats; Electroacupuncture; Esophagitis; Gastrins; Gastrointestinal Motility; Motilin; Vasoactive Intestinal Peptide

We investigated whether the signal mechanism for relaxation may be affected by inflammation of the cat esophagus. Acute esophagitis was induced by perfusion with 0.1N HCI at a rate of 1 mL/min for 45 min over three consecutive days. We then isolated esophageal smooth muscle cells by enzymatic digestion with collagenase. We pre-contracted the isolated smooth cells with acetylcholine (ACh) (10(-5) M) and compared the agonist-induced relaxation of pre-con tracted normal cells with those of esophagitic cells. Vasoactive intestinal polypeptide (VIP) caused a dose-dependent relaxation in normal cells, and this curve was down shifted in esophagitic cells. Sodium nitroprusside (SNP) or SIN-1 (NO donor) produced dose-dependent relaxation in normal cells, which was not affected by esophagitis. 8-Br-cGMP (a cGMP ana log) also induced dose-dependent relaxation to a similar extent in both normal and esoph agitic cells. Forskolin (a cAMP activator) or db-cAMP (a cAMP analog) produced dose-dependent relaxation in normal cells, and this relaxation curve was down shifted in esoph agitic cells. Western blotting was used to determine what subtype of adenylyl cyclase was involved in the cAMP pathway. Western blot analysis of homogenates derived from esophageal smooth muscle using antibodies against adenylyl cyclase types II, III, IV and V/VI revealed the presence of type V and/or type VI only. This result suggests that relaxation via a cAMP-dependent pathway rather than a cGMP dependent-pathway is down regulated in cat acute esophagitis. This subsensitivity of the cAMP related pathway may be related to the activ ity of adenylyl cyclase V/VI.

Topics: Adenylyl Cyclases; Animals; Blotting, Western; Bucladesine; Cats; Cell Membrane Permeability; Colforsin; Cyclic AMP; Cyclic GMP; Dose-Response Relationship, Drug; Down-Regulation; Esophagitis; In Vitro Techniques; Isoenzymes; Molsidomine; Muscle Relaxation; Muscle, Smooth; Nitric Oxide Donors; Nitroprusside; Signal Transduction; Vasoactive Intestinal Peptide