Gastric distension and gastroparesis following pulmonary vein isolation for atrial fibrillation: a case report and review of the literature.

We present a case of marked gastric distension and gastroparesis in a patient with atrial fibrillation who underwent a pulmonary vein isolation, a procedure commonly performed in patients suffering from atrial fibrillation in order to regain sinus rhythm. Two days following the procedure, the patient presented with marked abdominal distension, and computed tomography imaging was consistent with gastroparesis and/or delayed gastric emptying. A tentative diagnosis of pylorospasm was made. After a first attempt with a conservative approach, gastroscopy with both pyloric dilatation and intra-pyloric botox injection was performed due to persisting discomfort. The symptoms gradually resolved following this intervention. Gastroparesis and gastrointestinal distension is a rare complication following pulmonary vein isolation, and is mainly thought to result from temporary damaging the vagal nerve. Since a rising number of patients undergo an ablation of the pulmonary veins as treatment for atrial fibrillation, gastroenterologists should become aware of this probably not so rare complication.

The missing link.

We present a case of a 28-year old woman who presented with bizarre wheezing breath sounds on expiration and dysphagia, with unexplained significant dilation of the esophagus mimicking achalasia finally leading to the diagnosis of a very small congenital tracheoesophageal fistula (TEF). Congenital TEF is usually detected shortly after birth and is typically accompanied by esophageal atresia. Congenital TEF without esophageal atresia (H-type fistula) can be missed in early life and diagnosis may be postponed until adulthood due to subtle symptoms. Diagnosis is usually based upon a combination of esophagoscopy, bronchoscopy, barium esophagography and CT-scan. The only clue can be the finding of a significant dilated aperistaltic esophagus, with subsequent more detailed CT reconstruction revealing a very tiny H-type TEF. It is important to raise the awareness of small H-type TEF as a possible cause of achalasia-like esophageal dilation in adulthood and of very unusual and bizarre wheezing breath sounds.

Effect of chemical sympathectomy on scintigraphic gastric and small bowel transit in the rat.

Our aims were to measure gastric and small bowel transit of radiolabeled chow or liquids in rats and to assess the effect of pharmacologically induced chronic sympathectomy of at least 5 weeks duration. Three series of experiments were performed. In series I, four rats in each group underwent i.p. chloral hydrate anesthesia, tracheostomy with intubation and mechanical ventilation: they received by gavage 1.0 g rat chow dissolved in 1.5 ml saline labeled with 1.0 mCi 99mTc-DTPA In series II, four rats in each group were anesthetized with only i.p. chloral hydrate and received 1.5 ml labeled saline. Rats were placed on a gamma camera for dynamic acquisition of 1-min images for 7 h in series I, and 4 h in series II. Activity was quantitated in stomach and cecum; gastric emptying was analyzed by the power exponential model. In series III, four rats in each group were studied for 1 h on gamma camera and sacrificed after 5 h. At the end of each study, the stomach, small bowel, cecum and colon were removed and radioactivity counted in each organ in a dose calibrator. Quantitation of radioactivity by gamma camera was highly accurate: labeled chow in the stomach at 7 h was identical by external camera and counting of the excised organ (linear regression slope = 1.01, r = 0.97, P less than 0.0001). Similar precision was observed with labeled liquids (slope = 0.93, r = 0.93, P = 0.001). Chow emptied slower than liquid in both groups (P = 0.048). Ileocecal movement of isotope occurred by bolus transfers.(ABSTRACT TRUNCATED AT 250 WORDS)

Bioassay of nitric oxide released upon stimulation of non-adrenergic non-cholinergic nerves in the canine ileocolonic junction.

1. The release and the nature of the inhibitory non-adrenergic non-cholinergic (NANC) neurotransmitter was studied in the canine ileocolonic junction. A circular muscle strip of the canine ileocolonic junction served as donor tissue in a superfusion bioassay in which rings of rabbit aorta with the endothelium removed served as detector tissue. 2. The ileocolonic junction released a labile factor with vasodilator activity upon stimulation of non-adrenergic non-cholinergic (NANC) nerves in response to electrical impulses and the nicotinic receptor agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP). This release was respectively frequency- and concentration-dependent. 3. The release was reduced by the blocker of neuronal conductance, tetrodotoxin, and by the inhibitor of the nitric oxide (NO) biosynthesis NG-nitro-L-arginine. The biological activity was enhanced by superoxide dismutase and eliminated by haemoglobin. Hexamethonium abolished only the release in response to DMPP. 4. Injection of adenosine 5'-triphosphate (ATP) or vasoactive intestinal polypeptide (VIP) onto the cascade induced relaxations of the rabbit aorta but they were different from those induced by NO or the transferable factor. 5. Based on organ bath experiments in which the reactivity of different parts of the circular smooth muscle layer of the ileocolonic junction was investigated, a muscle strip of superficial circular muscle with submucosa was chosen as the detector strip in the bioassay cascade. 6. The ileocolonic junction dose-dependently relaxed in response to nitroglycerin and NO. NO was much more potent in the rabbit aorta than in the canine ileocolonic junction. 7. In conclusion, our results demonstrate the release of a transferable vasorelaxant factor in response to NANC nerve stimulation which behaves pharmacologically like NO but not like ATP or VIP. Therefore, we suggest that NO or a NO releasing substance is the inhibitory NANC neurotransmitter in the canine ileocolonic junction.

GABAA receptor-mediated stimulation of non-adrenergic non-cholinergic neurones in the dog ileocolonic junction.

1. The inhibitory effects of gamma-aminobutyric acid (GABA), the GABAA receptor agonist homotaurine and the GABAB receptor agonist (+/-)-baclofen were investigated on circular muscle strips of the dog terminal ileum and ileocolonic junction. 2. In the presence of atropine, GABA and homotaurine induced concentration-dependent relaxations, similar to the non-adrenergic non-cholinergic (NANC)-mediated relaxations evoked by electrical stimulation or by acetylcholine. The ileocolonic junction was more sensitive to GABA and homotaurine than the ileum. (+/-)-Baclofen had no effect. Cross desensitization only occurred between GABA and homotaurine. 3. The GABAA receptor antagonist bicuculline shifted the concentration-response curves to GABA and homotaurine to the right. The maximal relaxation to GABA remained unaffected. 4. GABA-induced relaxations were not inhibited by timolol, guanethidine, domperidone, hexamethonium and desensitization to ATP, but were abolished by tetrodotoxin. 5. Bicuculline, and pretreatment with GABA or (+/-)-baclofen had no effect on the NANC-evoked relaxations to electrical stimulation and acetylcholine. 6. In conclusion, GABA stimulates GABAA receptors located on inhibitory NANC neurones in the dog ileocolonic junction. Our results suggest that it is unlikely that GABA is the final inhibitory NANC neurotransmitter.