Microwave Ablation: A Potential Minimally Invasive Solution for Gastric Motility Disorders

Many gastric motility disorders, including gastroparesis, are caused by dysrhythmias occurring in the stomach musculature. Microwave ablation (MWA) offers potential as a minimally invasive endoscopic approach for targeted thermal destruction of the gastric musculature to disrupt irregular electrical rhythm within the stomach wall. An experimental study was conducted in a gel phantom to analyze the transient heating profile of a water-cooled 2.45 GHz MWA antenna enclosed within a PET balloon. Fiber-optic temperature sensors were used to collect temperature data at distances 1.5–7.5 mm from the balloon surface. Ablation profiles were also characterized in ex vivo porcine skeletal muscle. With 20 W applied power and cooling water temperature of 5 °C, temperature measured at 3.5 mm from the balloon surface exceeded the temperature at 1.5 mm from the balloon surface by 3 °C. In ex vivo tissue, for 40 W applied power, tissue within 2 mm of the balloon surface remained unablated. With adequate cooling and power, it may be feasible to thermally spare tissue within 2 mm of the MWA balloon applicator.

Histological, biochemical and pharmacologycal characterization of the gastric muscular layer in Chagas disease

PURPOSE: To assess in vitro the correlation between the number of neurons and the sensitivity to cholinergic drugs and acetylcholinesterase activity in chagasic patients. METHODS: A 3x1 cm strip of the muscle layer of the anterior part of the stomach, always close to the angular incisure, was removed from 10 chronic chagasic patients (6 men) submitted to megaesophagus or megacolon surgery and from 10 non-chagasic patients (4 men) submitted to other types of surgery (control group), aged on average 52.3 and 50.1 years, respectively, for histological and pharmacological studies. The action of cholinergic drugs was investigated in isolated preparations according to the superfusion method of Ferreira and Costa, and acetylcholinesterase activity was determined by the method of Ellman. For neuron count, the strips were cut into 8 µm sections according to the method standardized by Alcântara. RESULTS: There was a difference in number of neurons between the chagasic (5,6) and control (7,3) groups. Acetylcholinesterase activity, in moles of hydrolyzed substrate per minute per gram tissue, was reduced in chagasic patients (4,32) compared to the controls (7,30). No hypersensitivity of the gastric musculature to cholinergic drugs was detected, with a reduced maximum response to carbachol and betanechol in the chagasic group. CONCLUSIONS: The reduction of neurons in the myenteric plexus of the stomach of chronic chagasic patients can be demonstrated even in the absence of clinical chagasic gastropathy. The hypersensitivity of the gastric musculature to cholinergic drugs probably depends on intense denervation. The reduced acetylcholinesterase activity demonstrates the involvement of the cholinergic innervation in the stomach of chronic chagasic patients. There was no correlation between number of neurons, sensitivity to cholinergic drugs and acetylcholinesterase activity in the gastric musculature of chagasic and non-chagasic patients.

Vagotomy confined to the acid-secreting mucosa of the stomach

Chemoneurolysis, using varying concentrations of ethyl alcohol, was performed in dogs with a total gastric fistula in an attempt to denervate selectively only the acid-secreting mucosa, leaving the muscle innervated. Tests of gastric secretion and histological examination of gastric wall biopsies were performed both before and after chemoneurolysis. Chemoneurolysis resulted in a significant reduction in the number of parasympathetic fibres in the submucosa (p<0.01) and a decrease in insulin and pentagastrin stimulated acid secretion. The appearances of the myenteric plexus and gastric musculature were unchanged. The destruction of the submucosal neural tissue was, however, insufficient to produce a th erapeutically significant decrease in gastric acid output.

Gastric Ischemia: The Primary Factor in Neonatal Perforation

The incidence of perinatal asphyxia and evidence for gastric ischemia were investigated in six patients from the Yale-New Haven Hospital and 87 previously reported cases having neonatal gastric perforation. All our patients and 69 per cent of the collected series were found to have significant perinatal complications predisposing to asphyxia; five of our patients and 41 per cent of those reviewed had evidence of gastric ischemia as manifested by mucosal hemorrhage, ulceration, or necrosis. Gastric ischemia is the primary factor in neonatal perforation although pneumatic distention with separation of the gastric musculature, the effects of the acid pepsin response on the gastric mucosa, and direct trauma to the stomach wall are important contributing factors which make gastric perforation unique.