Correlation between pathological distal esophageal acid exposure and ineffective esophageal motility.

AIM: To assess the correlation between esophageal dysmotility, characterized as inefficient esophageal motility (IEM), and the presence of pathological acid reflux due to a structurally defective lower esophageal sphincter (LES), hiatus hernia. (HH), or esophagitis in patients with suspected gastroesophageal reflux disease (GERD). METHODS: 311 patients referred for GERD diagnostic procedures in a gastroesopahgeal motility laboratory were included in the study. Patients underwent an interview regarding their clinical symptoms, upper endoscopy (UE), stationary esophageal manometry, and 24-h esophageal pH-metry. The following risk factors of patients in the negative pH-metry group were compared to those in the positive pH-metry group: IEM, defective LES, HH, and esophagitis. The association between IEM and positive pH-metry results was first assessed by means of univariate analysis and later determined with multivariate logistic regression analysis. RESULTS: Out of the total of 311 studied patients, 208 met the inclusion criteria; 88 had normal and 120 had positive pH-metry results. Univariate analysis revealed that the occurrence of IEM, defective LES, and HH was significantly greater in the positive pH-metry group. Following logistic regression analysis, the occurrence of IEM remained significantly greater in the positive pH-metry group. CONCLUSIONS: IEM is associated with the presence of abnormal acid reflux, as assessed by 24-h esophageal pH-metry, regardless of the presence of defective LES, HH, or esophagitis.

Effects of nicotine administration in developing muscle fibers of rats offspring.

The authors studied the effects of nicotine in developing skeletal muscles of rats. Pregnant Wistar rats received an enteral dose of nicotine (2.5, 5.0 or 10mg/kg, respectively, in groups G2, G5, and G10) from the 10th to the 18th or 20th days of pregnancy. Myotube atrophy was observed mainly in 20-day-old fetuses of G10. Twenty-day-old control fetus and of G2 and G5 had a high sarcoplasmic expression of desmin (weaker in G10). Vimentin expression was similar in 18-day-old fetuses of the control, G2, and G5 groups, but it was weaker in 20-day-old fetuses of the G2 and G5 groups. This would indicate an acceleration of the maturation pattern of vimentin expression in these intoxicated fetus. In conclusion, high doses of nicotine induce myotube atrophy and decrease of the expression of intermediate filaments, whereas relatively low doses of nicotine (G2 and G5) induce an early decrease of vimentin expression with no myofiber atrophy.

Protective effect of pralidoxime on muscle fiber necrosis induced by organophosphate compounds.

OBJECTIVE: To determine the protective effect of pralidoxime on muscle fiber necrosis induced by organophosphate acute intoxication in rats. DESIGN: Adult male Wistar rats were given oral organophosphate compounds dissolved in glycerol formal: dichlorvos, isofenphos, metamidophos, and diazinon. Half of the animals also received pralidoxime mesylate (20 mg/kg, intraperitoneal). Control animals received only the solvent. Twenty-four hours after treatment, the diaphragm muscle was collected for histological counts of necrotic muscle fibers in transverse sections. RESULTS: Metamidophos- and isofenphos-treated animals showed the highest percentage of necrotic muscle fibers: 1.66 +/- 1.112 and 1.34 +/- 0.320, respectively. Diazinon-treated animals had a lower percentage of necrotic fibers: 0.40 +/- 0.032 (p < 0.05) compared to the first 2 products, and dichlorvos-treated animals showed the smallest: 0.05 +/- 0.021 (p < 0.05) when compared to the other 3 products. Pralidoxime reduced necrotic fibers about 20 times in metamidophos-treated animals, 10 times in isofenphos-treated animals and 6 times in diazinon-treated animals. Pralidoxime administration did not increase plasma cholinesterase activity in any group, although symptoms were reduced. CONCLUSIONS: Oxime reduced diaphragmatic muscle necrosis in experimental organophosphate intoxication, despite little effect on plasma cholinesterase. Since respiratory insufficiency is an important cause of mortality and morbidity in organophosphate intoxications, early oxime administration may be particularly beneficial.