Physaloptera brevivaginata has been found parasitising the stomach of two species of bats of the family Vesperti-lionidae, Myotis myotis and Myotis blythii, in Spain. A comparative study of the prevalences and mean intensities of parasitism by this physalopterid revealed no statistically significant differences between the two hosts. Likewise, no relationship was found between parasite intensity and host body weight. The histopathological study of the stomach lesion revealed destruction of the mucosa, with degeneration of the gastric glands, loss of the muscularis mucosae and focal necrosis at the points where the cephalic extremities of both sexes of this nematode attach to the mucosa. The present paper is the first study of gastric pathology caused by an adult physalopterid in bats.
a1_Leptin regulates energy homeostasis and body weight by balancing energy intake and expenditure. It was recently reported that leptin, released into the gut lumen during the cephalic phase of gastric secretion, is capable of initiating intestinal nutrient absorption. Vagal afferent neurons also express receptors for both CCK and leptin, which are believed to interact in controlling food intake. The present study was undertaken to investigate the central and peripheral effects of leptin on gastric emptying rate. Under anesthesia, male Sprague-Dawley rats (250-300 g) were fitted with gastric Gregory cannulas (n=12) and some had additional cerebroventricular cannulas inserted into their right lateral ventricles. Following recovery, the rate of gastric emptying of saline (300 mOsm/kg H2O) was determined after instillation into the gastric fistula (3 ml, 37°C, containing phenol red, 60 mg/l as a non-absorbable dilution marker). Gastric emptying rate was determined from the volume and phenol red concentrations recovered after 5 min. Leptin, injected intraperitoneally (ip; 10, 30, 60, 100 μg/kg) or intracerebroventricularly (icv; 5, 15 μg/rat) 15 min before the emptying, delayed gastric emptying rate of saline at the dose of 30 μg/kg or 15 μg/rat (p<0.001). When CCK 1 receptor blocker L-364,718 (1 mg/kg, ip), CCK 2 receptor blocker L-365,260 (1 mg/kg, ip) or adrenergic ganglion blocker bretylium tosylate (15mg/kg, ip) was administered 15 min before ip leptin (30 μg/kg) injections, leptin-induced delay in gastric emptying was abolished only by the CCK 1 receptor blocker (p<0.001)., a2_However, the inhibitory effect of central leptin on gastric emptying was reversed by adrenergic blockade, but not by either CCK antagonists. Our results demonstrated that leptin delays gastric emptying. The peripheral effect of leptin on gastric motility appears to be mediated by CCK 1 receptors, suggesting the release of CCK and the involvement of vagal afferent fibers. On the other hand, the central effect of leptin on gastric emptying is likely to be mediated by adrenergic neurons. These results indicate the existence of a functional interaction between leptin and CCK receptors leading to inhibition of gastric emptying and short-term suppression of food intake, providing an additional feedback control in producing satiety., B. Çakir, Ö. Kasimay, E. Devseren, B. Ç. Yeğen., and Obsahuje bibliografii a bibliografické odkazy
C-type natriuretic peptides (CNP) play an inhibitory role in smooth muscle motility of the gastrointestinal tract, but the effect of CNP on delayed rectifier potassium currents is still unclear. This study was designed to investigate the effect of CNP on delayed rectifier potassium currents and its mechanism by using conventional whole-cell patch- clamp technique in guinea-pig gastric myocytes isolated by collagenase. CNP significantly inhibited delayed rectifier potassium currents [IK (V)] in dose-dependent manner, and CNP inhibited the peak current elicited by depolarized step pulse to 86.1±1.6 % (n=7, P<0.05), 78.4±2.6 % (n=10, P< 0.01) and 67.7±2.3 % (n=14, P<0.01), at concentrations of 0.01 μmol/l, 0.1 μmol/l and 1 μmol/l, respectively, at +60 mV. When the cells were preincubated with 0.1 μmol/l LY83583, a guanylate cyclase inhibitor, the 1 μmol/l CNP-induced inhibition of IK (V) was significantly impaired but when the cells were preincubated with 0.1 μmol/l zaprinast, a cGMP-sensitive phosphodiesterase inhibitor, the 0.01 μmol/l CNP-induced inhibition of IK (V) was significantly potentiated. 8-Br-cGMP, a membrane permeable cGMP analogue mimicked inhibitory effect of CNP on IK (V). CNP-induced inhibition of IK (V) was completely blocked by KT5823, an inhibitor of cGMP-dependent protein kinase (PKG). The results suggest that CNP inhibites the delayed rectifier potassium currents via cGMP-PKG signal pathway in the gastric antral circular myocytes of the guinea-pig., H. Y. Xu, X. Huang, M. Yang, J.-B. Sun, L.-H. Piao, Y. Zhang, L. Gao, W.-X. Xu., and Obsahuje bibliografii a bibliografické odkazy