Pyloric resection and delayed gastric liquid emptying in rats.

BACKGROUND: Surgical resection of the distal stomach impairs gastric emptying. Generally, pylorus and the antrum are removed in the distal gastrectomy, however, the pylorus is removed individually under specific circumstances. We focus on the relation between the pyloric resection and the gastric liquid emptying. AIMS: The present investigation aimed to explore the pylorectomy how to influence gastric liquid emptying in rats. METHODS: Pylorectomy and end-to-end gastroduodenal anastomosis were conducted in rats. Electrodes were implanted in the gastrointestinal serosal surface near the stoma. Total stomach, proximal stomach, distal stomach and duodenal liquid emptying, myoelectricities in the gastrointestinal tract near the stoma, and structures were examined with scintigraphy, electrode recording in vivo, and electron microscopy, respectively. RESULTS: Delayed total stomach and distal stomach emptying were found in pylorectomy rats (p<0.001). However, there was no difference in the proximal stomach and the duodenal liquid emptying compared to the controls (p>0.05). The myoelectricity of 3-5 cpm (cycles/min) in antrum and 10-12 cpm in duodenum were found in the controls and no retrograde or antegrade myoelectricities were recorded in the duodenum and antrum. High-frequency myoelectricities (tachygastria) were recorded in the antrum near the stoma (p<0.01), the retrograde and antegrade myoelectricities propagating through the stoma were recorded, and the regenerated interstitial cells of Cajal were found in stoma under electron microscope observation in pylorectomy rat. CONCLUSIONS: The gastroduodenal incoordination and abnormal myoelectricity related to impaired contraction in the antrum caused the delayed liquid gastric emptying in pylorectomy rats.

[Impact of abnormal myoelectricity at gastroduodenal anastomosis on gastric emptying in rats].

OBJECTIVE: To explore the impact of abnormal myoelectricity at gastroduodenal anastomosis on gastric emptying in rats. METHODS: Rats were randomly divided into experimental group (n=16) and control group (n=16). Pylorectomy and end-to-end gastroduodenal anastomosis were performed in the experimental group and electrodes were implanted in the serosal surface adjacent to the anastomosis. Slow waves were recorded by the implanted electrode in vivo. Gastric emptying was examined by scintigraphy. RESULTS: At the first week after surgery, antral slow-wave frequency was significantly lower in the experimental group (0.8±1.4 vs. 3.3±1.2, P<0.01), as was the duodenal slow-wave frequency (2.1±0.6 vs. 11.1±0.7, P<0.01). There was no consecutive slow-waves transduction across the pylorus or the anastomosis. Within 12-16 weeks after operation, antral slow-wave frequency in the experimental group and the control group were (8.7±0.6) cpm and (4.0±0.4) cpm, respectively (P<0.01), and duodenal slow-wave frequency were (11.1±0.8) cpm and (10.8±0.7) cpm, respectively (P>0.05). Retrograde and antegrade myoelectricity transduction through the anastomosis were detected. The mean semi-emptying time in the proximal stomach was 14.7 min in the experimental group and 13.6 min in the control group (P>0.05). Radionuclide retention rate was 25.4% in the experimental group and 39.4% in the control group (P>0.05). The mean semi-emptying time in the distal stomach was 25.3 min in the experimental group and 10.5 min in the control group (P<0.01). Radionuclide retention rate was 46.4% in the experimental group and 18.7% in the control group (P<0.01). CONCLUSION: The abnormal myoelectricity in the region of gastroduodenal stoma may delay liquid gastric emptying in pylorectomy rats.

Effects of P2Y1 receptor on glial fibrillary acidic protein and glial cell line-derived neurotrophic factor production of astrocytes under ischemic condition and the related signaling pathways.

OBJECTIVE: The present study aimed to explore the role of P2Y(1) receptor in glial fibrillary acidic protein (GFAP) production and glial cell line-derived neurotrophic factor (GDNF) secretion of astrocytes under ischemic insult and the related signaling pathways. METHODS: Using transient right middle cerebral artery occlusion (tMCAO) and oxygen-glucose-serum deprivation for 2 h as the model of ischemic injury in vivo and in vitro, immunofluorescence, quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, enzyme linked immunosorbent assay (ELISA) were used to investigate location of P2Y(1) receptor and GDNF, the expression of GFAP and GDNF, and the changes of signaling molecules. RESULTS: Blockage of P2Y(1) receptor with the selective antagonist N(6)-methyl-2'-deoxyadenosine 3',5'-bisphosphate diammonium (MRS2179) reduced GFAP production and increased GDNF production in the antagonist group as compared with simple ischemic group both in vivo and in vitro. Oxygen-glucose-serum deprivation and blockage of P2Y(1) receptor caused elevation of phosphorylated Akt and cAMP response element binding protein (CREB), and reduction of phosphorylated Janus kinase2 (JAK2) and signal transducer and activator of transcription3 (STAT3, Ser727). After blockage of P2Y(1) receptor and deprivation of oxygen-glucose-serum, AG490 (inhibitor of JAK2) reduced phosphorylation of STAT3 (Ser727) as well as expression of GFAP; LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3-K), decreased phosphorylation of Akt and CREB; the inhibitor of mitogen-activated protein kinase kinase1/2 (MEK1/2) U0126, an important molecule of Ras/extracellular signal-regulated kinase (ERK) signaling pathway, decreased the phosphorylation of JAK2, STAT3 (Ser727), Akt and CREB. CONCLUSION: These results suggest that P2Y(1) receptor plays a role in the production of GFAP and GDNF in astrocytes under transient ischemic condition and the related signaling pathways may be JAK2/STAT3 and PI3-K/Akt/CREB, respectively, and that crosstalk probably exists between them.