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Objective: To study diabetic gastric motility changes and gastric vascular changes . Methods: 72 SPF male Wistar rats were the adaptive feeding week were randomly divided into experimental group and the control group , the experimental group animals induced by high-fat and high- sugar diet and a small dose of streptozotocin ( STZ ) injection destruction of pancreatic beta cells , manufacturing type 2 diabetes model . Respectively , at 4 weeks , 24 weeks, single photon emission tomography ( SPECT ) measurement of gastric emptying , observed blood endothelin ( ET - 1 ) , thrombomodulin ( TM ) , von Willebrand factor ( vWF ) , and observed under a microscope for the pathological changes of the gastric vessels . Results : 24 Weeks model rats plasma TM , vWF , ET - 1 significantly increased 4 weeks model group increased slightly . Microscope to see early vascular endothelial mild damage , microvascular compensatory increase gastric motility to accelerate . With the progression of the vascular endothelial damage further aggravate gastric mucosal microvascular gradually reduced , telangiectasia , submucosal and muscular vascular wall thickening , stenosis , wall / lumen ratio increased significantly delay gastric motility . Conclusion: changes in diabetic gastric motility gastric vascular changes , and vascular disease may cause gastric motility changes in the initial factor .
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