AIM: To study the mechanism of diabetic cardiomyopathy and abnormality of oxygen free radicals. METHODS: The contents of myocardial cytosolic cytochrome C, mitochondria cytochrome C, mitochondrial calcium, NO, MDA and the activity of SOD and NOS were determined in diabetic rats induced by STZ. The pathological changes were observed under transmission electron microscope. RESULTS: Compared to the normal and ganoderma group, the levels of mitochondrial NO, iNOS, MDA, calcium and plasma Cyt-C in rat myocardium were higher (P<0.05), while mitochondrial Cyt-C and SOD were lowered in model group (P<0.05). The bouncary indistinct, disorganization, a focal loss of muscular fibril, myocardium mitochondria swelling, pulmonary vascular endothelial cellular swelling and obstructed lumen of the capillary were also observed under transmission electronic microscope. CONCLUSION: The findings indicate that oxyradical and lipid peroxidation might be associated with the damage of myocardial mitochondria in NIDDM rats. Cyt-C and mitochondrial calcium is also involved in the process.

Background:Gastroesophageal reflux disease(GERD)is a common digestive system disease with typical symptoms of acid reflux and heartburn,and high sensitivity of esophagus is an important cause of heartburn and other symptoms.TRPV1 and NaV1.8 may play an important role in the regulation of esophageal hypersensitivity,and the specific mechanism is not yet clear.Aims:To detect the expression levels of TRPV1 and NaV1.8 in esophageal sensory neuron in GERD state and explore their role in mediating esophageal hypersensitivity.Methods:Twelve guinea pigs were randomly divided into control group and GERD group.The GERD guinea pig model was established by drinking hydrochloric-pepsinogen acid water,the body mass of guinea pigs was monitored,the esophageal inflammatory histological score was performed,and the successful construction of the GERD model was verified by measuring the expression indicators of inflammatory factors.The heart rate variability method was used to detect whether the guinea pigs were in the state of visceral hypersensitivity.The expression and co-expression of TRPV1 and NaV1.8 in esophagus,nodular ganglion and jugular ganglion were detected by immunofluorescence,Western blot and real-time fluorescence quantification.Results:Compared with the control group,the score of esophageal inflammatory histology in GERD group was much higher than that in the control group(0.96 vs.0.22).The contents of esophageal inflammatory factors interleukin(IL)-1β,IL-6 and tumor necrosis factor(TNF)-α were significantly increased(P<0.05),while the contents of anti-inflammatory factor IL-10 were decreased(P<0.05).The index of heart rate variability,low frequency to high frequency ratio(LF/HF)had no significant difference between the GERD group and the control group(P>0.05),and the LF/HF in the GERD group was higher than that in the control group after the molding(P<0.05).In esophagus and jugular,the expression levels of TRPV1 and NaV1.8 in GERD group were increased and the co-expression levels were up-regulated(P<0.05),while the expression levels in nodose were not significantly changed(P>0.05).Conclusions:In the case of esophageal acid exposure,the expression levels of TRPV1 and NaV1.8 in the esophageal mucosal epithelium increased,while the expression levels in jugular ganglion were up-regulated,thus promoting the transmission of pain signals in the vagus nerve pathway,and ultimately leading to the occurrence of esophageal hypersensitivity.

Gastroesophageal reflux disease (GERD) is a common digestive disease characterized by heartburn and acid reflux. In recent years, many studies have shown that esophageal hypersensitivity is an important pathophysiological mechanism involved in the occurrence and development of heartburn. Esophageal sensory receptors including transient receptor potential vanilloid 1 (TRPV1), prostaglandin E