Objective: To observe the effects of transection of cervical sympathetic trunk (TCST) on the cognitive function of traumatic brain injury (TBI) rats and the potential mechanisms. Methods: A total of 288 adult male SD rats were divided into 3 groups using a random number table: TBI group (n=96), TBI + TCST group (n=96) and Sham group (n=96). The water maze test was performed before TBI (T0) and at day 1 (T 1 ), day 2 (T 2 ), day 3 (T 3 ), 1 week (T 4 ), 2 weeks (T 5 ), 6 weeks (T 6 ) and 12 weeks (T 7 ) after TBI. The levels of α1-adrenergic receptors (α1-ARs), α2-adrenergic receptors (α2-ARs), toll-like receptor 4 (TLR-4) and P38 in hippocampi were detected by real-time PCR. Hippocampal P38 expression was assayed by Western blot. The expressions of interleukin-6 (IL-6), tumor necrosis factor (TNF-α) and brain-derived neurotrophic factor (BDNF) were examined by immunohistochemistry. Noradrenaline (NE) expression in plasma was evaluated by ELISA. The respiratory control ratio (RCR) of brain mitochondria was detected using a Clark oxygen electrode. Results: TCST effectively improved the cognitive function of TBI rats. TCST significantly inhibited sympathetic activity in the rats and effectively inhibited inflammatory responses. The expression of BDNF at T 1 -T 6 in TBI+TCST group was higher than that in TBI group ( P <0.05). Furthermore, P38 expression was inhibited more effectively in TBI+TCST group ( P <0.05), than in TBI group ( P <0.05), and the RCR of the brain was significantly higher in TBI+TCST group than in TBI group ( P <0.05). Conclusions: TCST can enhance cognitive function in TBI rats by inhibiting sympathetic activity, reducing inflammatory responses and brain edema, upregulating BDNF and improving brain mitochondrial function.

ObjectiveThe aim of this study was to observe the effects of extracorporeal shock waves (ECSWs) on neuralgia in diabetic rats.Materials and methodsDiabetic neuralgia model was established in rats via injection of streptozotocin. The rats were divided into diabetic neuralgia group (Group A, n=6) and ECSW treatment group (Group B, n=6). Another six rats were taken as control group (Group C, n=6). The mechanical withdrawal threshold (MWT) and thermal withdrawal latencies (TWLs) were measured at specific points throughout the experiment, and the sciatic nerve was bluntly severed under anesthesia after the last measurement. The protein expressions of Sphk1 and TNF-α were detected by Western blot, and the mRNA expressions of Sphk1 and TNF-α were detected by reverse transcription PCR. The structure of the sciatic nerve was observed by electron microscopy.ResultsCompared with Group C, MWT and TWLs were decreased significantly in Groups A and B (P< 0.05). The protein expressions of TNF-α and Sphk1 in Groups A and B were both significantly higher than those in Group C (P<0.05), with higher expression in Group A than in Group B (P<0.05). The mRNA expressions of TNF-α and Sphk1 were similar. Electron microscopy showed the intact structure of the myelin sheaths of the sciatic nerve fibers in Group C, whereas the structure of the nerve fibers was damaged, with a large number of vacuoles in the myelin sheath in Group A. In Group B, the vacuoles were occasionally formed on the sciatic nerve myelin sheath, with more compact and tidy layer arrangement compared with Group A.ConclusionECSWs can relieve neuralgia in diabetic rats. Sphk1 and TNF-α may be involved in the occurrence and development of diabetic peripheral neuralgia.

The effects of steroid on diaphragmatic contractility and endurance were examined in 24 New Zealand rabbits. Diaphragmatic contractility was determined by measuring gastric pressure (Pga) with the lower thorax and the abdomen of the animal being fixed with a rigid cast. Endurance procedure was done by continuous 15 Hz stimulation of the bilateral phrenic nerves, and diaphragmatic endurance was expressed as the time from the initiation of the endurance procedure to the moment when transdiaphragmatic pressure 15 Hz (Pdi-15 Hz) decreased to 25% of Pdimax-15 Hz. Our data suggested that intravenous administration of dexamethasone 2.5 mg daily for 7 days did not affect the diaphragmatic contractility significantly, but could cause a significant decrease in diaphragmatic endurance. When delivered intravenously at the dose of 2.0 mg daily for 14 days, dexamethasone induced a significant decrease both in diaphragmatic contractility and endurance. The recovery of the diaphragmatic strength from fatigue, however, was not influenced by dexamethasone in either circumstance. The influence of dexamethasone on diaphragmatic contractility and endurance may have important clinical implications.

Background: Diabetes is one of the most common diseases in today’s society. Diabetes can cause multiple vascular lesions in the body, renal insufficiency, blindness, and so on. However, the evidence concerning the role of extracorporeal shock wave therapy in diabetic vascular disease is insufficient. Objectives: Observation of the effect of shock wave on vascular lesions in diabetic rats. Study Design: This study used an experimental design. Setting: The research took place in the laboratory research center at The Third Military Medical University. Methods: Eighteen healthy adult male Sprague Dawley rats were randomly divided into 3 groups: normal control group (group A), diabetic group (group B), and diabetes + shock wave treatment group (group C). Groups B and C were established by intraperitoneal injection of streptozotocin 60 mg/kg to demonstrate a diabetic rat model. Shock wave treatment was performed on the left lower extremity femoral artery in group C for 1 week (T1), 2 weeks (T2), 3 weeks (T3), and 4 weeks (T4) while the other 2 groups were reared normally. At the end of T4 shock wave treatment, the femoral arteries of each group were observed under an electron microscope. The expression of vascular endothelial growth factors (VEGF), endothelial nitric oxide synthase (eNOS), and angiotensin type 1 (AT1) were measured by western blot, and the changes of VEGF expression were detected by real-time polymerase chain reaction. Results: The VEGF and eNOS in group C were higher than those in group B (P < 0.05). The AT1 of the rats in the B and C groups was significantly higher than that in the A group (P < 0.05), but the C group was significantly lower than the B group (P < 0.05). After shock wave therapy, the surface of vascular endothelium in group C was flatter and smoother than that in group B, and the endothelial basement membrane and foot process were relatively tight. Limitations: Potential mechanisms that underlie the relationship between vascular dysfunction and diabetic neuropathy pain were not examined in this study. Conclusions: Shock wave may promote the formation of new blood vessels and improve vasomotor function by upregulating VEGF, eNOS, and downregulation of AT1 in diabetic rats and improve the damage of blood glucose to blood vessels to some extent. Key words: Shock wave, diabetic rats, vascular dysfunction, neovascularization