Study on the Mechanism of mTOR-Mediated Autophagy during Electroacupuncture Pretreatment against Cerebral Ischemic Injury.

This study is aimed at investigating the association between the electroacupuncture (EA) pretreatment-induced protective effect against early cerebral ischemic injury and autophagy. EA pretreatment can protect cerebral ischemic and reperfusion injuries, but whether the attenuation of early cerebral ischemic injury by EA pretreatment was associated with autophagy is not yet clear. This study used the middle cerebral artery occlusion model to monitor the process of ischemic injury. For rats in the EA pretreatment group, EA pretreatment was conducted at Baihui acupoint before ischemia for 30 min for 5 consecutive days. The results suggested that EA pretreatment significantly increased the expression of autophagy in the cerebral cortical area on the ischemic side of rats. But the EA pretreatment-induced protective effects on the brain could be reversed by the specific inhibitor 3-methyladenine of autophagy. Additionally, the Pearson correlation analysis indicated that the impact of EA pretreatment on p-mTOR (2481) was negatively correlated with its impact on autophagy. In conclusion, the mechanism of EA pretreatment at Baihui acupoint against cerebral ischemic injury is mainly associated with the upregulation of autophagy expression, and its regulation of autophagy may depend on mTOR-mediated signaling pathways.

Effects of electroacupuncture of different intensities on energy metabolism of mitochondria of brain cells in rats with cerebral ischemia-reperfusion injury.

OBJECTIVE: To observe the effects of electroacupuncture (EA) of different intensities on lactate dehydrogernase (LDH), succinate dehydrogenase (SDH) and ATPase in brain tissue of rats with cerebral ischemia-reperfusion injury (CI/R). METHODS: Forty male SD rats were uniformly randomized into sham operation group (group A), CI/R group (group B), CI/R+5 mA EA (group C), CI/R+3 mA EA (group D) and CI/R+1 mA EA (group E) groups with eight rats in each group. Transient general brain ischemia was induced by four-vessel occlusion and reperfusion. The rats in group C, group D and group E were punctured and stimulated at Baihui (GV20), Mingmen (GV4) and Zusanli (ST36) with the same intermittent and rarefaction-dense wave (30 to 50 Hz) and different electric current intensities: 5 mA, 3 mA and 1 mA for 20 min after CI/R. Then the activities of Na(+)-K(+)-ATPase, SDH and LDH in mitochondria of brain tissue were measured by spectrophotometry. The ischemic cerebral cortex tissue was taken for observing the ultrastructure changes of impaired nerve cells. RESULTS: Compared with group A, the activities of LDH, SDH and Na(+)-K(+)-ATPase were lowerer in the group B (P<0.05 or P<0.01). However, the activities of LDH, SDH and Na(+)-K(+)-ATPase were higher in the group D than those in the group B (P<0.05 orP<0.01). In group A, the anatomical structure of the cerebral cortex cells was basically normal; in group B, the neuronal cellular structures were severely damaged, the neuronal mitochondria got swelling, the mitochondrial cristae were broken, the medullated nerve fifibers were not integrated. In group C, group D and group E, the ultrastructure of impaired neuron were improved. Group D was the best among three groups above. CONCLUSION: EA of 3 mA intensity could strengthen aerobic metabolism by elevating the activities of SDH and LDH, meanwhile maintaining the ionic equilibrium in the exterior and interior brain cell and relieving the cellular edema by reinforcing the activities of Na(+)-K(+)-ATPase.

Protective effects of the preconditioning with different doses of sodium aescinate on tourniquet-induced ischemic reperfusion.

OBJECTIVE: To evaluate the protective effects of sodium aescinate (SA) preconditioning on the tourniquet-induced ischemia-reperfusion (I/R) injury after limbs operation. METHODS: Seventy-five patients with grade I-II issued by American Society of Anesthesiology undergoing lower limb operation were randomly assigned to 3 groups: the control group, low-dose SA-treated group and high-dose SA-treated group; each group enrolled 25 patients. The patients were treated with 5 mg and 10 mg SA 30 min before tourniquet inflation in the two treatment groups separately, while the patients in the control group received normal saline. Venous blood samples were obtained before tourniquet was inflated (T0 baseline). And 5 (T1), 10 (T2), 20 (T3) min after tourniquet was released. The nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined by commercial kits. Meanwhile, arterial pressure (MAP) and heart rate (HR) were monitored from an automatic invigilator. RESULTS: In the control group, MDA and NO levels were increased, and SOD and MAP were decreased significantly after tourniquet deflation compared to T0 baseline (P<0.05). After tourniquet deflation, MDA and NO levels in the two treated groups were significantly decreased; meanwhile, SOD levels and MAP were increased, and the variations of HR were more stable compared with the control group (all P<0.05). There was no significant difference in all of the above between the two treated groups (P>0.05). CONCLUSION: The protective effects of SA preconditioning on tourniquet-induced limb I/R injury might possibly contribute to the increasing of SOD levels, and MAP and the decreasing of MDA and NO levels.

[Pulmonary alveolar proteinosis treated with whole-lung lavage utilizing extracorporeal membrane oxygenation: a case report and review].

OBJECTIVE: To improve the treatment of severe hypoxaemia in patients with pulmonary alveolar proteinosis (PAP). METHODS: The clinical data of a patient with pathologically proven PAP treated with whole-lung lavage utilizing extracorporeal membrane oxygenation (ECMO) were described and the literature was reviewed. RESULTS: This 57-year-old man was admitted because of cough and progressive dyspnea for 12 months. His PaO(2) was 46 mm Hg (1 mm Hg = 0.133 kPa) and saturation of pulse oximeter (SpO(2)) was from 85% to 88% with oxygen 5 L/min by nasal cannula. His chest CT, bronchoscopy with bronchoalveolar lavage and transbronchial biopsies were consistent with PAP. Whole-lung lavage was performed in the operation room under general anesthesia. A double-lumen tube was intubated in order to selectively ventilate and lavage a single lung independently. During mechanical ventilation for both lungs, the SpO(2) was from 80% to 90%, but when a single right lung ventilation was tried, the SpO(2) (from 68% to 80%) dropped significantly. To ensure adequate oxygen supply during lavage, a veno-arterial ECMO was set up by inserting catheters percutaneously into the right femoral artery and right femoral vein respectively. Then the SpO(2) improved, from 89% to 97% during single right lung ventilation. The left lung was lavaged with a total of 20.8 L of normal saline. The SpO(2) ranged from 80% to 94% during the lavage. After the lavage, the patient no longer experienced shortness of breath. Then 28 days later the right lung was lavaged without the aid of ECMO. A month after the second lavage, his chest CT showed marked improvement in infiltrates of both lungs. CONCLUSION: When a patient with PAP has refractory hypoxemia prior to the lavage procedure, ECMO should be considered in order to avoid severe hypoxaemia with fatal consequences during lavage.