Clinical practice guidelines for prevention and treatment of postoperative gastrointestinal disorder with Integrated Traditional Chinese and Western Medicine (2023).

Postoperative gastrointestinal disorder (POGD) was a common complication after surgery under anesthesia. Strategies in combination with Traditional Chinese Medicine and Western medicine showed some distinct effects but standardized clinical practice guidelines were not available. Thus, a multidisciplinary expert team from various professional bodies including the Perioperative and Anesthesia Professional Committees of the Chinese Association of Integrative Medicine (CAIM), jointly with Gansu Province Clinical Research Center of Integrative Anesthesiology/Anesthesia and Pain Medical Center of Gansu Provincial Hospital of Traditional Chinese Medicine and WHO Collaborating Center for Guideline Implementation and Knowledge Translation/Chinese Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) Center/Gansu Provincial Center for Medical Guideline Industry Technology/Evidence-based Medicine Center of Lanzhou University, was established to develop evidence-based guidelines. Clinical questions (7 background and 12 clinical questions) were identified through literature reviews and expert consensus meetings. Based on systematic reviews/meta-analyses, evidence quality was analyzed and the advantages and disadvantages of interventional measures were weighed with input from patients' preferences. Finally, 20 recommendations were developed through the Delphi-based consensus meetings. These recommendations included disease definitions, etiologies, pathogenesis, syndrome differentiation, diagnosis, and perioperative prevention and treatment.

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.

Electroacupuncture pretreatment attenuates blood­brain barrier disruption following cerebral ischemia/reperfusion.

Disruption of the blood-brain barrier (BBB) and subsequent brain edema are major contributors to the pathogenesis of ischemic stroke, however, current clinical therapeutic methods remains unsatisfactory. Electroacupuncture (EA) pretreatment has a protective effect against cerebral ischemia/reperfusion (I/R). However, the underlying mechanisms remain to be fully elucidated. In the present study, the effect of EA pretreatment on BBB disruption was investigated in a focal I/R rat model. Male Sprague-Dawley rats (280-320 g) were pretreated with EA at the acupoint 'Baihui' (GV20) 30 min/day, for five days consecutively prior to focal cerebral I/R, which was induced by middle cerebral artery occlusion (MCAO) for 2 h. The results demonstrated that the infarction volume, brain water content and neurological deficits increased in the MCAO model rats at 3 h and 24 h post-reperfusion, and were attenuated significantly by EA pretreatment. Furthermore, electron microscopy examination confirmed a reduction in brain edema reduction in the EA pretreated rats. Western blot analysis revealed that the tight junction proteins between endothelial cells, including claudin-5, occludin, were significantly degraded, while the protein expression of phosphorylated (p-)caveolin-1 and p-Akt increased following reperfusion, all of which were alleviated by EA pretreatment. However, no significant differences were observed in the expression of caveolin-1 or Akt. Overall, the results demonstrated that EA pretreatment significantly reduced BBB permeability and brain edema, which were correlated with alleviation of the degradation of tight junction proteins and inhibition of the expression of p-caveolin-1 in the endothelial cells.

Electroacupuncture pretreatment induces tolerance against cerebral ischemia/reperfusion injury through inhibition of the autophagy pathway.

Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment­induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule­associated protein 1A light chain 3 (LC3)­II and Beclin 1 were significantly increased 12 h post­I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3­II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.

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.

P6 Electroacupuncture Improved QTc Interval Prolongation by Upregulation of Connexin43 in Droperidol Treated Rats.

Aim. This study investigated the effect of P6 EA on droperidol-induced QTc interval prolongation and Cx43 expression in ventricular muscle of rats. Methods. Twenty-four rats were randomly divided into control group (C), droperidol group (D), or EA group (E). C group rats were injected with normal saline. D group rats were injected with droperidol 0.13 mg/kg. E group rats were pretreated with EA at left P6 acupoint for 30 min and then injected with droperidol (0.13 mg/kg). QTc intervals were recorded at lead II in ECG within 120 min. Cx43 expression was measured by RT-PCR and western blotting. Result. Droperidol significantly prolonged QTc intervals compared with controls at 5 min, 10 min, 15 min, and 30 min (P < 0.05). P6 EA could significantly abbreviate the prolongation of QTc interval compared with droperidol group at 5 min, 10 min, 15 min, and 30 min (P < 0.05). Cx43 mRNA and proteins were significantly increased by P6 EA compared with droperidol group at 120 min (P < 0.05). There were no significant differences in Cx43 mRNA and protein expression between droperidol and control group at 120 min (P > 0.05). Conclusion. P6 EA could improve QTc interval prolongation induced by droperidol, which may relate to upregulation of Cx43 mRNA and protein. Antiemetic dose of droperidol had minor effects on Cx43 mRNA and protein expression at 120 min.

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.