Clinical analysis of 84 cases of conversion from gynecologic laparoscopic surgery to laparotomy / 中国综合临床

Objective:To analyze the causes and influencing factors of conversion from laparoscopic surgery to laparotomy.Methods:To analyze and summarize the clinical data of 84 patients who converted to laparotomy in 16 203 cases of laparoscopic surgery from August 2017 to August 2020 in the Department of Gynecology of the Affiliated Hospital of Qingdao University, each patient converted to surgery was matched with 2 patients who underwent simple laparoscopic surgery. The patients were divided into conversion to laparotomy group (84 cases) and control group (168) cases, and analyze the influencing factors of laparoscopic conversion to laparotomy. χ 2 test or corrected χ 2 test or Fisher exact probability method were used for the comparison of counting data between groups, and conditional regression analysis was used for the multivariate analysis of case control design. Results:The conversion rate of gynecologic laparoscopic surgery to laparotomy was 0.52%(84/16 203). The reasons for 84 cases of conversion from laparoscopic surgery to open surgery were as follows: pelvic adhesion 50.0%(42/84), unexpected malignant tumor 19.0%(16/84), tumor oversize or special shape and location 14.3%(12/84), hemostasis difficulty 7.1%(6/84), multiple uterine fibroids 3.5%(3/84), simultaneous surgery 3.5%(3/84), bladder injury 1.2%(1/84), and subcutaneous emphysema 1.2%(1/84) during the operation. There were no significant differences in body mass index and comorbidities (diabetes, hypertension, coronary heart disease, thyroid disease) between the two groups (all P>0.05). And the history of endometriosis was 36.9% (31/84) and the history of pelvic surgery in the transperitoneal group was 60.7% (51/84) higher than that in the conversion to laparotomy group of 20.8% (35/84), 30.6% (51/84) (χ 2=7.482, 21.42, P=0.006). The results of conditional regression analysis showed that that surgical history( OR=3.979, 95% CI 2.010-7.874, P<0.001 and thyroid history ( OR=15.333, 95% CI 1.087-216.346, P=0.005) increased the risk of conversion to laparotomy; Hypertension history ( OR=0.203, 95% CI 0.067-0.622, P=0.005) reduced the risk of conversion to laparotomy. Further analysis of which operation type affected the conversion to laparotomy showed that cesarean section ( OR=2.105, 95% CI 1.109-4.351, P=0.044), myomectomy ( OR=11.605, 95% CI 3.306-40.735, P<0.001), and ovarian cyst removal ( OR=7.914, 95% CI 2.157-21.037, P=0.002) affected the conversion to laparotomy. Conclusion:The main reason for conversion from gynecologic laparoscopic surgery to laparotomy is pelvic adhesion. The history of surgery and thyroid disease are the risk factors for conversion to laparotomy. Among them, myomectomy and ovarian cyst removal are important factors for conversion to laparotomy. Before operation, appropriate clinical operation methods should be selected according to the patient's medical history and condition to ensure the patient's safety.

Effect of laparoscopic surgery for pancreatic cancer after neoadjuvant chemotherapy / 中华外科杂志

Objective: To evaluate the safety and feasibility of laparoscopic surgery after neoadjuvant chemotherapy for pancreatic cancer. Methods: Clinical data of 8 patients underwent laparoscopic surgery after neoadjuvant chemotherapy for pancreatic cancer at Fudan University Shanghai Cancer Center from September 2019 to June 2020 were reviewed retrospectively. There were 5 males and 3 females,aged from 47 to 72 years old. All patients underwent abdominal enhanced CT and PET-CT before operation to accurately evaluate the tumor stage and exclude distant metastasis. Results: Neoadjuvant chemotherapy with AG regimen(gemcitabine 1 000 mg/m2 and albumin bound paclitaxel 125 mg/m2) was received for 2 to 6 cycles before surgery. All 8 patients successfully completed the operation,including 5 cases of pancreaticoduodenectomy,2 cases of radical antegrade modular pancreatosplenectomy(RAMPS),and 1 case of total pancreatectomy. No conversion to laparotomy or laparoscopic assisted surgery. The operation time was 240 to 450 minutes,the blood loss was 100 to 500 ml,the postoperative length of stay was 10 to 16 days. During the follow-up period up to December 31, 2020, there was 1 case suffered grade B pancreatic leakage and abdominal infection. The numbers of resected lymph nodes were 9 to 31. All patients received R0 resection. The follow-up times were 4.5 to 9.5 months. One patient underwent RAMPS was diagnosed as liver metastasis after 2 months of the operation,and the other 7 patients still survived without tumor recurrence. Conclusion: Minimally invasive surgery of pancreatic cancer after neoadjuvant chemotherapy is safe and feasible in experienced pancreatic minimally invasive centers.

YANG Jun's clinical experience of acupuncture for oculomotor paralysis / 中国针灸

Professor YANG Jun's clinical experience of acupuncture and moxibustion for oculomotor paralysis is summarized. Professor YANG Jun pays attention to disease differentiation and syndrome differentiation in the treatment of this disease. According to the characteristics of oculomotor paralysis, "early diagnosis and seeking treatment from the source" is advocated. According to the etiology and pathogenesis, professor YANG divides oculomotor paralysis into three types: the syndrome of wind-evil attacking collaterals, the syndrome of spleen-stomach weakness and the syndrome of qi-deficiency and blood-stasis. As such, the acupoints are selected according to syndrome differentiation, and several different acupuncture methods (pricking needling at eyelids, penetrating needling and lifting eyelids and contralateral- balance needling on the healthy side) are adopted to improve the symptoms of oculomotor paralysis. It is also suggested to use the combination of scalp acupuncture and electroacupuncture to achieve the best dose-effect state. Moreover, local stimulation around the eyes is important to achieve the effects of "qi reaching affected area".

Emerging Role of PD-1 in the Central Nervous System and Brain Diseases / 神经科学通报·英文版

Programmed cell death protein 1 (PD-1) is an immune checkpoint modulator and a major target of immunotherapy as anti-PD-1 monoclonal antibodies have demonstrated remarkable efficacy in cancer treatment. Accumulating evidence suggests an important role of PD-1 in the central nervous system (CNS). PD-1 has been implicated in CNS disorders such as brain tumors, Alzheimer’s disease, ischemic stroke, spinal cord injury, multiple sclerosis, cognitive function, and pain. PD-1 signaling suppresses the CNS immune response via resident microglia and infiltrating peripheral immune cells. Notably, PD-1 is also widely expressed in neurons and suppresses neuronal activity via downstream Src homology 2 domain-containing protein tyrosine phosphatase 1 and modulation of ion channel function. An improved understanding of PD-1 signaling in the cross-talk between glial cells, neurons, and peripheral immune cells in the CNS will shed light on immunomodulation, neuromodulation, and novel strategies for treating brain diseases.

Advances in basic and translational research in neuroendocrine neoplasms / 中华胃肠外科杂志

With the development of diagnostic techniques and the improvement of people's living standards, the detection rate of neuroendocrine tumor has been increasing and people are paying more and more attention to it. With multiple treatment modalities, the clinical research progress of neuroendocrine tumor is remarkable. However, due to the tumor heterogeneity, metastasis and recurrence of neuroendocrine tumor remains a difficult problem for clinicians. The efficacy of neuroendocrine tumor still needs to be improved. Therefore, the biological behavior of neuroendocrine tumor needs to be further studied. In recent years, with the development of molecular biology, the basic and transformation research of neuroendocrine tumor has made some progress. In this paper, we focus on the hot topics of neuroendocrine tumor, such as multiomics (copy number variation, genomics, transcriptomics), tumor microenvironment (immune microenvironment, tumor microvasculature, tumor-associated fibroblasts, etc.), preclinical research model construction (cell lines, organoids, patient derived xenograft models, genetically engineered mice), etc. Specifically, the related clinical transformation significance will be elaborated.

Current Situation of Methamphetamine Abuse and Related Research Progress / 法医学杂志

Drug problem is a major social and public security problem in the world. Drug abuse poses a great threat to economic development, social stability and public health. In recent years, synthetic drugs represented by methamphetamine have surpassed traditional drugs such as morphine, heroin, ketamine and become one of the most abused drugs in the world. In order to solve the problem of drug abuse, it is of great theoretical value and practical significance to carry out all-round and multi-level scientific research on drug-related issues. Based on the current situation of drug abuse, this article reviews research progresses on the epidemiology of methamphetamine abuse, the monitoring technology, the basic researches on toxicity damage, the withdrawal drug screening, the related clinical comorbidity and the testing technologies, comprehensively presenting the development trend of methamphetamine abuse related issues.

Environmental risks of antibiotics in soil and the related bioremediation technologies / 生物工程学报

Antibiotics are widely used and prevalently distributed in the environment. The issue of antibiotic resistance genes has posed a huge threat to the global public health. Soil is an important sink of antibiotics in the environment. Antibiotic exposure may introduce adverse effects on soil organisms, and bring indirect but potential risks to human health. Therefore, it is urgent to take actions to remediate antibiotics-contaminated soil. This review summarized effects of antibiotics on phenotype growth of plants, physiological characteristics and community structure of animals, composition and structure of microbial communities, and transmission of antibiotic resistance genes among organisms in soil. Additionally, the potential and prospects of employing antibiotic-resistant soil plants, animals, microorganisms, and their combinations to treat antibiotics-contaminated soil were illustrated. Last but not least, the unaddressed issues in this area were proposed, which may provide insights into relevant research directions in the future.

Insights into the applications of 3D bioprinting for bioremediation technologies / 生物工程学报

A plethora of organic pollutants such as pesticides, polycyclic and halogenated aromatic hydrocarbons, and emerging pollutants, such as flame retardants, is continuously being released into the environment. This poses a huge threat to the society in terms of environmental pollution, agricultural product quality, and general safety. Therefore, effective removal of organic pollutants from the environment has become an important challenge to be addressed. As a consequence of the recent and rapid developments in additive manufacturing, 3D bioprinting technology is playing an important role in the pharmaceutical industry. At the same time, an increasing number of microorganisms suitable for the production of biomaterials with complex structures and functions using 3D bioprinting technology, have been identified. This article briefly discusses the principles, advantages, and disadvantages of different 3D bioprinting technologies for pollutant removal. Furthermore, the feasibility and challenges of developing bioremediation technologies based on 3D bioprinting have also been discussed.

Advances in biodegradation of sulfonamides antibiotics in aerobic activated sludge system / 生物工程学报

Sulfonamides (SAs) are a kind of antibiotics widely used in medical treatment and livestock breeding. However, they have poor degradability in human and animal intestines, and will enter the sewage treatment system through the discharge of feces and urine. The aerobic activated sludge (AAS) in wastewater treatment plant was found to be able to effectively transform SAs. This article summarizes the advances in biodegradation of SAs in aerobic activated sludge system, which includes the biodegradation mechanisms, the main biodegradation pathways, and the environmental factors affecting the degradation efficiency. Challenges encountered in the current research were discussed, with the aim to provide scientific basis for optimizing the biodegradation of SAs in wastewater treatment process.

Environmental scientists & microbiologists from China & EU: take the responsibility to cherish the Earth homeland / 生物工程学报

Humanity shares the common interest to protect the environment and to maintain a healthy global ecosystem. International collaboration is key in this context, to advance the necessary science and technology. The National Science Foundation of China (NSFC) and European Commission (EC) have agreed to collaborate in innovative knowledge and technology in the field of bioremediation of polluted environments and biodegradation of plastics. In this context, projects on bioremediation of soils, wastewater and sediment matrices and on microbial degradation of plastics were supported. This special issue aimed to introduce these projects and their progresses in the related fields. In total, 23 papers have been collected in this issue, covering both fundamental and applied researches.

Protective effects of endogenous carbon monoxide against myocardial ischemia-reperfusion injury in rats / 生理学报

The present study is aimed to explore the effects of endogenous carbon monoxide on the ischemia-reperfusion in rats. Wistar rats were intraperitoneally injected with protoporphyrin cobalt chloride (CoPP, an endogenous carbon monoxide agonist, 5 mg/kg), zinc protoporphyrin (ZnPP, an endogenous carbon monoxide inhibitor, 5 mg/kg) or saline. Twenty-four hours after injection, the myocardial ischemia-reperfusion model was made by Langendorff isolated cardiac perfusion system, and cardiac function parameters were collected. Myocardial cGMP content was measured by ELISA, and the endogenous carbon monoxide in plasma and myocardial enzymes in perfusate at 10 min after reperfusion were measured by colorimetry. The results showed that before ischemia the cardiac functions of CoPP, ZnPP and control groups were stable, and there were no significant differences. After reperfusion, cardiac functions had significant differences among the three groups (P < 0.05). Compared with pre-ischemia, the cardiac function decreased and obvious cardiac arrest was shown in control and ZnPP groups, while the cardiac function in CoPP group did not change significantly, maintaining a relatively stable level. At the same time, three groups' carbon monoxide level, myocardial enzymology and the cardiac function recovery time after reperfusion also had significant differences (P < 0.05). Compared with those in control group, recovery after reperfusion was faster, activities of creatine kinase and lactic dehydrogenase were significantly decreased, plasma CO and myocardial cGMP contents were significantly increased in CoPP group, while these changes were completely opposite in ZnPP group. It is concluded that endogenous carbon monoxide can maintain cardiac function, shorten the time of cardiac function recovery, and play a protective role in cardiac ischemia-reperfusion.

Spinal CCL2 Promotes Central Sensitization, Long-Term Potentiation, and Inflammatory Pain via CCR2: Further Insights into Molecular, Synaptic, and Cellular Mechanisms / 神经科学通报·英文版

Mounting evidence supports an important role of chemokines, produced by spinal cord astrocytes, in promoting central sensitization and chronic pain. In particular, CCL2 (C-C motif chemokine ligand 2) has been shown to enhance N-methyl-D-aspartate (NMDA)-induced currents in spinal outer lamina II (IIo) neurons. However, the exact molecular, synaptic, and cellular mechanisms by which CCL2 modulates central sensitization are still unclear. We found that spinal injection of the CCR2 antagonist RS504393 attenuated CCL2- and inflammation-induced hyperalgesia. Single-cell RT-PCR revealed CCR2 expression in excitatory vesicular glutamate transporter subtype 2-positive (VGLUT2) neurons. CCL2 increased NMDA-induced currents in CCR2/VGLUT2 neurons in lamina IIo; it also enhanced the synaptic NMDA currents evoked by dorsal root stimulation; and furthermore, it increased the total and synaptic NMDA currents in somatostatin-expressing excitatory neurons. Finally, intrathecal RS504393 reversed the long-term potentiation evoked in the spinal cord by C-fiber stimulation. Our findings suggest that CCL2 directly modulates synaptic plasticity in CCR2-expressing excitatory neurons in spinal lamina IIo, and this underlies the generation of central sensitization in pathological pain.

TNF-α/TNFR1 Signaling is Required for the Full Expression of Acute and Chronic Itch in Mice via Peripheral and Central Mechanisms / 神经科学通报·英文版

Increasing evidence suggests that cytokines and chemokines play crucial roles in chronic itch. In the present study, we evaluated the roles of tumor necrosis factor-alpha (TNF-α) and its receptors TNF receptor subtype-1 (TNFR1) and TNFR2 in acute and chronic itch in mice. Compared to wild-type (WT) mice, TNFR1-knockout (TNFR1-KO) and TNFR1/R2 double-KO (DKO), but not TNFR2-KO mice, exhibited reduced acute itch induced by compound 48/80 and chloroquine (CQ). Application of the TNF-synthesis inhibitor thalidomide and the TNF-α antagonist etanercept dose-dependently suppressed acute itch. Intradermal injection of TNF-α was not sufficient to evoke scratching, but potentiated itch induced by compound 48/80, but not CQ. In addition, compound 48/80 induced TNF-α mRNA expression in the skin, while CQ induced its expression in the dorsal root ganglia (DRG) and spinal cord. Furthermore, chronic itch induced by dry skin was reduced by administration of thalidomide and etanercept and in TNFR1/R2 DKO mice. Dry skin induced TNF-α expression in the skin, DRG, and spinal cord and TNFR1 expression only in the spinal cord. Thus, our findings suggest that TNF-α/TNFR1 signaling is required for the full expression of acute and chronic itch via peripheral and central mechanisms, and targeting TNFR1 may be beneficial for chronic itch treatment.

Expression and Role of Voltage-Gated Sodium Channels in Human Dorsal Root Ganglion Neurons with Special Focus on Nav1.7, Species Differences, and Regulation by Paclitaxel / 神经科学通报·英文版

Voltage-gated sodium channels (Navs) play an important role in human pain sensation. However, the expression and role of Nav subtypes in native human sensory neurons are unclear. To address this issue, we obtained human dorsal root ganglion (hDRG) tissues from healthy donors. PCR analysis of seven DRG-expressed Nav subtypes revealed that the hDRG has higher expression of Nav1.7 (~50% of total Nav expression) and lower expression of Nav1.8 (~12%), whereas the mouse DRG has higher expression of Nav1.8 (~45%) and lower expression of Nav1.7 (~18%). To mimic Nav regulation in chronic pain, we treated hDRG neurons in primary cultures with paclitaxel (0.1-1 μmol/L) for 24 h. Paclitaxel increased the Nav1.7 but not Nav1.8 expression and also increased the transient Na currents and action potential firing frequency in small-diameter (<50 μm) hDRG neurons. Thus, the hDRG provides a translational model in which to study "human pain in a dish" and test new pain therapeutics.

Sex-Dependent Glial Signaling in Pathological Pain: Distinct Roles of Spinal Microglia and Astrocytes / 神经科学通报·英文版

Increasing evidence suggests that spinal microglia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain following intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID (a caspase-6 inhibitor) and the astroglial inhibitors L-α-aminoadipate (L-AA, an astroglial toxin) and carbenoxolone (a connexin 43 inhibitor), as well as U0126 (an ERK kinase inhibitor) and D-JNKI-1 (a c-Jun N-terminal kinase inhibitor). We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast, intrathecal L-AA reduced neuropathic pain but not inflammatory pain in both sexes. Intrathecal U0126 and D-JNKI-1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain.

Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7 : Differential activities of Nav1.7-targeting monoclonal antibodies / 神经科学通报·英文版

The voltage-gated Na channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody (SVmab) reduces Na currents and pain and itch responses in mice. Here, we investigated whether recombinant SVmab (rSVmab) binds to and blocks Nav1.7 similar to SVmab. ELISA tests revealed that SVmab was capable of binding to Nav1.7-expressing HEK293 cells, mouse DRG neurons, human nerve tissue, and the voltage-sensor domain II of Nav1.7. In contrast, rSVmab showed no or weak binding to Nav1.7 in these tests. Patch-clamp recordings showed that SVmab, but not rSVmab, markedly inhibited Na currents in Nav1.7-expressing HEK293 cells. Notably, electrical field stimulation increased the blocking activity of SVmab and rSVmab in Nav1.7-expressing HEK293 cells. SVmab was more effective than rSVmab in inhibiting paclitaxel-induced mechanical allodynia. SVmab also bound to human DRG neurons and inhibited their Na currents. Finally, potential reasons for the differential efficacy of SVmab and rSVmab and future directions are discussed.

Arthroscopic treatment of tibial intercondylar ridge avulsion fracture with double-root line double tunnel fixation technique / 中国骨伤

<p><b>OBJECTIVE</b>To discuss arthroscopic technique of double-root line double tunnel fixation for tibial intercondylar ridge avulsion fracture and its short-term followvup observational results.</p><p><b>METHODS</b>From May 2012 to June 2017, 21 cases of tibial intercondylar ridge avulsion fractures were treated with arthroscope double line double tunnel. Among the patients, 16 males and 5 females were ranging in age from 17 to 45 years old, with an average of 29.6 years old, and injury to surgery time 3 to 6 days, with an average of 3.6 days. All the patients underwent arthroscopic exploration, fracture reduction, double root line fixation. The knee function was assessed at 3 and 6 months postoperatively using the Lysholm knee score, and the healing and resection of the patients were followed by X-ray examination.</p><p><b>RESULTS</b>All patients were followed up for 7 to 23 months, with an average of 12.8 months. All patients after fracture were bone healing, knee activity were gained their previous normal levels (ranged, 0° to 130 °), and no limb dysfunction. The average scores of Lysholm knee were(93.52±7.10) and(95.95±6.34) points in 3 months and 6 months after operation.</p><p><b>CONCLUSIONS</b>Arthroscopic treatment of tibial intercondylar ridge avulsion fractures with double root line is simple and reliable, and can provide an ideal internal fixation method for tibial intercondylar ridge avulsion fractures.</p>

Investigation of the Relationship between Cognitive Function and MRI Manifestation in Patients with SHPT / 中国医科大学学报

Objective To investigate the relationship between cognitive function and magnetic resonance imaging (MRI) manifestations in patients with secondary hyperparathyroidism (SHPT) by analyzing brain MRI diffusion-weighted imaging,diffusion tensor imaging,serological markers,and cognitive function.Methods We evaluated 49 random patients with SHPT.We adopted two functional scales to evaluate cognitive function and performed MRI fractional anisotropy (FA) and apparent diffusion coefficient (ADC) to evaluate white matter function of brain functional areas.We recorded serological markers,and conducted statistical analysis to analyze correlation among cognitive function scores,brain MRI in white matter functional areas,and biochemical parameters.Results We found that at the frontal area,the FA and ADC values were correlated with the MMSE language and memory function scores;at the parietal area,the FA and ADC values were correlated to the MoCA visuospatial executive function scores;the other areas had no significant correlation with cognitive function scale score.Cognitive function was negatively correlated with immunoreactive parathyroid hormone (iPTH) levels but positively correlated with education level,while it was not correlated with sex,age,blood pressure,and serum calcium levels in patients with SHPT.Conclusion In patients with SHPT,cognitive function is correlated with iPTH level and education level.The FA and ADC values of brain MRI in the frontal and parietal lobes might play a diagnostic role in evaluating cognitive function and locating injury for patients with SHPT,which requires clinical attention.

Sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway: An experimental study

Objective To study whether sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway. Methods H9c2 myocardial cell lines were cultured and divided into control group (C group), hypoxia reoxygenation group (H/R group), sevoflurane pretreatment + hypoxia reoxygenation group (SP group) and sevoflurane combined with Compound C pretreatment + hypoxia reoxygenation group (ComC group), and the cell proliferation activity and apoptosis rate, myocardial enzyme levels in culture medium as well as the expression of apoptosis genes and p-AMPK in cells were determined. Results p-AMPK expression in cells of H/R group was significantly lower than that of C group, SP group was significantly higher than that of H/R group; cell proliferation activity value and Bcl-2 expression in cells of H/R group were significantly lower than those of C group, SP group were significantly higher than those of H/R group, ComC group were significantly lower than those of SP group; apoptosis rate, LDH, CK and AST levels as well as the Bax and Caspase-3 expression in cells of H/R group were significantly higher than those of C group, SP group were significantly lower than those of H/R group, ComC group were significantly higher than those of SP group. Conclusions Sevoflurane pretreatment can activate AMPK signaling pathway to inhibit the myocardial apoptosis caused by hypoxia reoxygenation.

Sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway: An experimental study

OBJECTIVE@#To study whether sevoflurane pretreatment inhibits the myocardial apoptosis caused by hypoxia reoxygenation through AMPK pathway.@*METHODS@#H9c2 myocardial cell lines were cultured and divided into control group (C group), hypoxia reoxygenation group (H/R group), sevoflurane pretreatment + hypoxia reoxygenation group (SP group) and sevoflurane combined with Compound C pretreatment + hypoxia reoxygenation group (ComC group), and the cell proliferation activity and apoptosis rate, myocardial enzyme levels in culture medium as well as the expression of apoptosis genes and p-AMPK in cells were determined.@*RESULTS@#p-AMPK expression in cells of H/R group was significantly lower than that of C group, SP group was significantly higher than that of H/R group; cell proliferation activity value and Bcl-2 expression in cells of H/R group were significantly lower than those of C group, SP group were significantly higher than those of H/R group, ComC group were significantly lower than those of SP group; apoptosis rate, LDH, CK and AST levels as well as the Bax and Caspase-3 expression in cells of H/R group were significantly higher than those of C group, SP group were significantly lower than those of H/R group, ComC group were significantly higher than those of SP group.@*CONCLUSIONS@#Sevoflurane pretreatment can activate AMPK signaling pathway to inhibit the myocardial apoptosis caused by hypoxia reoxygenation.