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Objective:To investigate the effect of regional cerebral oxygen saturation (rSO 2) combined with neurophysiological blood pressure monitoring on brain protection and myocardial protection during carotid endarterectomy (CEA) in patients with carotid stenosis and coronary heart disease. Methods:One hundred patients with carotid artery stenosis complicated with coronary heart disease treated in Jinhua Central Hospital from June 2021 to June 2022 were randomly divided into control group and experimental group. All patients were scheduled to undergo CEA. Fifty patients in the control group were administered with empirically increasing basic blood pressure by 20% - 30%, and 50 patients in the experimental group were administered with blood pressure under the guidance of rSO 2 combined with motor evoked potentials (MEPs) and somatosensory evoked potentials (EPS). The neurological function indexes of the two groups [neuron specific enolase (NSE), central nerve specific protein (S100-β)], myocardial function indicators [cardiac troponin I (cTnI), B-type natriuretic peptide (BNP)], clinical indicators (eye opening time, extubation time, recovery room stay time, hospital stay) and the incidence of postoperative complications [delirium (POD), cognitive dysfunction (POCD), neurological impairment] were compard between the two groups. Results:Two sets of postoperative NSE and S100-β both increased ( P<0.05), but NSE and S100 in the experimental group after surgery were lower than those in the control group: (0.82 ± 0.14) μg/L vs. (1.18 ± 0.28) μg/L, (290.13 ± 27.25) mg/L vs. (301.98 ± 28.56) mg/L, the differences were statistically significant ( P<0.05). After surgery, cTnI and BNP increased in both groups ( P<0.05), but the cTnI and BNP in the experimental group were lower than those in the control group: (2.87 ± 0.74)] μg/L vs. (3.36 ± 0.83) μg/L, (3.01 ± 0.85) μg/L vs. (3.89 ± 0.92) μg/L, the differences were statistically significant ( P<0.05). The opening time, extubation time, recovery room stay time, and hospitalization time in the experimental group were shorter than those in the control group: (16.79 ± 3.15) min vs. (20.55 ± 3.83) min, (29.38 ± 4.66) min vs. (40.14 ± 4.57) min, (66.82 ± 15.80) min vs. (89.35 ± 24.78) min, (11.24 ± 4.89) d vs. (14.56 ± 6.74) d, there were statistical differences ( P<0.05). The incidence of postoperative complications in the experimental group was lower than that in the control group: 12.00% (6/50) vs. 28.00% (14/50), there was statistical difference ( P<0.05). Conclusions:The application of rSO 2 combined with neurophysiological blood pressure monitoring in CEA of patients with carotid artery stenosis and coronary heart disease has a good effect, which has brain protection and myocardial protection, can shorten the recovery time of anesthesia and hospitalization time, and reduce the incidence of postoperative complications.
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@#Objective To investigate the brain protective effects of ropivacaine on cerebral ischemia-reperfusion injury in rats and its influence on cyclic adenosine-adenosine synthase/stimulator of interferon gene (cGAS/STING) pathway.Methods SD rats were randomly divided into sham operation group,model group,low-dose ropivacaine group (0.075 mg/kg),medium-dose ropivacaine group(0.15 mg/kg),and high-dose ropivacaine group (0.30 mg/kg),positive control group(nimodipine,5 mg/kg),with 8 rats in each group,except for the sham operation group,the rats in the other groups were given suture method to construct a rat model of cerebral ischemia and reperfusion,and the neurological deficit scores of the rats in each group on the 0th,3rd,and 7th day of administration were measured;hematoxylin-eosin staining (HE) was used to detect the pathological changes of brain tissues in each group;2、3、5-Triphenyte-trazoliumchloride(TTC) method was used to detect cerebral infarction area; enzyme-linked immunosorbent (ELISA) was used to detect the levels of tumor necrosis factor(TNF-α),interleukin(IL-1β),IL-6,superoxide dismutase(SOD) and malondialdehyde (MDA) in brain tissue; qRT-PCR was used to detect the level of mitochondrial DNA (mtDNA);Western blotting was used to detect the expression of cGAS/STING pathway protein in the brain tissues.Results Compared with the sham operation group,the brain tissue of the rats in the model group was seriously damaged,cerebral infarction area,the nerve defect score,TNF-α,IL-1β,IL-6,MDA levels in brain tissue,Cytoplasmic mtDNA level,cGAS and STING proteins expression were significantly increased,and the SOD levels in brain tissue were significantly reduced (P<0.05);compared with those in the model group,the brain tissue damage of the rats in the ropivacaine groups and the positive control group was relieved,cerebral infarction area,the nerve defect score,TNF-α,IL-1β,IL-6,MDA levels in brain tissue,Cytoplasmic mtDNA level,cGAS,STING proteins expression were significantly reduced,and SOD levels in brain tissue were significantly increased (P<0.05). Conclusion Ropivacaine has a certain protective effect on cerebral ischemia-reperfusion injury,and can inhibit cGAS/STING pathway.
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To compare the neuroprotective and anti-dementia pharmacological effects of chiral oxiracetam, glutamate and calcium ions were used to establish neuronal injury models in vitro, and the protective effects of chiral oxiracetam on primary neurons were assayed by MTT. Permanent bilateral common carotid artery occlusion (2-VO)-induced rats were randomly divided into sham group, model group, galantamine 3 mg‧kg-1 group, oxiracetam groups (30, 100 and 200 mg‧kg-1), S-oxiracetam groups (30, 100 and 200 mg‧kg-1) and R-oxiracetam 200 mg‧kg-1 group. The animal experiments in the present study were performed in accordance with the Ethical Guidelines of the Laboratory Animal Welfare Ethical Committee of Peking Union Medical College. Morris water maze and step-down test were applied to evaluate the cognitive dysfunction induced by cerebral hypoperfusion in rats. Oxiracetam, S-oxiracetam and R-oxiracetam exerted protective effects on primary neuronal damage caused by various stimuli, and oxiracetam and S-oxiracetam showed better neuro-protective effects. Morris water maze and step-down results showed that oxiracetam, S-oxiracetam and R-oxiracetam improved the cognition of 2-VO rats. In summary, S-oxiracetam exerted a better neuro-protective effect than oxiracetam and R-oxiracetam.
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Stroke is the most common disease of the central nervous system, with high disability and mortality, which seriously affects the quality of life of patients and causes a huge disease burden. However, the overall treatment effect is still unsatisfied at present. Myeloperoxidase (MPO), a kind of peroxidase derived from neutrophils, may play an important role in stroke development through many ways, and has great potential in early diagnosis, clinical treatment and prognosis evaluation of stroke. This article reviews the research progress of MPO in stroke, aiming to provide new ideas for better diagnosis and treatment of stroke in clinic.
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@#Objective To investigate the protective effect of complement C5a receptor 1 (C5aR1) antagonist on cerebral ischemia-reperfusion （CIR） in mice.Method Mice were randomly divided into sham operation group,cerebral ischemia-reperfusion group (model group) and C5aR1 antagonist （PMX53）group.At 3 h before,24 h after and 48 h after cerebral reperfusion timepoint,the PMX53 group was given with PMX53,the sham group and the model group were given same volume of saline by intraperitoneall injection.At 72 h after cerebral reperfusion timepoint,neurological deficits score of mice were evaluated by the modified Longa method,the infarcted brain volume was calculated after TTC staining,the cerebral tissue water content of the ischemic hemisphere was calculated by dry and wet weight method,the mRNA expression of inflammatory factors in the ischemic hemisphere were detected by real-time PCR,and the relative expression of ZO-1 in cerebral tissue of the ischemic hemisphere was calculated by Western blot.Results At 72 h after cerebral reperfusion,compared with the model group,neurological deficits function score,cerebral water content,cerebral infarction volume and inflammatory cytokines (IL-1β,TNF-α) were significantly decreased in the PMX53 group (all P<0.05),ZO-1 expression was significantly higher in the PMX53 group (P<0.05).Conclusion C5aR1 antagonist can improve the neurological function score after CIR,reduce the volume of cerebral infarction,reduce the degree of cerebral edema and inflammatory response,and has a protective effect on the blood-brain barrier.
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Objective:To investigate the effects of different doses of dexmedetomidine on intestinal mucosal barrier function, cognitive function and brain protection in patients undergoing heart valve replacement.Methods:The clinical data of 135 patients with heart valve replacement from April 2019 to April 2020 in the First Affiliated Hospital of Chengdu Medical College were retrospectively analyzed. Among them, 54 patients received low-dose of dexmedetomidine after induction of anesthesia (low-dose group), 38 patients received high-dose of dexmedetomidine (high-dose group), and 43 patients did not use dexmedetomidine (control group). Before surgery (T 1), 1 h after surgery (T 2), end of surgery (T 3) and 72 h after surgery (T 4), the levels of intestinal mucosal barrier function indexes D-lactate and diamine oxidase (DAO) were detected by spectrophotometry, the levels of brain injury indexes central nervous system specific protein (S100β) and neuron-specific enolase (NSE) were detected by double antibody sandwich enzyme-linked immunosorbent assay; before surgery and 3 d after surgery, the cognitive function was assessed by the mini-mental state examination (MMSE) and Montreal cognitive assessment (MoCA) scale before and 3 days after surgery. Result:There was no statistical difference in T 1, T 2 and T 4 D-lactic acid among 3 groups ( P>0.05); the T 3 D-lactic acid in low-dose group was significantly lower than that in high-dose group and the control group: (7.87 ± 1.59) mg/L vs. (8.99 ± 1.82) and (9.32 ± 1.74) mg/L, the high-dose group was significantly lower than the control group, and there were statistical differences ( P<0.05). There was no statistical difference in T 1 and T 2 DAO among 3 groups ( P>0.05); the T 3 and T 4 DAO in low-dose group was significantly lower than that in high-dose group and control group: (2.77 ± 0.23) kU/L vs. (3.58 ± 0.25) and (4.30 ± 0.26) kU/L, (2.08 ± 0.25) kU/L vs. (2.40 ± 0.20) and (2.71 ± 0.23) kU/L, the high-dose group was significantly lower than the control group, and there were statistical differences ( P<0.05). There were no statistical differences in MMSE score and MoCA score before surgery among 3 groups ( P>0.05); the MMSE score and MoCA score 3 d after surgery in low-dose group were significantly higher than those in high-dose group and control group: (22.76 ± 0.54) scores vs. (21.41 ± 0.47) and (20.21 ± 0.43) scores, (24.90 ± 0.51) scores vs. (24.01 ± 0.48) and (23.12 ± 0.49) scores, the high-dose group was significantly higher than the control group, and there were statistical differences ( P<0.05). There was no statistical difference in T 1, T 2 and T 4 S100β among 3 groups ( P>0.05); the T 3 S100β in low-dose group was significantly lower than that in high-dose group and control group: (4.09 ± 2.01) μg/L vs. (5.48 ± 1.10) and (6.10 ± 1.58) μg/L, and there were statistical differences ( P<0.05). There was no statistical difference in T 1 and T 4 NSE among 3 groups ( P>0.05); the T 2 and T 3 NSE in low-dose group was significantly lower than that in high-dose group and control group: (17.20 ± 4.13) μg/L vs. (20.29 ± 3.77) and (22.35 ± 3.80) μg/L, (19.40 ± 3.92) μg/L vs. (23.46 ± 5.26) and (25.18 ± 5.32) μg/L, and there were statistical differences ( P<0.05). Conclusions:Administration of 0.5 μg/(kg·h) dexmedetomidine during heart valve replacement under cardiopulmonary bypass can reduce intestinal mucosal damage, protect brain against injury in a certain degree, and improve cognitive function.
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Objective:To introduce the early results of total aortic arch replacement (TAA) without cardiopulmonary bypass (CPB) and without interruption of cerebral blood supply, using the technique of arch branches preferential reconstruction and whole brain perfusion for brain protection.Methods:Between June 2020 and March 2021, a total of 9 Stanford type A aortic dissection patients we performed total arch replacement by using the technique of arch branches preferential reconstruction and whole brain perfusion without cardiopulmonary bypass and without interruption of blood supply to the brain. The method of this reconstruction technique is as follows: A 24F aortic cannula was inserted into the true lumen at the root of the transverse innominate artery (IA) to connect one end of the artery for cardiopulmonary bypass. The access was connected to 14F artery via Y-connector and inserted into IA cavity to maintain blood supply to brain. Without cardiopulmonary bypass, the 10 mm branch of the four branch artificial blood vessel was anastomosed with the innominate artery IA. The perfusion collateral was connected to the second end of the artery of CPB (single pump and double tubes) to continue to supply blood for IA. The left common carotid artery (LCA) and left subclavian artery (LSCA) were reconstructed by the same method. When IA and LCA were anastomosed, the distal blood supply was not interrupted. After the three branches of the aortic arch were anastomosed, we started to turn the machine, then cooled down and blocked the ascending aorta to further complete the operation of the aortic root and arch. During the period of lower body circulatory arrest, the whole brain was perfused with low flow.Results:No intraoperative death or perioperative complications occurred in all patients, and they were discharged smoothly. The cardiopulmonary bypass time was (192.4±58.1) min, the aortic clamping time was (128.3±52.4) min, the lower body circulatory arrest time was (29.1±1.3) min, and the postoperative awake time was (8.2±3.7) h.Conclusion:Off-pump arch branches preferential reconstruction can provide physiological whole brain perfusion, shorten the cardiopulmonary bypass time and aortic occlusion time, and the operation is safe and effective.
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Aim To explore the regulatory effect of Danggui-chuanxiong herb pair (GX) on JAK-STAT signaling pathway in rats with cerebral ischemia/reper-fusion injury (I/R). Methods The I/R injury rat model was constructed by modified suture occlusion method. After 24 hours of perfusion, Zea Longa scoring method was used to score the neurological function, TTC staining to detect the cerebral infarct volume of rats, HE staining to observe the pathological changes of brain tissues, the biochemical method to determine the MDA, SOD, GSH-Px expression, ELISA to detect the expression of NF-κB, VEGF, ICAM-1 and PAH in brain tissues, and immunohistochemical method to detect JAK2, p-STAT3, AKT And ERK1/2 expression of the brain tissue ischemic penumbra area. Results Compared with sham group, model rats had severe neurological damage, larger cerebral infarction, necrosis, edema, inflammation, disorder of nerve cell arrangement, abnormal cell enlargement, vacuole-like changes, neuron reduction and other pathologies in brain tissues. The expression JeveJs of MDA, NF-κB, VEGF, PAI-1 and ICAM-1 in brain tissues of model group significantly increased, and the expression levels of GSH-Px and SOD were significantly reduced. Compared with model group, the neurological scores of rats in GX
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AIM: To investigate the protective effect of ginsenoside Rb1 on brain through Cav-1 in mice with cerebral ischemia-reperfusion injury. METHODS: One hundred and twenty C57/B6 mice were randomly divided into sham operation group, model group, model + ginsenoside Rb1 group, ginsenoside Rb1+ Cav-1 siRNA group, ginsenoside Rb1+siNC group, 24 in each group. The model of cerebral ischemia-reperfusion injury in mice was established by middle cerebral artery occlusion (MCAO). The ginsenoside Rb1 group received intraperitoneally injection of ginsenoside Rb1 (40 mg/kg); the sham operation group and model group were intraperitoneally injected with an equal amount of physiological saline immediately after modeling. For the ginsenoside Rb1+ cav-1 siRNA group and the ginsenoside Rb1+siNC group, cav-1 siRNA and siNC were injected into the lateral ventricle 24 h before molding, respectively, and the other operations were the same as the ginsenoside Rb1 group. The neurobehavioral scores of the mice in each group were measured at 24 h after reperfusion, and the water content of brain tissue, cerebral infarction volume, Cav-1 mRNA and Cav-1, Bcl-2 and Bax protein expressions in the cerebral cortex penumbra were measured in each group. RESULTS:Compared with the sham operation group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the model group were significantly increased (P<0.05), and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly decreased (P<0.05). Compared with the model group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the ginsenoside Rb1 group were significantly decreased, and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly increased (P<0.05). Compared with the ginsenoside Rb1 group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the ginsenoside Rb1 + cav-1 siRNA group were significantly increased, and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly decreased (P<0.05). CONCLUSION: Ginsenoside Rb1 can protects brain for mice with cerebral ischemia-reperfusion injury. After Cav-1 siRNA decreased the expression of Cav-1 protein in the brain tissue of mice, it significantly reverses the cerebral protective effect of ginsenoside Rb1, indicating that Cav-1 protein mediated the cerebral protective effect of ginsenoside Rb1 on cerebral ischemia reperfusion injury mice.
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Objective To summarize the brain protection application experiences of combined internal and external blood shunt technologies for the in-situ three-fenestration revascularization of aortic arch.Methods From Feb 2017 to Jun 2018,8 patients with aortic arch leisons were treated by the in-situ three-fenestration techniques,including 3 aortic dissection,2 aortic aneurysm,3 postoperative TEVAR patients.We adopt the method of internal and external blood shunt technologies for brain protection using the vascular sheath for fenestration combined with carotid shunt tube skills,and using TCD to monitor the blood flow of brain.Results All operations completed successfully,and TCD showed no significant cerebral ischemia when aortic stent was used to cover the three branches of the aorta.The mean time of brain protection was (17.62 ± 6.87) minutes.One patient developed transient cerebral ischemia after surgery,and another one developed cerebral infarction.Conclusions The brain protection strategy of internal bypass combined with external converter technology maintain the brain blood flow,while is simple and feasible,it cannot completely avoid neurological complications.
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OBJECTIVE：To in vestigate the effects of dexmedetomidine （Dex）on SIRT 1/Akt/GSK3β/β-catenin signaling pathway in cerebral injury of sepsis model rats ，and explore the mechanism of its protecitve effect on cerebral injury. METHODS ： A total of 80 male SD rats were randomly divided into sham operation group （Sham group ），sepsis group （CLP group ），CLP+Dex group（10 μg/kg Dex），CLP+Dex+Sirtinol group （10 μg/kg Dex+2 μL/100 g SIRT 1 inhibitor sirtinol ），with 20 mice in each group. Two hours before modeling ，CLP+Dex+Sirtinol group was injected with sirtinol via lateral ventricle. Sepsis model was induced by cecal ligation and perforation in each group （in sham group ，only operation was performed but no ligation was performed）. At 0，3，6 h after modeling ，CLP+Dex group and CLP+Dex+Sirtinol group were given Dex （10 μg/kg） intraperitoneally，Sham group and CLP group were given constant volume of normal saline intraperitoneally. Cerebral tissue water content，Evans blue （EB）content，apoptosis in cerebral cortex ，the levels of IL- 1β and TNF-α in cerebral tissue as well as the protein expression of SIRT 1，p-Akt，p-GSK3β and β-catenin in hippocampus were detected 24 h after last medication. RESULTS ： Compared with Sham group ，cerebral tissue water content ，EB content ，the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were increased significantly（P＜0.05），while the protein expression of SIRT 1， p-Akt，p-GSK3β and β-catenin in hippocampus were decreased significantly （P＜0.05）. Compared with CLP group ，cerebral tissue water content ，EB content ，the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were decreased significantly in CLP+Dex group （P＜0.05），while the protein expression of SIRT 1，p-Akt，p-GSK3β and β-catenin in hippocampus were increased significantly （P＜0.05）. Sirtinol could significantly reverse the above-mentioned cerebral protection and factor regulation effects of Dex （P＜0.05）. CONCLUSIONS ：Dex can protect the cerebral tissue of sepsis model rats，which may play an anti-inflammatory and anti-apoptotic role by activating SIRT 1/Akt/GSK3β/β-catenin signaling pathway ，so as to reduce cerebral edema ，protect blood-brain barrier and reduce cerebral injury.
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Objective Few studies are reported on the protective effect of valproic acid (VPA) against traumatic brain injury (TBI) by down-regulating the protein expressions of matrix metalloproteinase-9 (MMP-9) and aquaporin-4 (AQP-4) in the brain tissue. This study aimed to investigate the neuroprotective effects of different doses of VPA against TBI in experimental rats. Methods We randomly divided 100 adult male rats into five groups of equal number, sham operation, TBI model, and low- (30 mg), medium- (150 mg) and high-dose (300 mg) VPA treatment. At 1, 3, 7 and 14 days after modeling by controlled cortex impact, we obtained the modified Neurological Severity Scores (mNSS), measured the VPA concentration in the venous blood, and then killed the rats and harvested the brain tissue for determination of the water content using the dry-wet method and the expressions of MMP-9 and AQP-4 by Western blot and immunohistochemistry. Results At 1, 3, 7 and 14 days after modeling, the mNSSs in the high-dose VPA group were 4.6 ± 1.3, 3.8 ± 1.3, 3.0 ± 0.7 and 1.8 ± 0.8, respectively, significantly lower than 8.4 ± 0.9, 7.0 ± 0.7, 5.8 ± 1.0 and 4.5 ± 1.3 in the TBI group (P < 0.05), decreasing in a time-dependent manner, with statistically significant difference between any two dose groups (P < 0.05). At 1, 3 and 7 days, the water contents in the brain tissue were (76.2 ± 0.7)%, (76.9 ± 1.7)% and (73.9 ± 1.3)% in the high-dose VPA group, significantly lower than (79.6 ± 0.8)%, (82.6 ± 0.8)% and (78.6 ± 0.7)% in the TBI group (P < 0.05), also decreasing in a time-dependent manner, with statistically significant difference between any two dose groups (P < 0.05). At 1 and 3 days, the expressions of MMP-9 and AQP-4 in the brain tissue were markedly down-regulated in the VPA groups in a dose-dependent manner as compared with those in the TBI group (P < 0.05), with statistically significant difference between any two dose groups (P < 0.05), and meanwhile immunohistochemistry showed large numbers of cells with positive expressions of MMP-9 and AQP-4, which were reduced with the increased dose of VPA. Conclusion VPA has a neuroprotective effect against TBI in rats by inhibiting the expressions of MMP-9 and AQP-4 proteins in the brain tissue and alleviating brain edema. Within the range of the doses studied, higher-dose VPA produces a better effect.
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Objective Mild hypothermia (MHT) can effectively protect the brain in traumatic brain injury (TBI). This study was to investigate the effects of MHT on the calmodulin (CAM) expression and brain edema in the rat model of TBI. Methods Ninety adult SD rats were randomly divided into a sham operation, a normal temperature and an MHT group of equal number. Immediately after TBI, the rats of the MHT group maintained at a rectal temperature of (32 ± 0.5) °C for 6 hours. Modified neurological severity scores (mNSS) were obtained from 6 rats in each group at 1, 3, 5 and 7 days after modeling, and the rest of the animals subjected to brain MRI at 6, 12, 24 and 48 hours and then killed for determination of the CAM gene transcription and protein expression in the brain tissue by real-time PCR, immunohistochemistry and Western blot. Results The mNSSs were significantly higher in the MHT and normal temperature groups than in the sham operation control (P < 0.05) at all time points, neurological severity markedly decreased in the MHT group compared with the normal temperature group (P < 0.05). At 6, 12, 24 and 48 hours, the expression of CAM mRNA was remarkably down-regulated in the MHT group (1.83 ± 0.19, 1.72 ± 0.12, 1.59 ± 0.06 and 1.60 ± 0.07) in comparison with the normal temperature group (2.76 ± 0.25, 2.49 ± 0.18, 2.04 ± 0.14 and 1.65 ± 0.09) (P < 0.05), even lower in the MHT than in the normal temperature group (P < 0.05), but higher in both of the two groups than in the sham operation group (P < 0.05). At 6, 12, 24 and 48 hours, the volume of brain edema was significantly reduced in the MHT group ([32.14 ± 4.52], [36.52 ± 4.10], [42.10 ± 4.38] and [46.25 ± 5.02] mm3) as compared with the normal temperature group ([48.56 ± 5.35], [53.13 ± 6.31], [59.23 ± 6.82] and [62.35 ± 7.25] mm3) (P < 0.05). Conclusion Mild hypothermia can improve the neurological function and reduce the CAM expression and brain edema in the brain tissue of rats with traumatic brain injury, which may be related to the neuroprotective effect of mild hypothermia.
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Aim To investigate the effects of sevoflurane postconditioning on oxidative stress and the expression of silent information regulation (SIRT1) and peroxisome proliferator-activated receptor γ coactivator la (PGC-1α) in hippocampus of rats subjected to hemorrhagic shock and resuscitation. Methods Male SD rats were randomly divided into sham surgery group (Sham group), shock and resuscitation group (Shock group) and 2.4% sevoflurane postconditioning group (Sevo group). The rats in Sevo group were inhaled 2.4% sevoflurane when received resuscitation after hemorrhagic shock, while rats in Sham and Shock group were treated with 95% O2 and 5% CO2 in the corresponding period. MAP and arterial blood gases were measured at TO (start bleeding), Tl (30 min after bleeding),T2 (start resuscitation), and T3 (30 min after resuscitation). After 24h of surgery,rats with successful model were chosen for the detection of various indexes. The content of malonaldehyde (MDA) in hippocampus and the activity of superoxide dismutase (SOD) in mitochondria isolated from hippocampal tissue were detected. Western blot was used to analyze the protein relative expression levels of SIRT1 and PGC-la in hippocampus. Results Compared with Sham group, the content of MDA increased, the activity of SOD decreased, and the expression of SIRT1 and PGC-1α a increased in Shock group (P < 0. 05). Compared with Shock group, the content of MDA decreased, the activity of SOD increased, and the expression of SIRT1 and PGC-1α increased in Sevo group (P < 0. 05). Conclusions Sevoflurane postconditioning can alleviate oxidative stress in hippocampus of a model rat of hemorrhagic shock and resuscitation, which may be correlated with the up-regulation of the protein relative expression levels of SIRT1 and PGC-1α.
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Objective To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) signaling pathway in the expression of aquaporin 4 (AQP4) in brain tissue of rats with cardiopulmonary resuscitation (CPR) during mild hypothermia. Methods Forty-eight healthy male Sprague-Dawley (SD) rats were divided into sham operation group, normal temperature group and mild hypothermia group according to random number table method, with 16 in each group. The rat model of cardiac arrest-cardiopulmonary resuscitation (CPR) was established by asphyxia method. The sham operation group only experienced venous catheterization and tracheal intubation. The mild hypothermia group was treated with hypothermia 0.5 hours after restore of spontaneous circulation (ROSC, maintaining esophageal temperature at 32-34 ℃); the normal temperature group was treated at room temperature after ROSC (maintaining esophageal temperature at 36-38 ℃). Brain tissue was harvested at 6 hours after ROSC, and histopathological changes were observed by hematoxylin-eosin (HE) staining. The water content of brain tissue was determined by dry-wet specific gravity method. The protein expressions of phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK), p38MAPK and AQP4 in brain tissue were determined by Western Blot. Results Compared with the sham operation group, the nerve cells in the normal temperature group were reduced in size, cytoplasmic loosening, nuclear pyknosis, and in apoptotic body formation, water content of brain tissue was significantly increased [(83.64±2.53)% vs. (77.95±0.94)%, P < 0.05], the protein expressions of p-p38MAPK, p38MAPK, AQP4 were significantly increased (p38MAPK/β- actin: 1.010±0.217 vs. 0.427±0.090, p-p38MAPK/p38MAPK: 0.451±0.172 vs. 0.191±0.141, AQP4/β- actin: 3.129±0.754 vs. 1.598±0.464, all P < 0.05). Compared with the normal temperature group, the degree of necrosis of nerve cells in the mild hypothermia group was reduced, the water content of brain tissue was significantly decreased [(80.49±2.05)% vs. (83.64±2.53)%, P < 0.05], the protein expression of p38MAPK, p-p38MAPK and AQP4 in brain tissue were significantly decreased (p38MAPK/β- actin: 0.590±0.162 vs. 1.010±0.217, p-p38MAPK/p38MAPK: 0.298±0.076 vs. 0.451±0.172, AQP4/β- actin: 2.061±0.340 vs. 3.129±0.754, all P < 0.05). Conclusion Mild hypothermia may regulate the expression of AQP4 in brain tissue of CPR rats through p38MAPK signaling pathway, and reduce brain edema, thereby exerting brain protection.
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Objective To explore the differences in brain protection between anterograde cerebral perfusion( ACP) and retrograde cerebral perfusion( RCP) in aortic arch surgery. Methods Aortic arch circulatory surgery, ACP and RCP tech-niques were searched at the Cochrane Library, PubMed, EMBASE, Wanfang Database and the Chinese Biomedical Database from January 2013 to December 2018. Cohort studies were then performed with early postoperative death, transient neurological dysfunction(TND), stroke, and transient ischemic attack(TIA). For each study, data on endpoints in the ACP and RCP groups were used to generate risk ratios( RR) and 95％ confidence intervals( CI) . The funnel chart was used to test publication bias. Results A total of 6692 patients were enrolled in 12 studies, of which 3902 patients received low-temperature circula-tory arrest plus ACP, and 2790 patients received low-temperature circulatory arrest plus RCP. Summary analysis showed that the early postoperative death(RR=0. 83, 95％CI=0. 51-1. 35,P=0. 46), stroke(RR=1. 09, 95％CI=0. 91-1. 31, P=0.33),transient neurological dysfunction(RR=0.81, 95％CI=0.17-3.91,P=0.80) and transient ischemic attack(RR=1.00,95％CI=0.74-1.34,P=1.00) in both groups were no significant differences(all P>0.05). Conclusion There are no significant differences in postoperative mortality and neurological dysfunction between antegrade cerebral perfusion and retrograde cerebral perfusion in the aortic arch surgery. Combined with hypothermic circulatory arrest, it can be selected ac-cording to the actual situation of aortic arch surgery.
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Objective@#To explore the differences in brain protection between anterograde cerebral perfusion(ACP) and retrograde cerebral perfusion(RCP) in aortic arch surgery.@*Methods@#Aortic arch circulatory surgery, ACP and RCP techniques were searched at the Cochrane Library, PubMed, EMBASE, Wanfang Database and the Chinese Biomedical Database from January 2013 to December 2018. Cohort studies were then performed with early postoperative death, transient neurological dysfunction(TND), stroke, and transient ischemic attack(TIA). For each study, data on endpoints in the ACP and RCP groups were used to generate risk ratios(RR) and 95% confidence intervals(CI). The funnel chart was used to test publication bias.@*Results@#A total of 6 692 patients were enrolled in 12 studies, of which 3 902 patients received low-temperature circulatory arrest plus ACP, and 2 790 patients received low-temperature circulatory arrest plus RCP. Summary analysis showed that the early postoperative death(RR=0.83, 95%CI=0.51-1.35, P=0.46), stroke(RR=1.09, 95%CI=0.91-1.31, P=0.33), transient neurological dysfunction(RR=0.81, 95%CI=0.17-3.91, P=0.80) and transient ischemic attack(RR=1.00, 95%CI=0.74-1.34, P=1.00) in both groups were no significant differences(all P>0.05).@*Conclusion@#There are no significant differences in postoperative mortality and neurological dysfunction between antegrade cerebral perfusion and retrograde cerebral perfusion in the aortic arch surgery. Combined with hypothermic circulatory arrest, it can be selected according to the actual situation of aortic arch surgery.
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Objective To explore how the bundle comprehensive brain protection treatments affects cerebral oxygen metabolism,endothelial cell function and intracranial pressure of patients with severe craniocerebral trauma.Methods One hundred and twenty patients with severe craniocerebral trauma were selected from January 2014 to November 2016 in our hospital.The patients were randomly divided into control group and observation group (n=60).Patients from the control group were given normal treatment;whilst patients from the observation group were additionally treated with bundle comprehensive brain protection treatments.The cerebral oxygen metabolism levels (jugular bulb venous oxygen saturation [SjVO2],cerebral extraction of oxygen [CEO2] and arteriovenous oxygen difference [AVDO2]),endothelin (ET) level and intracranial pressure (ICP) were calculated and compared before and after treatment.Results The levels of SjVO2,CEO2 and AVDO2,and ET and ICP levels showed no significant differences between the obvseration group and control group before treatment (P＞0.05).After treatment,the levels of SjVO2,CEO2 and AVDO2 in the observation group were significantly higher than those in the control group (P＜0.05);as compared with those in the control group,the ET and ICP levels in the observation group were significantly decreased (P＜0.05).Conclusion The bundle comprehensive brain protection treatments could improve cerebral oxygen metabolism and endothelial function,and decrease the ET and ICP levels of patients with severe craniocerebral trauma,which has important value in clinical practice.
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Objective To study the protective effect of Xingnaojing combined with alprostadil on brain after acute ischemic stroke in rats.MethodsSixty patients with acute ischemic stroke were enrolled in zhejiang xin'an international hospital from March 2014 to March 2016.They were randomly divided into control group and treatment group, 30 cases in each group.The control group received conventional treatment plus alprostadil, the treatment group in the control group based on the combination of Xingnaojing treatment.Two groups of patients after treatment, are given nursing intervention, such as routine diet guidance, nutritional support, health education.The levels of serum oxidative stress (MDA), vascular endothelial growth factor (VEGF) and vascular endothelial growth factor (VEGF) were compared between the two groups before and after treatment.The levels of cerebral blood flow (CBFV) were recorded before and after treatment Observe the adverse reactions during treatment.ResultsAfter 14 days of treatment, the NIHSS score of the treatment group was lower than that of the control group and the ADL score was higher than that of the control group.The difference between the two groups was statistically significant (P<0.05).Before treatment, the oxidative stress indexes MDA and Hcy were no significant difference between the two groups.After treatment, the oxidative stress indexes MDA and Hcy were lower than the control group(P<0.05).Before treatment, the levels of VEGF and CBFV in the two groups were no significant difference between the two groups.After treatment, the levels of VEGF and CBFV in the two groups were significantly higher than those in the control group (P<0.05).The adverse reaction rate between the 2 groups was similar, and there was no significant adverse reaction, there was no significant difference between the two groups.ConclusionXingnaojing combined with alprostadil has a certain clinical effect on acute ischemic stroke, and has a good protective effect on brain tissue after reperfusion.
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In recent years, remote ischemic preconditioning is found as a novel way to protect the brain, which may be achieved through nerve pathways, humoral factors or nerve-humoral interaction. The molecular mechanisms for the protection might be related to mitochondria ATP-sensitive potassium channel, mitogen-activated protection kinase, mammalian target of rapamycin, including nitric oxide synthase and cannabinoid receptors. The aim of this review is to explain the mechanism of action of remote ischemic preconditioning on brain protection, as well as the possible direction of clinical application.