Objective To evaluate the effects of dexmedetomidine (DEX) on cell apoptosis induced by endoplasmic reticulum stress and c-Jun N-terminal kinase (JNK) pathway during one-lung ventilation (OLV) in rats.Methods Sixty male Sprague-Dawley rats were randomly allocated into 6 groups (n =10 each):sham operation group (Sham group),OLV group,OLV + atipamezole (α2 receptor antagonist) group (AD group),OLV + atipamezole + DEX group (DEX+AD group),OLV + low-dose DEX group (DEX-L group) and OLV + high-dose DEX group (DEX-H group).The animals were anesthetized with 10％ chloral hydrate 4.5 ml/kg,tracheostomized and mechanically ventilated.Bilateral lungs were ventilated for 2.5 h in Sham group.The right lung was ventilated for 2.0 h followed by 0.5 h two-lung ventilation in OLV group.In DEX-L and DEX-H groups,DEX was infused intravenously for 1 h at a rate of 2.5 μg · kg-1 · h-1 and 5.0 μg · kg-1 · h-1,respectively,starting from 1 h prior to OLV.Atipamezole 250 μg/kg was injected intravenously at 1 h prior to OLV in AD group.Atipamezole 250 μg/kg was injected intravenously at the onset of DEX infusion (5.0 μg · kg-1 · h-1) in DEX+AD group.The rats were sacrificed and left lungs were removed for determination of weight to dry lung weight ratio (W/D),cell apoptosis in lung tissues (by TUNEL),and expression of glucose-regulated protein 78 (GRP78) mRNA and protein,JNK mRNA and phosphorylated JNK (p-JNK) protein (by RT-PCR and Western blot).Pathological changes of lungs were examined and the injured alveolus rate (IAR) was counted under light microscope.The changes in ultrastructure of lung tissues were observed under transmission electron microscope.Apoptosis index (AI) was calculated.Results W/D,AI and IAR were significantly higher in OLV,AD and DEX+AD group than in Sham group,while lower in DEX-L and DEX-H groups than in OLV,AD and DEX+AD groups.The pathological changes of the structure of lung tissues were observed in OLV,AD and DEX+AD groups,while the pathological changes were significantly alleviated in DEX-L and DEX-H groups.In OLV,AD and DEX + AD groups,there was apoptosis in lots of pulmonary vascular endothelial cells and alveolar epithelial cells,while cell apoptosis was significantly reduced after administration of DEX.The expression of GRP78 mRNA and protein,JNK mRNA and p-JNK protein was significantly higher in OLV,AD and DEX+AD groups than in Sham group,and lower in DEX-L and DEX-H groups than in OLV,AD and DEX +AD groups.Conclusion DEX pretreatment can protect lungs during OLV,and inhibited JNK signaling pathway and reduced cell apoptosis induced by endoplasmic reticulum stress may be involved in the mechanism.

Chondrosarcoma ; Humans ; Laryngeal Neoplasms ; Male ; Middle Aged

Objective To explore the effects and mechanisms of anti-endothelial cell antibody (AECA )in the alveolar cell apoptosis of the emphysema rats induced by smoking,and to discuss the intervention effects of methylprednisolone.Methods 39 male Sprague-Dawley rats were randomly divided into normal control group,model group,and intervention group,with 13 rats in each group.Emphysema models were established in the latter two groups.After exposing to cigarette smoking for one month,methylprednisolone injected intraperitoneally in the intervention group(10 mg/kg,1 time/d),6d/week.On the 90th day,inferiora vena cave blood samples were collected and all rats were sacrificed.The levels of AECA were detected in bronchial alveolar lavage fluid (BALF )and serum,respectively.Pathological changes were observed in lung tissues stained by hematoxylin eosin, quantitative determination of lung average mean linear intercept(MLI)and mean alveolar number(MAN)were preformed. Results Compared with normal group and intervention group,the levels of AECA in BALF and serum,MLI in the model group were higher(P<0.05 ),but the levels of MAN was lower (P<0.05);There is a positive correlation between AECA in BALF and MLI of rats(r=0.821,P<0.05),a negative correlation between AECA in BALF and MAN(r=-0.894,P<0.05.Conclusions ACEA may enroll the pathogenesis of emphysema in rats induced by smoking and related with the severity.Methylprednisolone may inhibit the formation of emphysema by reducing the expression level of AECA in airway.

Objective To evaluate the effect of sevoflurane on unfolded protein response-related cell apoptosis during acute lung injury in rats undergoing cardiopulmonary bypass ( CPB) . Methods For-ty-eight clean-grade healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 250-300 g, were allocated into 3 groups ( n=16 each) using a random number table method: sham operation group ( Sham group) , CPB group and sevoflurane group ( Sev group) . Left common carotid artery and right internal jugu-lar vein were only cannulated in group Sham. After establishing CPB, the flow rate was gradually adjusted to the maximum (100 ml·kg-1·min-1) and maintained for 60 min in group CPB. Two percent sevoflurane was inhaled for 30 min, and 15 min later the model of CPB was established in Sev group. Rats were sacri-ficed at 1 h after the end of CPB, lungs were removed and lung tissues were obtained. The pathological changes and ultrastructure of lung tissues were examined with a light microscope and with an electron micro-scope, respectively. The wet to dry weight ratio ( W∕D ratio) , apoptosis in lung cells ( by TUNEL assay) , expression of glucose-regulated protein 78 ( GRP78) , CCAAT∕enhancer-binding protein homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and caspase-12 mRNA was determined by real-time polymerase chain reaction. The expression of GRP78, CHOP, phosphorylated JNK (p-JNK) and caspase-12 was de-tected by Western blot. The index of quantitative assessment of histologic lung injury ( IQA) was measured, and apoptotic index ( AI) was calculated. Results Compared with Sham group, the W∕D ratio, IQA and AI were significantly increased, the expression of GRP78, CHOP, JNK and caspase-12 was up-regulated ( P<0. 05) , and the pathological changes of lung tissues were accentuated in CPB group. Compared with CPB group, the W∕D ratio, IQA and AI were significantly decreased, the expression of GRP78, CHOP, JNK and caspase-12 was down-regulated ( P<0. 05) , and the pathological changes of lung tissues were sig-nificantly attenuated in Sev group. Conclusion The mechanism by which sevoflurane mitigates acute lung injury induced by CPB is related to inhibiting unfolded protein response related cell apoptosis in lung tissues of rats.

Objective: To evaluate the effect of dexmedetomidine on pyroptosis during lung ischemia-reperfusion (I/R) in rats. Methods: Adult male Sprague-Dawley rats, weighing 250-320 g, were used in this study.The model of isolated lung perfusion was established using an IL-2 Isolated Perfused Rat or Guinea Pig Lung System after the rats were anesthetized.Thirty lungs in which an ex vivo lung perfusion model was successfully established were divided into 3 groups (n=10 each) by a random number table method: control group (C group), I/R group and dexmedetomidine group (DEX group). The lungs were continuously perfused with K-H solution for 150 min in C group.After 15 min of perfusion, lungs were subjected to 60-min suspension of ventilation and perfusion, followed by 75 min of reperfusion and ventilation to establish the model of lung I/R injury in I/R and DEX groups.In DEX group, dexmedetomidine 10 nmol/L was added to K-H solution at the beginning of reperfusion.Lung tissues were obtained for determination of wet/dry weight ratio (W/D ratio) and for examination of pathological changes (with a light microscope) and ultrastructure (using an electron microscope), and the alveolar damage rate (IAR) was calculated.The expression of pyroptosis-related factors including NOD-like receptor family protein 3 (NLRP3), caspase-1, interleukin-1β (IL-1β), IL-18 and gasdermin D (GSDMD) protein and mRNA was detected by Western blot or by real-time polymerase chain reaction. Results: Compared with C group, the W/D ratio and IAR in lung tissues were significantly increased, and the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was up-regulated in I/R and DEX groups (P<0.05). Compared with I/R group, the W/D ratio and IAR in lung tissues were significantly decreased, the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was down-regulated (P<0.05), and the pathological changes were significantly attenuated in DEX group. Conclusion The mechanism by which dexmedetomidine reduces isolated rat lung I/R injury may be related to inhibiting pyroptosis.

Objective:To evaluate the value of autologous platelet-rich plasma (aPRP) separation-retransfusion for blood conservation in the patients undergoing thoracolumbar laminectomy.Methods:Sixty American Society of Anesthesiologists Physical Status classification Ⅰ or Ⅱ patients, aged 18-60 yr, with body mass index of 19-30 kg/m 2, scheduled for elective thoracolumbar laminectomy, were divided into 2 groups ( n=30 each) using a random number table method: conventional blood conservation group (group C) and aPRP blood conservation group (group aPRP). Group C received tranexamic acid and autologous blood salvage-retransfusion. Group aPRP received aPRP separation-retransfusion, tranexamic acid and autologous blood salvage-retransfusion. The volume of allogeneic blood transfused, percentage of patients who did not need the allogeneic blood transfusion and adverse reactions were recorded. Venous blood samples were collected for blood routine examination and for determination of the plasma concentrations of interleukin-6 (IL-6) and IL-10 at 1 day before operation (T 0), when the volume of blood loss reached 500 ml (T 1), immediately after surgery (T 2), and at 24 and 48 h after surgery (T 3, 4). The incidence of hypoxemia and amount of 24-h wound drainage were recorded. Results:Compared with group C, the amount of allogeneic red blood cells, plasma transfused and 24-h wound drainage were significantly decreased ( P<0.05), the percentage of patients who did not need the allogeneic red blood cell and plasma transfusion was increased (30% vs 47%, 10% vs 60%, P<0.05), the plasma concentrations of IL-6 and IL-10 at T 2-4 were significantly decreased ( P<0.05), and the incidence of hypoxemia in PACU was decreased in group aPRP (27% vs 10%, P<0.05). Conclusions:aPRP separation-retransfusion can provide marked improvement in conventional blood conservation in the patients undergoing thoracolumbar laminectomy.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.