ObjectiveTo study the changes of levels of α subunits of stimulatory (Gsα) and inhibitory guanine nucleotide binding protein (Giα) in newborn guinea pig (0 2 days old) myocardium undergoing global ischemic reperfusion, and influences on the changes by St.Thomas Ⅱ and cold blood cardioplegic solution.MethodsThirty newborn guinea pigs were randomly assigned to three groups. GroupⅠ ( n = 10): the newborn hearts suffered by hypothermic global ischemia; group Ⅱ( n =10): the newborn hearts arrested by St. Thomas Ⅱ , and group Ⅲ ( n = 10): the newborn hearts arrested by cold blood cardioplegic solution. Levels of Gsα and Giα were investigated with Western blot analysis.ResultsNo differences of levels of Gsα and Giα were found in three groups before ischemia ( P gt;0.05). The level of Gsα after ischemia was significantly decreased than before ischemia in groupⅠand group Ⅱ ( P lt; 0 01), whereas no pronounced changes in group Ⅲ ( P gt;0.05) were noted after ischemia. The level of Gsα in group Ⅲ was not significantly changed after reperfusion compared with before ischemia( P gt;0 05), and it was much higher than those in groupⅠand group Ⅱ ( P lt; 0 01). Level of Giα was found not markedly changed in group Ⅲ after reperfusion compared with that before ischemia, but was notable higher in groupⅠand group Ⅱ( P lt;0.01). ConclusionsSignificant decrease of level of Gsα, whereas marked increase of level of Giα are found in myocardium of newborn guinea pig undergoing hypothermic (20℃) ischemic reperfusion. No impact of St. Thomas Ⅱ on these changes is verified, but recovery to the level of Gsα and Giα before ischemia is achieved by cold blood cardioplegic solution after ischemia and reperfusion. Unbalance between Gsα and Giα is the one of the mechanisms of ischemic reperfusion injury for immature myocardium.
Objective To observe the influences of depolarized arrest and hyperpolarized arrest on alternation of fluidity of myocardial cell membrane during cardiopulmonary bypass (CPB) and evaluate the protective effects on myocardium of hyperpolarized arrest. Methods Seventy-two felines were randomized into three groups, each group 24. Control group: 180 minutes of CPB was conducted without aortic and vena caval cross-clamping. Depolarized arrest group: hearts underwent 60 minutes of global ischemia after aortic cross-clamping (ACC) followed by 90 minutes of reperfusion. The cardioplegic solution consisted of St. Thomas solution (K+16mmol/L). Hyperpolarized arrest group: the protocol was the same as that in depolarized arrest group except that the cardioplegic solution consisted of St.Thomas solution with pinacidil (50 mmol/L,K+5mmol/L). Microviscosity, the reciprocal of fluidity of myocardial membrane was measured in all groups by using fluorescence polarization technique. (Results )Microvis cosity of myocardial cell in depolarized arrest group during ACC period was significantly higher than that before ACC and kept on rising during reperfusion period. Microviscosity of myocardial cell in hyperpolarized arrest group during ACC was trending up and reperfusion periods as well, but markedly lower compared to that in depolarized arrest group at corresponding time points(Plt;0.01). Conclusion Hyperpolarized arrest is more effective in protecting myocardial cells from ischemia-reperfusion injury than depolarized arrest during CPB by maintaining better fluidity of myocardial membrane.
ObjectiveTo summarize the research progress of severed limb preservation by perfusion and to analyze difference in effect of severed limb preservation by different perfusate. MethodsThe domestic and foreign related literature about severed limb preservation by perfusion was extensively reviewed and analyzed. ResultsCurrently the main perfusate includes organ perfusate,free radical scavengers,energy mixture,blood substitutes,and whole blood.They can reduce the skeletal muscle's ischemia-reperfusion injury in different degrees. ConclusionDifferent perfusate can reduce the skeletal muscle's ischemia-reperfusion injury in different degrees,but the best effect of perfusate and personalized preservation method need further study.
【Abstract】ObjectiveOn the basis of traditional transplantation model, a successful model of pancreaticoduodenal transplantation (PDT) were established in rats, which is the foundation of basic and clinical transplantation research. Methods We improved the technique of microoperation on donor and harvested high-quality graft. The dual cuff technique was applied to end-to-end anastomose proximal part of abdominal aorta and portal vein with left renal aorta and vein of recipient, and distal part of abdominal aorta was connected with Y-tube. External secretion was performed by duodenum stoma. The PDT model was finished without blocking systemic circulation and portal vein system. Random blood glucose levels and drainage were monitored postoperatively to evaluate the function of endocrine and ectocrine. Results Thirty operations were done. The total procedure of transplantation lasted 2 hours. Moreover the operation on recipient and the reconstruction of vessels took only (26±5) and (25±5) minutes, respectively. The success rate was elevated to 100%. The ectocrine function was restored within 2 hours after operation. Except for 3 cases of non-function graft because of thrombosis in cannula, the glucose level of the remaining recipients was reduced to normal level 6 h or 24 h after transplantation. The survival rate of graft function was 90% (27/30). Conclusion This model is finished without special equipment and can recover the endocrine function in advance. It is a simple and stable model, which might be used in research of the theoretical problems involved in clinical pancreas transplantation.
Objective To examine the effect of endothelial progenitor cell (EPC) on lung ischemia-reperfusion injury (LIRI). Methods Twenty-four recipients were randomized into 3 groups including a sham group, a LIRI group, and an EPC group. Rats in the sham group only received anesthesia. Rats in the LIRI and EPC groups received left lung transplantation and received saline or EPC immediately after reperfusion. The partial pressure of oxygen to fraction of inspiratory oxygen (PaO2/FiO2) ratio, wet-to-dry weight ratio and protein levels in the transplanted lung and inflammation-related factors levels in serum were examined. Histological change of transplanted lung were analyzed. The nuclear factor (NF)-κB in the transplanted lung was detected. Results Compared with the LIRI group, the PaO2/FiO2 ratio dramaticly increased, and the wet-to-dry weight ratio and protein level significantly decreased by EPC after reperfusion. The lung histological injury was attenuated by EPC. The pro-inflammatory factors in serum were down-regulated, whereas IL-10 was up-regulated in the EPC group. The expression of NF-κB was decreased by EPC. Conclusion EPC ameliorated LIRI after lung transplantation. The protection of EPC partly associated with anti-inflammation.
Objective To investigate the effects of ischemic postconditioning （IPO） on inflammatory response inischemia-reperfusion （IR） injury of rat lungs in vivo. Methods Forty SD rats were randomly divided into 5 groups inclu-ding a sham surgery group （S group），a 30-minute IR group （I/R-30 group），a 120-minute IR group（IR-120 group），a 30-minute IPO group （IPO-30 group），and a 120-minute IPO group （IPO-120 group）. There were 8 rats in each group. All therats received left thoracotomy after anesthesia. In the sham surgery group，a line was only placed around the left hilum butnot fastened. In the I/R-30 group and I/R-120 group，a line was fastened to block the blood flow of the left lung for 1 hour，then loosened for reperfusion for 30 minutes and 120 minutes respectively. In the IPO-30 group and IPO-120 group，afterblocking the blood flow of the left lung for 1 hour，the left hilum was fastened for 10 seconds and loosened for 10 seconds（repeating 3 times for 1 minute），then the line was loosened for 30 minutes and 120 minutes respectively. The levels of interleukin-10 （IL-10） in lung tissues and soluble intercellular adhesion molecule-1 （sICAM-1） in plasma were measured. Histopathological changes of lung tissues were observed and diffuse alveolar damage （DAD） scores was calculated.Results The levels of plasma sICAM-1 in the I/R-30 group and I/R-120 group were significantly higher than that of S group ［（2.140±0.250）μg/L vs. （0.944±0.188）μg/L，P=0.003；（2.191±0.230）μg/L vs. （0.944±0.188）μg/L，P=0.003］. IL-10levels in lung tissues in the I/R-30group and I/R-120 group were also significantly higher than that of S group［（15.922±0.606）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.037；（17.421±1.232）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.042］. Pathologic lesions of lung tissues in the I/R-30 group and I/R-120 group were more severe than that of S group. After IPO, plasma sICAM-1 levels in the IPO-30 group and IPO-120 group were significantly lower than those in the I/R-30group and I/R-120 group respectively ［（1.501±0.188）μg/L vs.（2.140±0.250）μg/L，P=0.038；（1.350±0.295）μg/L vs.（2.191±0.230）μg/L，P=0.005］. IL-10 levels in lung tissues in the IPO-30 group and IPO-120 group were significantly higherthan those in the I/R-30 group and I/R-120 group respectively ［（20.950±1.673）pg/mg pro vs.（15.922±0.606）pg/mgpro，P=0.008；（25.334±1.173）pg/mg pro vs.（17.421±1.232）pg/mg pro，P=0.006］. DAD scores in the IPO-30 group andIPO-120 group were significantly lower than those in the I/R-30 group and I/R-120 group respectively ［6.8±1.4 vs. 11.5±1.9，P=0.007；7.5±1.6 vs. 13.2±1.7，P=0.005］. Pathological lesions of the lung tissues of IPO groups were less severe than those of I/R groups. Conclusion IPO can attenuate IR injury by inhibiting inflammatory response in rat lungs.
【 Abstract 】 Objective To investigate the protective effect of peroxisome proliferator-activated receptor γ (PPAR γ ) activator 15-deoxyprostaglandin J2 (15d-PGJ2) in rat hepatic ischemia-reperfusion injury and its mechanism. Methods The models of 70% warm ischemia-reperfusion injury were established in SD rats, rats were randomly divided into 4 groups: sham operation group, ischemia-reperfusion group, 15d-PGJ2 group and 15d-PGJ2+GW9662 group. After reperfusion, serum AST and ALT levels were determined; the liver tissues were removed for measurement of activity of NF-κB and myeloperoxidase (MPO), TNF-α content and expression of ICAM-1. Results Compared with sham operation group, the serum levels of ALT and AST, and the activities of MPO and NF- κ B, TNF- α content and expression of ICAM-1 in ischemia-reperfusion group, 15d-PGJ2 group and 15d-PGJ2+GW9662 group were greatly improved (P ＜ 0.05). Compared with ischemia-reperfusion group, the serum levels of ALT and AST and the activities of MPO and NF- κ B, TNF- α content and expression of ICAM-1 in 15d-PGJ2 group were significantly decreased (P ＜ 0.05). Compared with 15d-PGJ2 group, the serum levels of ALT and AST, and the activities of MPO and NF- κ B, TNF- α content and the expression of ICAM-1 in 15d-PGJ2+GW9662 group were obviously increased (P ＜ 0.05). Conclusion PPAR γ activator 15d-PGJ2 could protect against ischemia-reperfusion injury in rats, with its possible mechanism of inhibiting NF-κB activation and down-regulating TNF-α content and ICAM-1 expression in a PPARγ dependent fashion.
Acute lung injury is a kind of common complication after cardiopulmonary bypass. Acute lung injury is attributed to the ischemia-reperfusion injury and systemic inflammatory response syndrome. Several factors common in cardiac surgery with cardiopulmonary bypass may worsen the risk for acute lung injury including atelectasis, transfusion requirement, older age, heart failure, emergency surgery and prolonged duration of bypass. Targets for prevention of acute lung injury include mechanical, surgical and anesthetic interventions that aim to reduce the contact activation, systemic inflammatory response, leukocyte sequestration and hemodilution associated with cardiopulmonary bypass. We aim to review the etiology, risk factors and lung protective strategies for acute lung injury after cardiopulmonary bypass.