The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanism...The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.展开更多
The effects of tacrolimus postconditioning on protein-serine-threonine kinases （Akt） phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male ...The effects of tacrolimus postconditioning on protein-serine-threonine kinases （Akt） phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion （P〈0.05, P〈0.01）. The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced （P〈0.01） in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.展开更多
AIM: To investigate the effects of selenium in rat retinal ischemia reperfusion(IR) model and compare pretreatment and post-treatment use.METHODS: Selenium pre-treatment group(n =8) was treated with intraperitoneal(i....AIM: To investigate the effects of selenium in rat retinal ischemia reperfusion(IR) model and compare pretreatment and post-treatment use.METHODS: Selenium pre-treatment group(n =8) was treated with intraperitoneal(i.p.) selenium 0.5 mg/kg for7 d and terminated 24 h after the IR injury. Selenium posttreatment group( n = 8) was treated with i. p. selenium0.5 mg/kg for 7d after the IR injury with termination at the end of the 7d period. Sham group(n =8) received i.p.saline injections identical to the selenium volume for 7d with termination 24 h after the IR injury. Control group(n =8) received no intervention. Main outcome measures were retina superoxide dismutase(SOD), glutathione(GSH),total antioxidant status(TAS), malondialdehyde(MDA),DNA fragmentation levels, and immunohistological apoptosis evaluation.RESULTS: Compared to the Sham group, selenium pre-treatment had a statistical difference in all parameters except SOD. Post-treatment selenium also resulted in statistical differences in all parameters except the MDA levels. When comparing selenium groups, the pre-treatment selenium group had a statistically higher success in reduction of markers of cell damage such as MDA and DNA fragmentation. In contrast, the post-selenium treatment group had resulted in statisticallyhigher levels of GSH. Histologically both selenium groups succeeded to limit retinal thickening and apoptosis. Pre-treatment use was statistically more successful in decreasing apoptosis in ganglion cell layer compared to post-treatment use.CONCLUSION: Selenium was successful in retinal protection in IR injuries. Pre-treatment efficacy was superior in terms of prevention of tissue damage and apoptosis.展开更多
Intestinal ischemia is a severe disorder with a variety of causes.Reperfusion is a common occurrence during treatment of acute intestinal ischemia but the injury resulting from ischemia/reperfusion(IR)may lead toeven ...Intestinal ischemia is a severe disorder with a variety of causes.Reperfusion is a common occurrence during treatment of acute intestinal ischemia but the injury resulting from ischemia/reperfusion(IR)may lead toeven more serious complications from intestinal atrophy to multiple organ failure and death.The susceptibility of the intestine to IR-induced injury(IRI)appears from various experimental studies and clinical settings such as cardiac and major vascular surgery and organ transplantation.Where as oxygen free radicals,activation of leukocytes,failure of microvascular perfusion,cellular acidosis and disturbance of intracellular homeo-stasis have been implicated as important factors inthe pathogenesis of intestinal IRI,the mechanisms underlying this disorder are not well known.To date,increasing attention is being paid in animal studies to potential pre-and post-ischemia treatments that protect against intestinal IRI such as drug interference with IR-induced apoptosis and inflammation processes and ischemic pre-conditioning.However,better insight is needed into the molecular and cellular events associated with reperfusion-induced damage to develop effective clinical protection protocols to combat this disorder.In this respect,the use of ischemic post-conditioning in combination with experimentally prolonged acidosis blocking deleterious reperfusion actions may turn out to have particular clinical relevance.展开更多
目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)...目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)中的作用。方法将24只大鼠饲养7天后,随机分成3组:假手术(Sham)组、缺血再灌注(ischemia/reperfusion,IR)组、缺血后处理(ischemic post-conditioning,IPO)组。模型构建完毕24 h进行检测大鼠血清中心肌肌钙蛋白I(cTnI)和白介素6(IL-6)表达水平,取材检测大鼠心肌梗死面积,检测大鼠心肌组织中MALAT1转录表达水平的差异,HMGB1、Toll样受体4(Toll-like receptor4,TLR4)蛋白含量差异。结果与Sham组比较,IR、IPO组血清中cTnI、IL-6水平明显升高,心肌梗死面积明显增加,心肌组织中MALAT1表达水平显著上调,HMGB1、TLR4水平明显升高(P<0.05)。与IR组比较,IPO组cTnI浓度显著降低,心肌梗死面积显著减小,心肌组织中lncRNA-MALAT1相对表达量降低,HMGB1、TLR4蛋白含量降低(P<0.05)。结论及时的缺血后处理可有效减缓大鼠心肌缺血-再灌注的损伤程度,其相关机制可能与抑制MALAT1调节控制HMGB1、TLR4表达水平之间有一定的关联。展开更多
Objective:To evaluate pharmacological mimetic action of herbal extract Desmodium gangeticum (DC) roots on ischemia reperfusion injury.Methods:With the help of Langendroff perfusion technique,ischemic post condition(PO...Objective:To evaluate pharmacological mimetic action of herbal extract Desmodium gangeticum (DC) roots on ischemia reperfusion injury.Methods:With the help of Langendroff perfusion technique,ischemic post condition(POC) mimetic action of DG methanol root extract was evaluated and compared by using standard drugs that acts as muscarinic receptor agonist and antagonist,namely acetylcholine(Ach) and atropine(Atr) respectively in an isolated rat heart. Results:The physiological parameters like left ventricular developed pressure,end diastolic pressure and working index of isolated rat heart showed significant recovery in DG root extract administrated rat heart,similar to the recovery by POC.Kymogram results showed muscarinic receptor agonist like action for DG methanol root extract,confirmed in rat heart by muscarnic receptor agonist(acetylcholine) and anatoginst(atropine).Administration of DC root extract prior to reperfusion showed better antioxidant status in myocardial tissue homogenate and mitochondrial,complemented by the levels of cardiac specific marker proteins in myocardial tissue and perfusate.Even though DG methanol root extract mimics its action similar to that of Ach,the myocardial protection mediated by the extract was superior to Ach,due to the presence of antioxidants in the crude extract.Conclusions:DG methanol root extract provides myocardial protection towards IRI by stimulating muscarinic receptors.展开更多
Post-stroke depression is associated with reduced expression of brain-derived neurotrophic factor （BDNF）. In this study, we evaluated whether BDNF overexpression affects depression-like behavior in a rat model of po...Post-stroke depression is associated with reduced expression of brain-derived neurotrophic factor （BDNF）. In this study, we evaluated whether BDNF overexpression affects depression-like behavior in a rat model of post-stroke depression. The middle cerebral artery was occluded to produce a model of focal cerebral ischemia. These rats were then subjected to isolation-housing combined with chronic unpredictable mild stress to generate a model of post-stroke depression. A BDNF gene lentiviral vector was injected into the hippocampus. At 7 days after injection, western blot assay and real-time quantitative PCR revealed that BDNF expression in the hippo- campus was increased in depressive rats injected with BDNF lentivirus compared with depressive rats injected with control vector. Furthermore, sucrose solution consumption was higher, and horizontal and vertical movement scores were increased in the open field test in these rats as well. These findings suggest that BDNF overexpression in the hippocampus of post-stroke depressive rats alleviates depression-like behaviors.展开更多
目的探讨尼可地尔联合远程缺血后适应(RIPostC)对急性ST段抬高型心肌梗死(STEMI)急诊经皮冠状动脉介入(PCI)的心肌保护作用。方法单中心、前瞻性、随机对照研究。连续纳入2018年1月至2021年9月在新乡医学院附属焦作市人民医院心内科病...目的探讨尼可地尔联合远程缺血后适应(RIPostC)对急性ST段抬高型心肌梗死(STEMI)急诊经皮冠状动脉介入(PCI)的心肌保护作用。方法单中心、前瞻性、随机对照研究。连续纳入2018年1月至2021年9月在新乡医学院附属焦作市人民医院心内科病房接受PCI治疗的STEMI患者208例。按随机数字表法分为4组:A组(52例):常规PCI;B组(52例):RIPostC+常规PCI;C组(52例):尼可地尔+常规PCI;D组(52例):RIPostC+尼可地尔+常规PCI。于PCI术前后检测心肌灌注、心律失常、炎症反应、血管内皮功能、心肌损伤及心功能指标;记录术后12个月内主要不良心血管事件(MACE,包括再发心肌梗死、再发心力衰竭、心原性休克和心原性死亡)。结果(1)D组PCI术后即刻校正的TIMI血流帧数计数(CTFC)、术后24 h Curtis-Walker评分及恶性心律失常发生率均低于A组,术后2 h ST段回落幅度高于A组(均为P<0.01);(2)PCI术后48 h,D组的高敏C反应蛋白(hs-CRP)、白细胞介素6(IL-6)、丙二醛(MDA)和血管内皮生长因子(VEGF)水平均低于A、B和C组,超氧化物歧化酶(SOD)和一氧化氮(NO)水平均高于A、B和C组(均为P<0.001);B、C组的hs-CRP、IL-6、MDA和VEGF水平均低于A组,SOD和NO水平均高于A组(均为P<0.001);(3)PCI术后12 h和48 h,D组的高敏心肌肌钙蛋白I(hs-cTnI)水平均低于A、B和C组,B、C组的hs-cTnI水平均低于A组(均为P<0.001);(4)PCI术后1个月和12个月,D组的左心室射血分数(LVEF)水平均高于A、B和C组,B、C组的LVEF水平均高于A组(均为P<0.001);(5)PCI术后12个月内,4组患者的MACE发生率无统计学差异(χ^(2)=4.396,P=0.22)。结论单纯尼可地尔或RIPostC在PCI中均具有改善心肌灌注、拮抗氧化应激、抑制炎症反应、改善血管内皮、保护心肌细胞和改善心功能等作用,尼可地尔联合RIPostC的心肌保护作用明显优于单纯尼可地尔或RIPostC,联用具有协同、叠加效果。展开更多
基金supported by the National Natural Science Foundation of China,No.81271387the Research Special Fund of Public Welfare and Health Department of China,No.201402009a grant form the National Key Technology R&D Program in China,No.Z141107002514031
文摘The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.
基金supported by the Hubei Provincial Natural Science Foundation of China(No.2012FFB04406)
文摘The effects of tacrolimus postconditioning on protein-serine-threonine kinases （Akt） phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion （P〈0.05, P〈0.01）. The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced （P〈0.01） in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.
文摘AIM: To investigate the effects of selenium in rat retinal ischemia reperfusion(IR) model and compare pretreatment and post-treatment use.METHODS: Selenium pre-treatment group(n =8) was treated with intraperitoneal(i.p.) selenium 0.5 mg/kg for7 d and terminated 24 h after the IR injury. Selenium posttreatment group( n = 8) was treated with i. p. selenium0.5 mg/kg for 7d after the IR injury with termination at the end of the 7d period. Sham group(n =8) received i.p.saline injections identical to the selenium volume for 7d with termination 24 h after the IR injury. Control group(n =8) received no intervention. Main outcome measures were retina superoxide dismutase(SOD), glutathione(GSH),total antioxidant status(TAS), malondialdehyde(MDA),DNA fragmentation levels, and immunohistological apoptosis evaluation.RESULTS: Compared to the Sham group, selenium pre-treatment had a statistical difference in all parameters except SOD. Post-treatment selenium also resulted in statistical differences in all parameters except the MDA levels. When comparing selenium groups, the pre-treatment selenium group had a statistically higher success in reduction of markers of cell damage such as MDA and DNA fragmentation. In contrast, the post-selenium treatment group had resulted in statisticallyhigher levels of GSH. Histologically both selenium groups succeeded to limit retinal thickening and apoptosis. Pre-treatment use was statistically more successful in decreasing apoptosis in ganglion cell layer compared to post-treatment use.CONCLUSION: Selenium was successful in retinal protection in IR injuries. Pre-treatment efficacy was superior in terms of prevention of tissue damage and apoptosis.
文摘Intestinal ischemia is a severe disorder with a variety of causes.Reperfusion is a common occurrence during treatment of acute intestinal ischemia but the injury resulting from ischemia/reperfusion(IR)may lead toeven more serious complications from intestinal atrophy to multiple organ failure and death.The susceptibility of the intestine to IR-induced injury(IRI)appears from various experimental studies and clinical settings such as cardiac and major vascular surgery and organ transplantation.Where as oxygen free radicals,activation of leukocytes,failure of microvascular perfusion,cellular acidosis and disturbance of intracellular homeo-stasis have been implicated as important factors inthe pathogenesis of intestinal IRI,the mechanisms underlying this disorder are not well known.To date,increasing attention is being paid in animal studies to potential pre-and post-ischemia treatments that protect against intestinal IRI such as drug interference with IR-induced apoptosis and inflammation processes and ischemic pre-conditioning.However,better insight is needed into the molecular and cellular events associated with reperfusion-induced damage to develop effective clinical protection protocols to combat this disorder.In this respect,the use of ischemic post-conditioning in combination with experimentally prolonged acidosis blocking deleterious reperfusion actions may turn out to have particular clinical relevance.
文摘目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)中的作用。方法将24只大鼠饲养7天后,随机分成3组:假手术(Sham)组、缺血再灌注(ischemia/reperfusion,IR)组、缺血后处理(ischemic post-conditioning,IPO)组。模型构建完毕24 h进行检测大鼠血清中心肌肌钙蛋白I(cTnI)和白介素6(IL-6)表达水平,取材检测大鼠心肌梗死面积,检测大鼠心肌组织中MALAT1转录表达水平的差异,HMGB1、Toll样受体4(Toll-like receptor4,TLR4)蛋白含量差异。结果与Sham组比较,IR、IPO组血清中cTnI、IL-6水平明显升高,心肌梗死面积明显增加,心肌组织中MALAT1表达水平显著上调,HMGB1、TLR4水平明显升高(P<0.05)。与IR组比较,IPO组cTnI浓度显著降低,心肌梗死面积显著减小,心肌组织中lncRNA-MALAT1相对表达量降低,HMGB1、TLR4蛋白含量降低(P<0.05)。结论及时的缺血后处理可有效减缓大鼠心肌缺血-再灌注的损伤程度,其相关机制可能与抑制MALAT1调节控制HMGB1、TLR4表达水平之间有一定的关联。
文摘Objective:To evaluate pharmacological mimetic action of herbal extract Desmodium gangeticum (DC) roots on ischemia reperfusion injury.Methods:With the help of Langendroff perfusion technique,ischemic post condition(POC) mimetic action of DG methanol root extract was evaluated and compared by using standard drugs that acts as muscarinic receptor agonist and antagonist,namely acetylcholine(Ach) and atropine(Atr) respectively in an isolated rat heart. Results:The physiological parameters like left ventricular developed pressure,end diastolic pressure and working index of isolated rat heart showed significant recovery in DG root extract administrated rat heart,similar to the recovery by POC.Kymogram results showed muscarinic receptor agonist like action for DG methanol root extract,confirmed in rat heart by muscarnic receptor agonist(acetylcholine) and anatoginst(atropine).Administration of DC root extract prior to reperfusion showed better antioxidant status in myocardial tissue homogenate and mitochondrial,complemented by the levels of cardiac specific marker proteins in myocardial tissue and perfusate.Even though DG methanol root extract mimics its action similar to that of Ach,the myocardial protection mediated by the extract was superior to Ach,due to the presence of antioxidants in the crude extract.Conclusions:DG methanol root extract provides myocardial protection towards IRI by stimulating muscarinic receptors.
基金supported by a grant from the Experimental Animal Science and Technology Project of Zhejiang Province in China,No.2012C37083
文摘Post-stroke depression is associated with reduced expression of brain-derived neurotrophic factor （BDNF）. In this study, we evaluated whether BDNF overexpression affects depression-like behavior in a rat model of post-stroke depression. The middle cerebral artery was occluded to produce a model of focal cerebral ischemia. These rats were then subjected to isolation-housing combined with chronic unpredictable mild stress to generate a model of post-stroke depression. A BDNF gene lentiviral vector was injected into the hippocampus. At 7 days after injection, western blot assay and real-time quantitative PCR revealed that BDNF expression in the hippo- campus was increased in depressive rats injected with BDNF lentivirus compared with depressive rats injected with control vector. Furthermore, sucrose solution consumption was higher, and horizontal and vertical movement scores were increased in the open field test in these rats as well. These findings suggest that BDNF overexpression in the hippocampus of post-stroke depressive rats alleviates depression-like behaviors.
文摘目的探讨尼可地尔联合远程缺血后适应(RIPostC)对急性ST段抬高型心肌梗死(STEMI)急诊经皮冠状动脉介入(PCI)的心肌保护作用。方法单中心、前瞻性、随机对照研究。连续纳入2018年1月至2021年9月在新乡医学院附属焦作市人民医院心内科病房接受PCI治疗的STEMI患者208例。按随机数字表法分为4组:A组(52例):常规PCI;B组(52例):RIPostC+常规PCI;C组(52例):尼可地尔+常规PCI;D组(52例):RIPostC+尼可地尔+常规PCI。于PCI术前后检测心肌灌注、心律失常、炎症反应、血管内皮功能、心肌损伤及心功能指标;记录术后12个月内主要不良心血管事件(MACE,包括再发心肌梗死、再发心力衰竭、心原性休克和心原性死亡)。结果(1)D组PCI术后即刻校正的TIMI血流帧数计数(CTFC)、术后24 h Curtis-Walker评分及恶性心律失常发生率均低于A组,术后2 h ST段回落幅度高于A组(均为P<0.01);(2)PCI术后48 h,D组的高敏C反应蛋白(hs-CRP)、白细胞介素6(IL-6)、丙二醛(MDA)和血管内皮生长因子(VEGF)水平均低于A、B和C组,超氧化物歧化酶(SOD)和一氧化氮(NO)水平均高于A、B和C组(均为P<0.001);B、C组的hs-CRP、IL-6、MDA和VEGF水平均低于A组,SOD和NO水平均高于A组(均为P<0.001);(3)PCI术后12 h和48 h,D组的高敏心肌肌钙蛋白I(hs-cTnI)水平均低于A、B和C组,B、C组的hs-cTnI水平均低于A组(均为P<0.001);(4)PCI术后1个月和12个月,D组的左心室射血分数(LVEF)水平均高于A、B和C组,B、C组的LVEF水平均高于A组(均为P<0.001);(5)PCI术后12个月内,4组患者的MACE发生率无统计学差异(χ^(2)=4.396,P=0.22)。结论单纯尼可地尔或RIPostC在PCI中均具有改善心肌灌注、拮抗氧化应激、抑制炎症反应、改善血管内皮、保护心肌细胞和改善心功能等作用,尼可地尔联合RIPostC的心肌保护作用明显优于单纯尼可地尔或RIPostC,联用具有协同、叠加效果。
