目的探讨早期复苏后外周静脉-动脉血二氧化碳分压差对感染性休克患者预后的预测价值。方法采用前瞻性研究方法,选择2017年5月~2018年5月南京中医药大学附属中西医结合医院重症医学科收治的感染性休克患者,测定患者早期复苏6 h后中心静...目的探讨早期复苏后外周静脉-动脉血二氧化碳分压差对感染性休克患者预后的预测价值。方法采用前瞻性研究方法,选择2017年5月~2018年5月南京中医药大学附属中西医结合医院重症医学科收治的感染性休克患者,测定患者早期复苏6 h后中心静脉、动脉及外周静脉血血气分析,记录患者中心静脉、动脉及外周静脉血二氧化碳分压(PCO_2),计算患者外周静脉-动脉血二氧化碳分压差(Ppv-aCO_2)及中心静脉-动脉血二氧化碳分压差(Pcv-aCO_2),根据患者28 d预后将患者分为存活组及死亡组,采用Pearson相关性分析法分析Ppv-aCO_2与Pcv-aCO_2相关性,采用多因素Logistic分析筛选患者死亡的危险因素,并通过受试者工作特征曲线(ROC)评价各项指标预测患者预后的价值。结果共入选62例感染性休克患者,28 d存活35例,死亡27例。与存活组比较,死亡组患者急性生理与慢性健康评分Ⅱ(APACHEⅡ)(24.2±6.0 vs 20.5±4.9,P=0.011)及序贯器官衰竭的评分(SOFA)(14.9±4.7 vs 12.2±4.5,P=0.027)明显升高。6 h复苏后死亡组患者Pcv-aCO_2(5.5±1.6 vs 7.1±1.7,P<0.001),Ppv-aCO_2(7.1±1.8 vs 10.0±2.7,P<0.001),及动脉乳酸(Lac)(3.3±1.2 vs 4.2±1.3,P=0.003)明显高于存活组。Pearson相关性分析显示PpvaCO_2与Pcv-aCO_2明显相关,r=0.897,R^2=0.805,P<0.001。多因素Logistic回归分析显示Ppv-aCO_2和Lac是感染性休克患者28 d生存率的独立预后因素[(Ppv-aCO_2:β=0.625,P=0.001,相对危险度(OR)=1.869,95%CI:1.311~2.664;Lac:β=0.584,P=0.041,OR=1.794,95%CI:1.024~3.415)]。ROC曲线分析显示,Ppv-aCO_2、Pcv-aCO_2和Lac对感染性休克患者预后均有预测价值,其中Ppv-aCO_2的ROC曲线下面积(AUC)最大,为0.814(95%CI:0.696~0.931,P<0.001),最佳临界值为9.05 mmHg时,预测患者28 d死亡的敏感度为70.4%,特异度为88.6%;Lac的AUC=0.732(95%CI:0.607~0.858,P=0.002),最佳临界值为3.45 mmol/L时,敏感度为70.4%,特异度为74.3%;Pcv-aCO_2的AUC=0.766(95%CI:0.642~0.891,P<0.001),最佳临界值为7.05 mmHg时,敏感度为66.7%,特异度为80.0%。结论Ppv-aCO_2与Pcv-aCO_2相关,与感染性休克患者预后相关,可作为评估感染性休克患者28 d生存率的独立预后指标。展开更多
Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response...Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI), Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial in- farction, and heart failure) in patients with AMI.展开更多
Background Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions Plasmacytoid dendritic cells (pDCs) have been found to participate in the progres...Background Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions Plasmacytoid dendritic cells (pDCs) have been found to participate in the progression of atherosclerosis mainly through interferon ct (IFN-ct) production. Whether cilostazol influences pDCs activation is still not clear. In this study, we aimed to investigate the effects of cilostazol on cell activation and antigen presentation ofpDCs in vitro in this study. Methods Peripheral blood mononuclear cells isolated by Ficoll cen- trifugation and pDCs sorted by flow cytometry were used in this study. After pretreated with cilostazol for 2 h, cells were stimulated with CpG-A, R848 or virus for 6 h or 20 h, or stimulated with CpG-B for 48 h and then co-cultured with naive T cell for five days. Cytokines in supernatant and intracellular cytokines were analyzed by ELISA or flow cytometry respectively. Results Our data indicated that cilostazol could inhibit IFN-α and tumor necrosis factor α (TNF-α) production from pDCs in a dose-dependent manner. In addition, the ability of priming na ve T cells of pDCs was also impaired by cilostazol. The inhibitory effect was not due to cell killing since the viability of pDCs did not change upon cilostazol treatment. Conclusion Cilostazol inhibits pDCs cell activation and antigen presentation in vitro, which may explain how cilostazol protects against atherosclerosis.展开更多
OBJECTIVE: To observe the effect of Liandouqingmai recipe(Chinese herbal medicine compound preparation) on the quality of life(QOL) and inflammatory reaction of patients with coronary heart disease(CHD).METHODS: A tot...OBJECTIVE: To observe the effect of Liandouqingmai recipe(Chinese herbal medicine compound preparation) on the quality of life(QOL) and inflammatory reaction of patients with coronary heart disease(CHD).METHODS: A total of 101 CHD patients were randomized into two groups: treatment group(n=45)receiving standard treatment for CHD plus Liandouqingmai recipe, and control group(n=56) receiving standard treatment only. The control group contained 16 normal healthy subjects. Changes in hs-C-reactive protein(CRP), peripheral blood leucocytes(PBL), and interleukin(IL)-6 and IL-10 levels were measured. The Seattle Angina Questionnaire(SAQ) was used to determine patient QOL before and after treatment for 2 weeks.RESULTS: Before treatment, SAQ scores [physical limitation(PL), angina stability(AS), angina frequen-cy(AF), treatment satisfaction(TS), and disease perception(DP)] were not statistically different between groups. After treatment, AS and DP levels of controls were significantly increased compared with the other groups, while PL, AS, AF, TS, and DP levels of the treatment group were significantly increased compared with controls. Treatment group SAQ scores(PL, AS, AF, TS, and DP) were significantly higher than for controls. CHD patient IL-6 and IL-10 levels were significantly higher than controls.Before treatment, mean levels of IL-6, hs-CRP and PBL of the two groups were not statistically different. After treatment, mean levels of IL-6, IL-10,hs-CRP and PBL of the two groups were significantly decreased compared with their before treatment values, and levels of IL-6, hs-CRP, and PBL of the treatment group were lower than controls. Although mean IL-10 levels of both groups decreased, there was no significant difference in between-group and in-group comparisons before and after treatment. Mean levels of IL-6 and IL-10 in the normal group were lower than in CHD patients.SAQ scores of QOL were negatively associated with the inflammatory index(IL-6/IL-10), and there was a significant negative association of IL-10 with AS(r=﹣0.15, P<0.05).CONCLUSION: Inflammatory reactions in CHD patients are related to angina status. Coadministration of CHD standard treatment and Liandouqingmai recipe increased patient SAQ scores by decreasing IL-6, IL-10, hs-CRP, and PBL levels in CHD patients, which might inhibit endothelial inflammation to improve patient QOL.展开更多
Objective: To investigate the biomechanical effect of major extremity vessels to choose appropriate repair methods for vascular injuries of the extremities. Methods : The data of 385 patients (337 males and 48 fem...Objective: To investigate the biomechanical effect of major extremity vessels to choose appropriate repair methods for vascular injuries of the extremities. Methods : The data of 385 patients (337 males and 48 females, aged 18-71 years, mean = 32.6 years ) including 403 injured vessels, who suffered from vascular injuries of the extremities and were treated in our hospital from October 1960 to August 2005, were studied retrospectively in this article. We compared the results of different repair methods for the defect of vessels and evaluated different injured vessels for repairing arterial injuries with anastomosis and venous graft, respectively. Results: A significant difference was found between the defect lengths of the arteries repaired with anastomosis and venous graft ( P 〈 0. 0001 ). The upper limits of the confidence interval in the defect lengths of the brachial artery, the femoral artery and the popliteal artery were 3.43 cm, 2. 38 cm and 2. 42 cm, respectively, when repaired with anastomosis. The lower limits were 2.16 cm, 2.16 cm and 1. 63 cm, respectively, when repaired with venous graft. The defect length of each artery repaired with venous graft had linear correlation with the graft length. Conclusion - Because of the longitudinal biomechanical difference of different options of repair arterial injuries. human peripheral vessels, are necessary for different arterial injuries.展开更多
Objective: Type 2 diabetes coexistent with lower extremity artery disease (peripheral arterial disease (PAD)) can be observed in numerous patients. The mechanism compensating for ischemia and contributing to heal...Objective: Type 2 diabetes coexistent with lower extremity artery disease (peripheral arterial disease (PAD)) can be observed in numerous patients. The mechanism compensating for ischemia and contributing to healing is angiogenesis-the process of forming new blood vessels. The purpose of this study was to assess the likely impact of type 2 diabetes on the plasma levels of proangiogenic factor (vascular endothelial growth factor A (VEGF-A)) and angiogenesis inhibitors (soluble VEGF receptors type 1 and type 2 (sVEGFR-1 and sVEGFR-2)) in patients with PAD. Methods: Among 46 patients with PAD under pharmacological therapy (non-invasive), we identified, based on medical history, a subgroup with coexistent type 2 diabetes (PAD-DM2+, n=15) and without diabetes (PAD-DM2-, n=31). The control group consisted of 30 healthy subjects. Plasma levels of VEGF-A, sVEGFR-1, and sVEGFR-2 were measured using the enzyme-linked immunosorbent assay (ELISA) method. Results: The subgroups of PAD-DM2+ and PAD-DM2- revealed significantly higher concentrations of VEGF-A (P=-0.000007 and P=0.0000001, respectively) and significantly lower sVEGFR-2 levels (P=-0.02 and P=-0.00001, respectively), when compared with the control group. Patients with PAD and coexistent diabetes tended to have a lower level of VEGF-A and higher levels of sVEGFR-1 and sVEGFR-2 comparable with non-diabetic patients. Conclusions: The coexistence of type 2 diabetes and PAD is demonstrated by a tendency to a lower plasma level of proangiogenic factor (VEGF-A) and higher levels of anglogenesis inhibitors (sVEGFR-1 and sVEGFR-2) at the same time. Regardless of the coexistence of type 2 diabetes, hypoxia appears to be a crucial factor stimulating the processes of angiogenesis in PAD patients comparable with healthy individuals, whereas hyperglycemia may have a negative impact on angiogenesis in lower limbs.展开更多
文摘目的探讨早期复苏后外周静脉-动脉血二氧化碳分压差对感染性休克患者预后的预测价值。方法采用前瞻性研究方法,选择2017年5月~2018年5月南京中医药大学附属中西医结合医院重症医学科收治的感染性休克患者,测定患者早期复苏6 h后中心静脉、动脉及外周静脉血血气分析,记录患者中心静脉、动脉及外周静脉血二氧化碳分压(PCO_2),计算患者外周静脉-动脉血二氧化碳分压差(Ppv-aCO_2)及中心静脉-动脉血二氧化碳分压差(Pcv-aCO_2),根据患者28 d预后将患者分为存活组及死亡组,采用Pearson相关性分析法分析Ppv-aCO_2与Pcv-aCO_2相关性,采用多因素Logistic分析筛选患者死亡的危险因素,并通过受试者工作特征曲线(ROC)评价各项指标预测患者预后的价值。结果共入选62例感染性休克患者,28 d存活35例,死亡27例。与存活组比较,死亡组患者急性生理与慢性健康评分Ⅱ(APACHEⅡ)(24.2±6.0 vs 20.5±4.9,P=0.011)及序贯器官衰竭的评分(SOFA)(14.9±4.7 vs 12.2±4.5,P=0.027)明显升高。6 h复苏后死亡组患者Pcv-aCO_2(5.5±1.6 vs 7.1±1.7,P<0.001),Ppv-aCO_2(7.1±1.8 vs 10.0±2.7,P<0.001),及动脉乳酸(Lac)(3.3±1.2 vs 4.2±1.3,P=0.003)明显高于存活组。Pearson相关性分析显示PpvaCO_2与Pcv-aCO_2明显相关,r=0.897,R^2=0.805,P<0.001。多因素Logistic回归分析显示Ppv-aCO_2和Lac是感染性休克患者28 d生存率的独立预后因素[(Ppv-aCO_2:β=0.625,P=0.001,相对危险度(OR)=1.869,95%CI:1.311~2.664;Lac:β=0.584,P=0.041,OR=1.794,95%CI:1.024~3.415)]。ROC曲线分析显示,Ppv-aCO_2、Pcv-aCO_2和Lac对感染性休克患者预后均有预测价值,其中Ppv-aCO_2的ROC曲线下面积(AUC)最大,为0.814(95%CI:0.696~0.931,P<0.001),最佳临界值为9.05 mmHg时,预测患者28 d死亡的敏感度为70.4%,特异度为88.6%;Lac的AUC=0.732(95%CI:0.607~0.858,P=0.002),最佳临界值为3.45 mmol/L时,敏感度为70.4%,特异度为74.3%;Pcv-aCO_2的AUC=0.766(95%CI:0.642~0.891,P<0.001),最佳临界值为7.05 mmHg时,敏感度为66.7%,特异度为80.0%。结论Ppv-aCO_2与Pcv-aCO_2相关,与感染性休克患者预后相关,可作为评估感染性休克患者28 d生存率的独立预后指标。
文摘Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI), Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial in- farction, and heart failure) in patients with AMI.
文摘Background Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions Plasmacytoid dendritic cells (pDCs) have been found to participate in the progression of atherosclerosis mainly through interferon ct (IFN-ct) production. Whether cilostazol influences pDCs activation is still not clear. In this study, we aimed to investigate the effects of cilostazol on cell activation and antigen presentation ofpDCs in vitro in this study. Methods Peripheral blood mononuclear cells isolated by Ficoll cen- trifugation and pDCs sorted by flow cytometry were used in this study. After pretreated with cilostazol for 2 h, cells were stimulated with CpG-A, R848 or virus for 6 h or 20 h, or stimulated with CpG-B for 48 h and then co-cultured with naive T cell for five days. Cytokines in supernatant and intracellular cytokines were analyzed by ELISA or flow cytometry respectively. Results Our data indicated that cilostazol could inhibit IFN-α and tumor necrosis factor α (TNF-α) production from pDCs in a dose-dependent manner. In addition, the ability of priming na ve T cells of pDCs was also impaired by cilostazol. The inhibitory effect was not due to cell killing since the viability of pDCs did not change upon cilostazol treatment. Conclusion Cilostazol inhibits pDCs cell activation and antigen presentation in vitro, which may explain how cilostazol protects against atherosclerosis.
基金Supported by the Bureau of Traditional Chinese Medicine of Jiangsu Province(No.HZ07097)
文摘OBJECTIVE: To observe the effect of Liandouqingmai recipe(Chinese herbal medicine compound preparation) on the quality of life(QOL) and inflammatory reaction of patients with coronary heart disease(CHD).METHODS: A total of 101 CHD patients were randomized into two groups: treatment group(n=45)receiving standard treatment for CHD plus Liandouqingmai recipe, and control group(n=56) receiving standard treatment only. The control group contained 16 normal healthy subjects. Changes in hs-C-reactive protein(CRP), peripheral blood leucocytes(PBL), and interleukin(IL)-6 and IL-10 levels were measured. The Seattle Angina Questionnaire(SAQ) was used to determine patient QOL before and after treatment for 2 weeks.RESULTS: Before treatment, SAQ scores [physical limitation(PL), angina stability(AS), angina frequen-cy(AF), treatment satisfaction(TS), and disease perception(DP)] were not statistically different between groups. After treatment, AS and DP levels of controls were significantly increased compared with the other groups, while PL, AS, AF, TS, and DP levels of the treatment group were significantly increased compared with controls. Treatment group SAQ scores(PL, AS, AF, TS, and DP) were significantly higher than for controls. CHD patient IL-6 and IL-10 levels were significantly higher than controls.Before treatment, mean levels of IL-6, hs-CRP and PBL of the two groups were not statistically different. After treatment, mean levels of IL-6, IL-10,hs-CRP and PBL of the two groups were significantly decreased compared with their before treatment values, and levels of IL-6, hs-CRP, and PBL of the treatment group were lower than controls. Although mean IL-10 levels of both groups decreased, there was no significant difference in between-group and in-group comparisons before and after treatment. Mean levels of IL-6 and IL-10 in the normal group were lower than in CHD patients.SAQ scores of QOL were negatively associated with the inflammatory index(IL-6/IL-10), and there was a significant negative association of IL-10 with AS(r=﹣0.15, P<0.05).CONCLUSION: Inflammatory reactions in CHD patients are related to angina status. Coadministration of CHD standard treatment and Liandouqingmai recipe increased patient SAQ scores by decreasing IL-6, IL-10, hs-CRP, and PBL levels in CHD patients, which might inhibit endothelial inflammation to improve patient QOL.
文摘Objective: To investigate the biomechanical effect of major extremity vessels to choose appropriate repair methods for vascular injuries of the extremities. Methods : The data of 385 patients (337 males and 48 females, aged 18-71 years, mean = 32.6 years ) including 403 injured vessels, who suffered from vascular injuries of the extremities and were treated in our hospital from October 1960 to August 2005, were studied retrospectively in this article. We compared the results of different repair methods for the defect of vessels and evaluated different injured vessels for repairing arterial injuries with anastomosis and venous graft, respectively. Results: A significant difference was found between the defect lengths of the arteries repaired with anastomosis and venous graft ( P 〈 0. 0001 ). The upper limits of the confidence interval in the defect lengths of the brachial artery, the femoral artery and the popliteal artery were 3.43 cm, 2. 38 cm and 2. 42 cm, respectively, when repaired with anastomosis. The lower limits were 2.16 cm, 2.16 cm and 1. 63 cm, respectively, when repaired with venous graft. The defect length of each artery repaired with venous graft had linear correlation with the graft length. Conclusion - Because of the longitudinal biomechanical difference of different options of repair arterial injuries. human peripheral vessels, are necessary for different arterial injuries.
基金supported by the Nicolaus Copernicus University in Toruń,Ludwik Rydygier Collegium Medicum in Bydgoszcz,Poland(Grant No.2/WF-SD)
文摘Objective: Type 2 diabetes coexistent with lower extremity artery disease (peripheral arterial disease (PAD)) can be observed in numerous patients. The mechanism compensating for ischemia and contributing to healing is angiogenesis-the process of forming new blood vessels. The purpose of this study was to assess the likely impact of type 2 diabetes on the plasma levels of proangiogenic factor (vascular endothelial growth factor A (VEGF-A)) and angiogenesis inhibitors (soluble VEGF receptors type 1 and type 2 (sVEGFR-1 and sVEGFR-2)) in patients with PAD. Methods: Among 46 patients with PAD under pharmacological therapy (non-invasive), we identified, based on medical history, a subgroup with coexistent type 2 diabetes (PAD-DM2+, n=15) and without diabetes (PAD-DM2-, n=31). The control group consisted of 30 healthy subjects. Plasma levels of VEGF-A, sVEGFR-1, and sVEGFR-2 were measured using the enzyme-linked immunosorbent assay (ELISA) method. Results: The subgroups of PAD-DM2+ and PAD-DM2- revealed significantly higher concentrations of VEGF-A (P=-0.000007 and P=0.0000001, respectively) and significantly lower sVEGFR-2 levels (P=-0.02 and P=-0.00001, respectively), when compared with the control group. Patients with PAD and coexistent diabetes tended to have a lower level of VEGF-A and higher levels of sVEGFR-1 and sVEGFR-2 comparable with non-diabetic patients. Conclusions: The coexistence of type 2 diabetes and PAD is demonstrated by a tendency to a lower plasma level of proangiogenic factor (VEGF-A) and higher levels of anglogenesis inhibitors (sVEGFR-1 and sVEGFR-2) at the same time. Regardless of the coexistence of type 2 diabetes, hypoxia appears to be a crucial factor stimulating the processes of angiogenesis in PAD patients comparable with healthy individuals, whereas hyperglycemia may have a negative impact on angiogenesis in lower limbs.