经颅多普勒超声联合血流速度检测在颈内动脉支架置入术后高灌注损伤中的应用

目的探讨经颅多普勒超声(TCD)联合血流速度检测在颈内动脉支架置入术后高灌注损伤(CHS)中的应用。方法前瞻性选取2016年1月至2019年12月常熟市第二人民医院收治的80例接受颈动脉支架置入术患者为对象,均接受TCD检测。统计颈动脉支架置入术后CHS发生情况,收集患者年龄、性别、体质量指数、高血压、糖尿病、吸烟、饮酒、冠心病、高脂血症、脑梗死史、血压、颈动脉狭窄程度等资料,分析影响颈内动脉支架置入术后CHS发生的因素。并分析监测血流速度对CHS的诊断价值。结果80例接受颈内动脉支架置入术患者术后7例(8.75%)出现CHS。单因素分析显示CHS组与非CHS组患者在性别构成比、体重指数、高血压、糖尿病、吸烟、饮酒、冠心病、高脂血症、脑梗死史方面比较,差异均无统计学意义(P>0.05);CHS组患者年龄高于70岁、血压高于150 mmHg、颈动脉狭窄程度高于90%的占比高于非CHS组患者,CHS组收缩期峰值流速(PSV)、血管搏动指数(PI)水平高于非CHS组,差异均有统计学意义(P<0.05)。Logistic分析结果显示颈动脉狭窄程度(OR=6.439;95%CI:1.548~20.137)、PSV(OR=5.063;95%CI:1.271~16.062)、PI(OR=4.448;95%CI:1.190~13.863)为影响颈动脉支架置入术后CHS发生的独立危险因素;而年龄、血压与CHS无明显相关(P>0.05)。PSV诊断颈动脉支架置入术后CHS的AUC、敏感度、特异度分别为0.845(95%CI:0.747~0.917)、85.71%、78.08%;PI诊断颈动脉支架置入术后CHS的AUC、敏感度、特异度分别为0.814(95%CI:0.711~0.892)、71.43%、89.04%;颈动脉狭窄程度诊断颈动脉支架置入术后CHS的AUC、敏感度、特异度分别为0.769(95%CI:0.661~0.856)、85.71%、79.45%;联合监测诊断颈动脉支架置入术后CHS的AUC、敏感度、特异度分别为0.924(95%CI:0.842~0.971)、100.00%、72.65%。联合检测诊断颈动脉支架置入术后CHS的AUC高于PSV、PI、颈动脉狭窄程度单独检测(P<0.05)。结论颈动脉支架置入术后CHS患者大脑中动脉血流速度加快,监测PSV、PI有助于早期诊断CHS的发生。

糖尿病下肢血管病变球囊成形术后高灌注损伤患者的护理效果评价

目的比较两组球囊成形术后发生高灌注损伤的糖尿病患者是否采用加强护理干预的疗效差异。方法 18例糖尿病下肢血管病变患者,经皮经腔球囊成形术(PTA)后发生高灌注损伤,所有患者随机分为护理组(n=9)和对照组(n=9)。护理组采用我科制定的抬高患肢、加强屈伸运动和外敷硫酸镁等加强护理干预方法,对照组仅采用一般冷敷和暴露创口等对症护理计划。通过对照研究,评价加强护理干预对于减轻PTA术后高灌注引起的下肢疼痛、肿胀和皮下淤点等症状的疗效。结果两组相比较,护理组患者经加强护理干预后,下肢肿胀、疼痛及皮下淤点等症状改善评分较对照组有显著性差异(P<0.01)。结论糖尿病患者下肢PTA术后引起的高灌注损伤,经加强护理干预后,具有良好的治疗效果。

颈动脉支架术高灌注损伤因素分析

目的探讨颈内动脉狭窄支架置入术后高灌注损伤的危险因素。方法颈内动脉狭窄经过颈动脉支架成形术治疗的患者中术后出现高灌注损伤12例和未出现高灌注损伤的56例患者的临床资料进行分析，研究高灌注损伤与高血压、糖尿病、狭窄程度、侧枝代偿情况、血压变化情况、狭窄同侧大脑中动脉血流速度变化的相关性。结果结果提示狭窄程度（B=0．637；P=0．034；OR=1．891）、侧枝代偿情况（B=-1．955；P=0．021；OR=0．142）、血压变化（B=-1．818；P=0．011；OR=0．162）和血流速度的变化（B=1．278；P=0．031；OR=3．59）与高灌注损伤密切相关。结论患者的颈动脉狭窄程度越高，侧枝循环代偿越差，术后血压控制不好，术后同侧大脑中动脉的血流速度越快，则高灌注损伤的危险就越大。

Coexistence of hyperlipidemia and acute cerebral ischemia/reperfusion induces severe liver damage in a rat model

AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.

Management of cerebral ischemia due to Takayasu's arteritis

OBJECTIVE: To explore the management of cerebral ischemia caused by Takayasu's arteritis. METHODS: Ninety-three cases treated from June 1984 to September 1999 at the General Post & Telecom Hospital, the Sir Run Run Shaw Hospital, the First Affiliated Hospital of Zhejiang University, the Second Medical College of Beijing University, Beijing An Zhen Hospital, and the Beijing Union Medical College Hospital, including 10 men and 83 women, were reviewed. Of the 93 cases, bypasses from the ascending aorta to the axillary or subclavian artery and from graft to the carotid artery were performed in 47 cases. Subclavian to carotid bypass was performed in six cases. Percutaneous transluminal angioplasty (PTA) was used in five cases and stenting in one. RESULTS: Marked improvement was achieved in 30.3%, fair in 34.9%, improvement in 21.2%, unchanged in 4.6%, and death in 9.0% before discharge; 30.6%, 38.8%, 16.3%, 4.1%, and 2.0% respectively during a mean follow-up of 48 months, and recurrence requiring revision in 8.2%. CONCLUSION: Patients with occlusive lesions of all four cervical arteries always have severe cerebral ischemia and their distal runoff is always unvisualised by angiography. However, we found by exploration that the internal carotid artery is patent in all but one patient. Therefore, an ascending aorta to carotid bypass is feasible in most instances, and this can and should be done when the cerebral perfusion is jeopardized at a time when the patient is in a stable or relatively stable condition. Unfortunately, the cerebral re-perfusion syndrome is still a serious and not completely solved problem.