目的:探讨人尿激肽原酶(HUK)对急性脑梗死患者侧支循环与脑血流灌注的影响,以找寻新的药物来有效开放侧支循环,挽救缺血组织。方法:纳入急性大脑中动脉(MCA)脑梗死患者40例,采用随机对照的方法将被试分为HUK治疗组和对照组,每组各20例,...目的:探讨人尿激肽原酶(HUK)对急性脑梗死患者侧支循环与脑血流灌注的影响,以找寻新的药物来有效开放侧支循环,挽救缺血组织。方法:纳入急性大脑中动脉(MCA)脑梗死患者40例,采用随机对照的方法将被试分为HUK治疗组和对照组,每组各20例,于治疗前1天、治疗后第7天及第30天采集两组被试的扩散加权成像(DWI)和灌注加权成像(PWI)图像,比较两组治疗前后梗死中心区和缺血半暗带区的血流灌注情况。然后采用对比剂增强MRA(CE-MRA)技术比较两组治疗前后梗死周围区软脑膜侧支循环的建立情况。结果:1治疗后两组被试梗死中心区和缺血半暗带区的局部脑血流(r CBF)值均较治疗前增加,但与对照组相比,HUK治疗组增加更为明显,且治疗后两组间缺血组织r CBF值的差异有统计学意义(梗死中心区:0.86±0.43 vs 0.54±0.13,P<0.05;缺血半暗带区:2.11±0.36 vs 1.03±0.61,P<0.05)。2采用CE-MRA技术可显示侧裂和大脑半球凸面软脑膜侧支循环的建立,HUK治疗组侧支血管建立的评分较对照组明显提高(4.3±0.5 vs 3.2±0.7,P<0.05)。结论:HUK可有效改善急性脑梗死患者缺血组织的侧支循环和血流灌注;CE-MRA技术有望成为侧支血管成像的新手段。展开更多
The overall prevalence of dementia in Chinese people aged 60 years and older was 5.30%,imposing a heavy burden on the public and health care systems.Currently,there are no effective therapeutic strategies availa...The overall prevalence of dementia in Chinese people aged 60 years and older was 5.30%,imposing a heavy burden on the public and health care systems.Currently,there are no effective therapeutic strategies available to prevent Alzheimer’s disease(AD).Accumulating evidence implicates that the pathophysiological process of AD begins decades before the emergence of clinical symptoms.展开更多
文摘目的:探讨人尿激肽原酶(HUK)对急性脑梗死患者侧支循环与脑血流灌注的影响,以找寻新的药物来有效开放侧支循环,挽救缺血组织。方法:纳入急性大脑中动脉(MCA)脑梗死患者40例,采用随机对照的方法将被试分为HUK治疗组和对照组,每组各20例,于治疗前1天、治疗后第7天及第30天采集两组被试的扩散加权成像(DWI)和灌注加权成像(PWI)图像,比较两组治疗前后梗死中心区和缺血半暗带区的血流灌注情况。然后采用对比剂增强MRA(CE-MRA)技术比较两组治疗前后梗死周围区软脑膜侧支循环的建立情况。结果:1治疗后两组被试梗死中心区和缺血半暗带区的局部脑血流(r CBF)值均较治疗前增加,但与对照组相比,HUK治疗组增加更为明显,且治疗后两组间缺血组织r CBF值的差异有统计学意义(梗死中心区:0.86±0.43 vs 0.54±0.13,P<0.05;缺血半暗带区:2.11±0.36 vs 1.03±0.61,P<0.05)。2采用CE-MRA技术可显示侧裂和大脑半球凸面软脑膜侧支循环的建立,HUK治疗组侧支血管建立的评分较对照组明显提高(4.3±0.5 vs 3.2±0.7,P<0.05)。结论:HUK可有效改善急性脑梗死患者缺血组织的侧支循环和血流灌注;CE-MRA技术有望成为侧支血管成像的新手段。
文摘The overall prevalence of dementia in Chinese people aged 60 years and older was 5.30%,imposing a heavy burden on the public and health care systems.Currently,there are no effective therapeutic strategies available to prevent Alzheimer’s disease(AD).Accumulating evidence implicates that the pathophysiological process of AD begins decades before the emergence of clinical symptoms.