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血管狭窄

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Endovascular restenosis is an abnormal repairing response of vessel against injury. Following stent implantation, vessel contractibility reconstitution, local inflammation and thrombogenesis, intima hyperplasia, mainly vascular smooth muscle hyperplasia, are found.

血管内再狭窄是血管对抗损伤的一种异常修复反应,表现为支架植入后血管的收缩性重构,局部的炎症与血栓形成,以及以血管平滑肌细胞增殖为主的内膜增生。

GD can notedly decrease the expression of NF-κB and NF-κB mRNA in the abdominal aorta of AS rabbits damaged with sacculus proprius, and then may prevent the occurance of RS, which may he a part of the mechanism of preventive effect of GD.

冠心通络方减轻血管内膜增生、防止血管再狭窄的内在机制可能在于抑制NF-κB活性,进而抑制血管平滑肌细胞增殖、血管内膜增生。

Between 6th and 14th weeks afteconstricted bilateral renal arteries, the blood pressure in the majority of RHRSP with cerebral infarction was obviously higher than in RHRSP without cerebral infarction (28. 8±2. 24kPa~32. 3 ±2. 88kPa, 26. 2±2. 01~28. 3±2. 33kPa respectively). Severe hyalinosis, fibrosis, wall hypertrophy, lumen stenosis, and even microaneurysm formation in cerebral small arteries in RHRSP with cerebral infarction were found, while slight to mild arteriolosclerosis in RHRSP was found without cerebral infarction.

本实验发现,RHRSP在经受不同水平的低血压后,产生脑梗塞的大多数(32/38只)在肾动脉狭窄术后第六周至第十四周,血压为28.8±2.24 kPa~32.3±2.88 kPa(216±17mmHg~242±22mmHg),显著高于无脑梗塞的RHRSP,并且发现这些RHRSP的脑内小血管呈严重的透明样变、纤维素样变性,管壁增厚,管腔狭窄,部分有微动脉瘤形成;而无脑梗塞的RHRSP的血压为26.2±2.01kPa~28.3±2.33 kPa(200±15mmHg~212±17.5mmHg),其脑内小血管呈轻至中度的动脉硬化改变。

Various arterious stenosis diagnosed by CTA were 115 segment, DSA 108 segment.

CTA显示不同程度狭窄的血管段共115段; DSA显示不同程度狭窄的血管段共108段。

The article reviews mechanism of action of caroid artery resulting from hypertension, especially debates vascular endothelial injury resulting from shear stress of vascular wall caused by hypertension, which can also affect vasopermeability by affecting the morphans, structure and function of vascular endothelium.

本文综述高血压引起颈动脉狭窄的发生机制,重点探讨血压对血管壁所造成的切应力引起的血管内皮细胞受损,通过影响血管内皮细胞的形态、结构和功能,并影响血管通透性,从而有助于脂质沉积的病理学机制。

Stenosis of internal caroid antery was found in 32 of 48 branches in 24 case. 5 branches were occlusive and 11 branches were normal. 22 cases with large or moderate cerebral infarction volume (>5 cm3) confirmed by CT and MRI were smaller than those on MSCTPI as having abnormal perfusion lesions,which were moderate and obvious stenosis and occlusion on MSCTA. In 2 cases with small cerebral infarction volume(<5 cm3), MSCTPI and MSCTA revealed normal.

其中32支颈内动脉呈不同程度的狭窄,5支颈内动脉闭塞,11支血管无狭窄。22例在常规CT及MRI图像上为中及大体积梗死(>5 cm3)的患者,MSCTPI发现与梗死灶相对应的异常灌注区,且均比常规CT及MRI图像上病灶体积大, MSCTA显示颈内动脉呈中重度狭窄或闭塞。2例未发现明显灌注异常的患者,为小体积梗死灶(<5 cm3),MSCTA显示颈内动脉正常。

Stenosis of internal caroid antery was found in 32 of 48 branches in 24 case. 5 branches were occlusive and 11 branches were normal. 22 cases with large or moderate cerebral infarction volume (>5 cm3) confirmed by CT and MRI were smaller than those on MSCTPI as having abnormal perfusion lesions,which were moderate and obvious stenosis and occlusion on MSCTA.

其中32支颈内动脉呈不同程度的狭窄,5支颈内动脉闭塞,11支血管无狭窄。22例在常规CT及MRI图像上为中及大体积梗死(>5 cm3)的患者,MSCTPI发现与梗死灶相对应的异常灌注区,且均比常规CT及MRI图像上病灶体积大, MSCTA显示颈内动脉呈中重度狭窄或闭塞。2例未发现明显灌注异常的患者,为小体积梗死灶(<5 cm3),MSCTA显示颈内动脉正常。

The results suggested that vascular remodeling was the most prominent in LCA subjected to low shear stress accompanied by hypertension, which is regulated through the changing expression of p-Akt, p-p38, Rho GDIα. Tributyrin could affect the flow mediated carotid remodeling by both increasing apoptosis and decreasing proliferation of VSMCs through PI-3K/Akt, bcl-2, p53, p27. Tributyrin could have potential roles in treatment of vascular diseases, such as artherosclerosis and vascular restenosis, etc.

结果提示,高血压与切应力协同作用对血管重建的影响最为显著,Akt、p38和Rho GDIα信号通路参与了高血压与低切应力诱导的血管重建过程;Tributyrin对血管重建的干预作用是通过影响PI-3K信号通路,调节凋亡相关蛋白bcl-2以及细胞周期调控蛋白p53和p27的表达水平而实现的;Tributyrin有可能成为一种在动脉粥样硬化、血管再狭窄等疾病防治中有潜在临床应用价值的药物。

The severity of coronary atherosclerosis was underestimated by CAG. 38 segments were indicated for operation by IVUS. Post-stenting in 38 segments was checked with IVUS. 46 segments had good effect and 10 segments with no ideal effect needed high-pressure ballon re-expansion. This 10 segments with re-expansion were shown good effect by IVUS. Statistic analysis showed VA and LA were increased after post-stenting. PA and area stenosis rate were reduced. VA and PA had no difference , but LA and ASR had obvious difference between pre-high pressure and post-high pressure ballon re-expansion.

结果IVUS在显示血管壁的形态结构、斑块的性质方面敏感性高于CAG检查,诊断冠心病更准确,血管造影低估冠脉病变的严重程度;本组46处血管,经CAG和IVUS检查符合介入治疗干预指征的血管38处,IVUS指导置入支架的大小、长度以及置入的位置,支架置入术后,血管总截面积、管腔面积增加,斑块面积及面积狭窄率降低,并有显著性差异。

"In-stent restenosis of DES occurs in nearly 10% of all DES implanted oer time," senior inestigator Dr. Ron Waksman told Reuters Health."Although not diffuse as with bare metal stents, DES ISR still associated with late eents."

高级研究人员Ron Waksman博士告诉路透社健康版说:&10%的药物支架在植入一段时间后发生血管内支架再狭窄,虽然不像单纯金属支架的问题那样广泛,药物支架血管内支架再狭窄也与近期活动有联系。&

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