血流动力学障碍

结论颈动脉粥样硬化（CAS）所致颈动脉血流动力学障碍及斑块性质与各种类型脑梗死的发生密切相关。

Conclusion The carotid artery hemodynamics disturbance and plaque character which are induced by carotid atherosclerosis are close correlated with the occurrence of various kinds cerebral infarction .

方法5例因反复发作有血流动力学障碍的室性心动过速/心室颤动（VT/VF）均顺利植入ICD（其中双腔ICD2例），随访6～24个月，观察患者临床疗效及ICD工作情况。

Methods From August 2001 to August 2003 , 5 patients with recurrent ventricular tachycardia and fibrillation ( VT / VF ) received ICD .

利用环孢素A（CsA）致大鼠离休灌注肾急性血流动力学障碍模型研究了内皮源性舒张因子（EDRF）在CsA致肾毒性发生中的作用。

The model of CsA induced IPK acute hemodynamic disturbances was used to explore the possible role of endothelium derived rived relaxing factor ( EDRF ) in mediating CsA induced nephrotoxicity .

本研究应用环孢素A（CsA）致大鼠离体灌注肾急性血流动力学障碍模型，研究了川芎嗪对CsA肾毒性的防治作用。

The preventive effect of tetramethylpyrazine ( TMP ) on the cyclosporine A ( CsA ) induced nephrotoxicity was studied in the experimental model of CsA induced acute hemodynamic disorder of isolated perfused rat kidney ( IPK ) .

结果提示EDRF释放减少或灭活增多在CsA引起的IPK急性血流动力学障碍中可能具有重要意义。

These results suggested that the reduction of release or the increase of breakdown of EDRF might be of an important significance in CsA induced acute IPK hemodynamic disturbance .

主动脉内球囊反搏逐渐被越来越多的应用于存在严重血流动力学障碍的患者，已成为目前使用最广泛的心脏辅助装置之一。

Intra-aortic balloon counterpulsation ( IABP ) has been increasingly widely used in patients needing hemodynamic support and has become one of the most popular circulatory-assistance devices .

各种因素造成大脑中动脉狭窄或闭塞，通常能造成相应供血部位血流动力学障碍，脑卒中发生的危险性增高，急性主干闭塞更能带来同侧大脑半球的灾难性大面积脑梗死，甚至死亡。

Middle cerebral artery stenosis or occlusion due to various factors , usually cause corresponding hemodynamic disorders and stroke risk increases . Acute occlusion is more likely to lead to catastrophic large area infant of the ipsilateral cerebral hemisphere .

结论：ghrelin治疗可以部分纠正败血症休克大鼠的血流动力学紊乱和代谢障碍。

CONCLUSION : Treatment with ghrelin could correct partly the abnormalities of hemodynamics and metabolic disturbance in septic shock of rats .

认为老年人椎动脉型颈椎病的发病机制主要在于椎动脉受压，及／或引起的一系列生化改变，如血流动力学改变、微循环障碍、自由基损伤等等。

The mechanism of senile CSA mainly lies in oppressed vertebral artery , and / or . a series of evocable biochemical changes , such as kinetic change of blood stream , hindrance of microcirculation , damnification of free radical and so on .

血管纤维化增加动脉僵硬度，引发血流紊乱，最终造成血流动力学障碍，成为动脉粥样硬化发生发展的力学基础。

Vascular fibrosis may increase the wall stiffness , lead to turbulent blood flow , and eventually derange the hemodynamic function , which is the biomechanical basis for atherosclerosis .