Global cerebral perfusion parameters were measured using dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) in eight healthy volunteers examined during normal breathing and spontaneous hyperventilati...Global cerebral perfusion parameters were measured using dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) in eight healthy volunteers examined during normal breathing and spontaneous hyperventilation. DSC-MRI-based cerebral blood flow (CBF) de-creased during hyperventilation in all volun-teers (average decrease 29%), and the corre-sponding global CBF estimates were 73±19ml/ (min100g) during normal breathing and 52± 7.9ml/(min100g) during hyperventilation (mean ±SD, n=8). Furthermore, the hypocapnic condi-tions induced by hyperventilation resulted in a prolongation of the global mean transit time (MTT) by on average 14%. The observed CBF estimates appeared to be systematically over-estimated, in accordance with previously pub-lished DSC-MRI results, but reduced to more reasonable levels when a previously retrieved calibration factor was applied.展开更多
目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入2...目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入20-HETE阻断剂17-octadecynoic acid（17-ODYA）并过度通气致PETCO2 20 mm Hg时、加入外源性20-HETE并过度通气致PETCO2 20 mm Hg时,分别于各状态1、5、15、30、60min时测量大脑中动脉、小动脉的直径。结果整个实验过程体温和血液动力学维持稳定。与PETCO2 40 mm Hg时相比,过度通气致PETCO2 20 mm Hg时小动脉直径缩小（P＜0．05）;17-ODYA局部给药并过度通气致PETCO 20 mm Hg时小动脉直径差异无统计学意义（P＞0．05）;外源性20-HETE局部给药并过度通气时小动脉直径缩小（P＜0．05）;在上述各种状态时大脑中动脉直径均无明显变化（P＞0．05）。结论犬低碳酸血症时,20-HETE可能是诱发脑小动脉收缩的机制之一。展开更多
文摘Global cerebral perfusion parameters were measured using dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) in eight healthy volunteers examined during normal breathing and spontaneous hyperventilation. DSC-MRI-based cerebral blood flow (CBF) de-creased during hyperventilation in all volun-teers (average decrease 29%), and the corre-sponding global CBF estimates were 73±19ml/ (min100g) during normal breathing and 52± 7.9ml/(min100g) during hyperventilation (mean ±SD, n=8). Furthermore, the hypocapnic condi-tions induced by hyperventilation resulted in a prolongation of the global mean transit time (MTT) by on average 14%. The observed CBF estimates appeared to be systematically over-estimated, in accordance with previously pub-lished DSC-MRI results, but reduced to more reasonable levels when a previously retrieved calibration factor was applied.
文摘目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入20-HETE阻断剂17-octadecynoic acid（17-ODYA）并过度通气致PETCO2 20 mm Hg时、加入外源性20-HETE并过度通气致PETCO2 20 mm Hg时,分别于各状态1、5、15、30、60min时测量大脑中动脉、小动脉的直径。结果整个实验过程体温和血液动力学维持稳定。与PETCO2 40 mm Hg时相比,过度通气致PETCO2 20 mm Hg时小动脉直径缩小（P＜0．05）;17-ODYA局部给药并过度通气致PETCO 20 mm Hg时小动脉直径差异无统计学意义（P＞0．05）;外源性20-HETE局部给药并过度通气时小动脉直径缩小（P＜0．05）;在上述各种状态时大脑中动脉直径均无明显变化（P＞0．05）。结论犬低碳酸血症时,20-HETE可能是诱发脑小动脉收缩的机制之一。
