Ogoh Shigehiko, Sørensen Henrik, Hirasawa Ai, Sasaki Hiroyuki, Washio Takuro, Hashimoto Takeshi, Bailey Damian M, Secher Niels H
Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan.
The Copenhagen Muscle Research Centre, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Exp Physiol. 2016 Aug 1;101(8):1040-9. doi: 10.1113/EP085772. Epub 2016 Jun 21.
What is the central question of this study? Dynamic cerebral autoregulation (CA) is impaired by sympathetic blockade, and the external carotid artery (ECA) vascular bed may prevent adequate internal carotid artery blood flow. We examined whether α1 -receptor blockade-induced attenuation of dynamic CA is related to reduced ECA vasoconstriction. What is the main finding and its importance? α1 -Receptor blockade attenuated dynamic CA, but in contrast to our hypothesis did not affect the ECA blood flow response to acute hypotension. These findings suggest that the recovery of cerebral blood flow during acute hypotension is unrelated to vasoconstriction within the ECA territory. External carotid artery (ECA) vasoconstriction may defend internal carotid artery (ICA) blood flow during acute hypotension. We hypothesized that the α1 -receptor blockade-induced delay in ICA recovery to the baseline level from acute hypoperfusion is related to attenuated ECA vasoconstriction. The ICA and ECA blood flow were determined by duplex ultrasound during thigh-cuff release-induced acute hypotension while the α1 -receptor blocker prazosin [1 mg (20 kg)(-1) ] was administered to nine seated young healthy men. Both ICA (mean ± SD; by 17 ± 8%, P = 0.005) and ECA (by 37 ± 15%, P < 0.001) blood flow decreased immediately after occluded thigh-cuff release, with a more rapid ICA blood flow recovery to the baseline level (9 ± 5 s) than for the ECA blood flow (17 ± 5 s; P = 0.019). The ICA blood flow recovery from hypoperfusion was delayed with prazosin (17 ± 4 s versus control 9 ± 5 s, P = 0.006), whereas ECA recovery remained unchanged (P = 0.313) despite a similar reduction in mean arterial pressure (-20 ± 4 mmHg versus control -23 ± 7 mmHg, P = 0.148). These findings suggest that α1 -receptor blockade-induced attenuation of the ICA blood flow response to acute hypotension is unrelated to the reduction in ECA blood flow. The sympathetic nervous system via the ECA vascular bed does not contribute to dynamic CA during acute hypotension.
本研究的核心问题是什么?动态脑自动调节(CA)会因交感神经阻滞而受损,并且颈外动脉(ECA)血管床可能会阻碍颈内动脉的充足血流。我们研究了α1受体阻滞引起的动态CA减弱是否与ECA血管收缩减弱有关。主要发现及其重要性是什么?α1受体阻滞减弱了动态CA,但与我们的假设相反,它并未影响ECA对急性低血压的血流反应。这些发现表明,急性低血压期间脑血流的恢复与ECA区域内的血管收缩无关。急性低血压期间,颈外动脉(ECA)血管收缩可能会保护颈内动脉(ICA)的血流。我们假设,α1受体阻滞导致ICA从急性低灌注恢复到基线水平的延迟与ECA血管收缩减弱有关。在9名坐位年轻健康男性中,在大腿袖带松开诱导的急性低血压期间,通过双功超声测定ICA和ECA的血流,同时给予α1受体阻滞剂哌唑嗪[1 mg(20 kg)(-1)]。大腿袖带松开后,ICA(平均值±标准差;下降17±8%,P = 0.005)和ECA(下降37±15%,P < 0.001)的血流立即下降,ICA血流恢复到基线水平的速度(9±5秒)比ECA血流(17±5秒;P = 0.019)更快。使用哌唑嗪后,ICA从低灌注恢复的血流延迟(17±4秒,而对照组为9±5秒,P = 0.006),而尽管平均动脉压有类似程度的降低(-20±4 mmHg,对照组为-23±7 mmHg,P = 0.148),ECA的恢复仍未改变(P = 0.313)。这些发现表明,α1受体阻滞引起的ICA对急性低血压的血流反应减弱与ECA血流减少无关。急性低血压期间,通过ECA血管床的交感神经系统对动态CA没有作用。