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首页> 外文期刊>Journal of Clinical Ultrasound: JCU >Cerebrovascular regulation and vasoneuronal coupling.
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Cerebrovascular regulation and vasoneuronal coupling.

机译：脑血管调节和血管神经元偶联。

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Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegration of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit.
机译：维持脑灌注压力是预防脑缺血的先决条件。全身灌注压力的生理波动可通过脑血管自动调节得到补偿。 （1）全身血流动力学衰竭（例如，远端至严重的动脉狭窄），过度调节血管的能力可能导致脑灌注不足。 （2）脑血管自动调节功能异常和衰竭。或（3）两者。超声具有出色的时间分辨率，是非侵入性的，并且很容易用于后续研究。尽管其空间分辨率较差，但经颅多普勒超声检查已用于确定脑灌注储备研究，该研究可测量高碳酸血症或应用血管活性剂（例如乙酰唑胺）期间的脑血流速度（CBFV）。该方法评估了严重供血狭窄或大脑供血动脉闭塞的血液动力学受损患者的血管舒缩调节。在倾斜台检查过程中监测CBFV可直接测量大脑的自动调节能力。在系统性体位性低血压的患者中，尽管系统血压正常，但可能会维持或维持脑血管代偿功能，甚至更重要的是脑血管功能失调。在适当的神经元刺激过程中，CBFV变化反映了血管神经元偶联。神经元功能障碍与CBFV异常有关，例如先兆性偏头痛患者后脑动脉（PCA）局灶性脑功能障碍的先决条件，其中在扩散性抑郁症中，血管神经元偶联和局部缺血的巨大改变正在受到威胁。在这些患者中，极高的不对称性血管内泌尿激素耦合可能是触发机制。由于各种神经元刺激（例如，运动感觉或认知范式）的空间分辨率差，仅引起MCA CBFV总体变化中代表性不足的局部神经元区域，测试大脑中动脉（MCA）区域内的血管神经元偶联更加困难。但是，运动刺激诱发的CBFV可能被用于指示在急性脑缺血伴感觉运动性偏瘫的过程中血管神经元耦合的失整合，而且，似乎对运动缺陷具有预后价值。

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