Paulson O B, Waldemar G, Schmidt J F, Strandgaard S
Department of Neurology, Rigshospitalet, Copenhagen, Denmark.
Am J Cardiol. 1989 Feb 2;63(6):2C-5C. doi: 10.1016/0002-9149(89)90396-2.
Autoregulation of the cerebral circulation is the regulating mechanism that keeps cerebral blood flow (CBF) constant within wide limits of arterial pressure. The lower limit is defined as the value of mean arterial pressure below which CBF decreases below the plateau, and the upper limit as the value of mean arterial pressure above which CBF increases above the plateau (60 and 150 mm Hg, respectively). Two possible mechanisms for autoregulation are discussed, myogenic response and metabolic regulation. Stimulation of the sympathetic nervous system and antagonism of the renin-angiotensin system modulate CBF autoregulation by shifting the entire curve toward higher or lower values of arterial pressure, respectively. The autoregulatory curve is shifted toward higher arterial pressures in chronic hypertension. Therefore, the tolerance to acute decreases in arterial pressure is impaired. Concomitantly, the tolerance of the brain to acute increases in arterial pressure is improved. This shift in the limits of autoregulation is due to structural and functional (hemodynamic) changes in the cerebral resistance vessels. These adaptive changes are partly reversible after chronic treatment with antihypertensive agents. The pathophysiology of autoregulation should be taken into consideration before drugs are used to decrease arterial pressure acutely.
脑循环的自动调节是一种调节机制，可在动脉压的广泛范围内保持脑血流量（CBF）恒定。下限定义为平均动脉压的值，低于该值时CBF降至平台期以下，上限定义为平均动脉压的值，高于该值时CBF升至平台期以上（分别为60和150 mmHg）。讨论了自动调节的两种可能机制，即肌源性反应和代谢调节。刺激交感神经系统和拮抗肾素-血管紧张素系统分别通过将整个曲线向动脉压的更高或更低值移动来调节CBF自动调节。在慢性高血压中，自动调节曲线向更高的动脉压移动。因此，对动脉压急性降低的耐受性受损。同时，大脑对动脉压急性升高的耐受性得到改善。自动调节极限的这种变化是由于脑阻力血管的结构和功能（血流动力学）变化所致。在用抗高血压药物进行长期治疗后，这些适应性变化部分是可逆的。在使用药物急性降低动脉压之前，应考虑自动调节的病理生理学。
