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猫脑动脉肌源性调节的细胞机制。

A cellular mechanism for myogenic regulation of cat cerebral arteries.

作者信息

Harder D R

出版信息

Ann Biomed Eng. 1985;13(3-4):335-9. doi: 10.1007/BF02584252.

Abstract

Autoregulation of cerebral blood flow is accomplished through integration of metabolic, neurogenic and myogenic mechanisms. Myogenic mechanisms involve activation of cerebral arterial muscle cells as transmural pressure increases, providing a means through which vessel caliber can be regulated to maintain blood flow constant. The cellular mechanisms involved in this myogenic response may involve changes in the electrical potential across the plasma membrane. When isolated cat middle cerebral arteries are cannulated and prepared in a manner allowing manipulation of transmural pressure, the muscle cell membrane depolarizes as pressure increases. The degree of membrane depolarization in response to an elevated pressure is dependent upon extracellular Ca2+ [( Ca]o), increasing as [Ca]o is elevated and markedly decreasing as [Ca]o is reduced to low levels. When these arterial preparations are maintained at a physiological pressure of around 100 mm Hg, spontaneous action potentials can be recorded which increase in frequency upon further elevation in pressure. Vessels exhibiting such electrical activity can be observed to decrease in diameter as pressure is increased. Such finding suggest a membrane electrical mechanism for myogenic autoregulation of cerebral arteries.

摘要

脑血流量的自动调节是通过整合代谢、神经源性和肌源性机制来实现的。肌源性机制涉及随着跨壁压力增加,脑动脉肌细胞被激活,这提供了一种调节血管口径以维持血流量恒定的方式。参与这种肌源性反应的细胞机制可能涉及质膜跨膜电位的变化。当将分离的猫大脑中动脉插管并以允许操纵跨壁压力的方式制备时,随着压力增加,肌细胞膜去极化。响应压力升高的膜去极化程度取决于细胞外Ca2+[(Ca]o),随着[Ca]o升高而增加,而当[Ca]o降低到低水平时则明显降低。当这些动脉制剂维持在约100mmHg的生理压力时,可以记录到自发动作电位,随着压力进一步升高,其频率增加。可以观察到表现出这种电活动的血管随着压力增加而直径减小。这些发现提示了脑动脉肌源性自动调节的膜电机制。

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