Lombard J H, Willems W J, Harder D R, Stekiel W J
Circ Shock. 1986;18(2):131-40.
Although transmembrane potential (Em) appears to be an important regulator of vascular smooth muscle (VSM) contractile force in vivo, little is known of the electrophysiological changes in VSM during low flow states. In rats, VSM in small mesenteric veins depolarizes in the compensatory stage of hemorrhagic hypotension while the onset of peripheral vascular decompensation is associated with VSM hyperpolarization. Pretreatment with 30 mg/kg i.v. of methylprednisolone prevents the Em changes in mesenteric veins of hemorrhaged rats and reduces the depolarization of isolated vessels in response to norepinephrine, suggesting that some therapeutic agents may act by modifying the electrophysiological responses of VSM during the stress. Finally, adrenergic depolarization under resting conditions may contribute to a reduced ability of spontaneously hypertensive rats (SHR) to tolerate blood loss by reducing their compensatory venoconstrictor reserve relative to normotensive WKY controls. Although these observations suggest that vascular responses to hypotensive stress are related to the effects of the sympathetic nervous system upon VSM Em, further studies are required fully to elucidate the relative role of Em-dependent and Em-independent mechanisms in controlling active VSM tone during low flow states.
尽管跨膜电位（Em）似乎是体内血管平滑肌（VSM）收缩力的重要调节因子，但对于低流量状态下VSM的电生理变化却知之甚少。在大鼠中，小肠系膜静脉中的VSM在失血性低血压的代偿期会发生去极化，而外周血管失代偿的开始与VSM超极化有关。静脉注射30mg/kg甲基强的松龙预处理可防止出血大鼠肠系膜静脉的Em变化，并减少离体血管对去甲肾上腺素的去极化反应，这表明某些治疗药物可能通过改变应激期间VSM的电生理反应起作用。最后，静息条件下的肾上腺素能去极化可能导致自发性高血压大鼠（SHR）相对于正常血压的WKY对照降低其代偿性静脉收缩储备，从而降低耐受失血的能力。尽管这些观察结果表明血管对低血压应激的反应与交感神经系统对VSM Em的影响有关，但仍需要进一步研究以充分阐明Em依赖性和Em非依赖性机制在低流量状态下控制VSM主动张力中的相对作用。
