Seyama I, Irisawa H, Honda T, Takeda Y, Miwatani T
Jpn J Physiol. 1977;27(1):43-56. doi: 10.2170/jjphysiol.27.43.
The mechanisms of the action of hemolysin extracted from Vibrio parahaemolyticus in the S-A node and right atrium cells of rabbit were studied by means of the single sucrose gap and isometric tension recording methods. Hemolysin caused the membrane to depolarize reversibly without affecting the action potential generating mechanism. Lowering of [Na+]o inhibited membrane depolarization in the presence of hemolysin while the readmission of normal Tyrode solution induced depolarization. Tetrodotoxin (TTX) barely antagonized the depolarizing action of hemolysin but slowed the rate of development of depolarization. Therefore, this depolarization is considered to be primarily due to the increase in conductance to Na which TTX may not block. The dose-response relationship was obtained by measuring a change in membrane resistance. The concentration necessary to yield one-half of the maximum reduction of the membrane was determined to by 7.5 micrograms/ml. Accumulation of Na within the cell may be responsible for an increase of twitch tension observed during the action of a low concentration of hemolysin. On the other hand, a higher concentration of hemolysin seemed to promote exchange of intracellar Na with extracellular Ca, especially when the Na concentration of the perfusing solution was reduced, and led to stronger contracture.
采用单蔗糖间隙法和等长张力记录法，研究了从副溶血性弧菌中提取的溶血素对家兔窦房结和右心房细胞的作用机制。溶血素可使细胞膜发生可逆性去极化，但不影响动作电位的产生机制。降低细胞外液[Na⁺]可抑制溶血素存在时的膜去极化，而重新加入正常台氏液则可诱导去极化。河豚毒素（TTX）几乎不能拮抗溶血素的去极化作用，但可减缓去极化的发展速度。因此，这种去极化主要被认为是由于Na⁺电导增加，而TTX可能无法阻断。通过测量膜电阻的变化获得剂量-反应关系。使膜电阻最大降低一半所需的浓度测定为7.5微克/毫升。细胞内Na⁺的积累可能是低浓度溶血素作用期间观察到的收缩张力增加的原因。另一方面，较高浓度的溶血素似乎促进细胞内Na⁺与细胞外Ca²⁺的交换，尤其是当灌注液中的Na⁺浓度降低时，并导致更强的挛缩。
