Halperin J A, Brugnara C, Nicholson-Weller A
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
J Clin Invest. 1989 May;83(5):1466-71. doi: 10.1172/JCI114039.
The lytic effect of complement on human erythrocytes has been reported by others to increase when Na+ is substituted for K+ in the external medium. In this paper we have investigated the hypothesis that net loss of K+ through a K+ transport pathway protects erythrocytes from complement-induced colloidosmotic swelling and lysis. Antibody-sensitized human erythrocytes containing different intracellular cation concentrations (nystatin treatment) were exposed to low concentrations of guinea pig serum in media of different cation composition; complement lysis was assessed by the release of hemoglobin and the volume of the surviving cells estimated by their density distribution profiles. Complement-dependent swelling and lysis of erythrocytes (a) were limited by the presence of an outwardly directed K+ electrochemical gradient and (b) were enhanced by carbocyanine, a specific inhibitor of the Ca2+-activated K+ transport pathway, and by absence of Ca2+ in the external medium. We propose that during complement activation a rising cytosolic calcium triggers the Ca2+-activated K+ permeability pathway, the Gardos effect, produces a net K+, Cl- and water loss, and thus limits the colloidosmotic swelling and lysis of erythrocytes.
其他人曾报道，当用Na⁺替代细胞外介质中的K⁺时，补体对人红细胞的溶解作用会增强。在本文中，我们研究了一种假说，即通过K⁺转运途径导致的K⁺净流失可保护红细胞免受补体诱导的胶体渗透压肿胀和溶解。将含有不同细胞内阳离子浓度的抗体致敏人红细胞（制霉菌素处理）置于不同阳离子组成的介质中，暴露于低浓度豚鼠血清中；通过血红蛋白释放评估补体溶解情况，并根据存活细胞的密度分布曲线估算其体积。红细胞依赖补体的肿胀和溶解：(a) 受外向K⁺电化学梯度的限制；(b) 因Ca²⁺激活的K⁺转运途径的特异性抑制剂羰花青以及细胞外介质中Ca²⁺的缺失而增强。我们提出，在补体激活过程中，胞质钙升高会触发Ca²⁺激活的K⁺通透性途径，即加尔多斯效应，导致K⁺、Cl⁻和水的净流失，从而限制红细胞的胶体渗透压肿胀和溶解。
