Kidder G W
Am J Physiol. 1984 Jan;246(1 Pt 1):G40-7. doi: 10.1152/ajpgi.1984.246.1.G40.
The sudden potential drop (SPD) with its associated resistance drop, previously noted during anoxia when serosal pH was slightly decreased, can also be produced by substrate deprivation and reversed by addition of substrate. During a critical portion of the response, alternate stable high and low potential difference states can be selected by current pulsing. High Ca2+ in the serosal solution prevents the SPD response, and any condition preventing an SPD response will reverse the post-SPD potential. Although pH 1 mucosal solutions do not damage the tissue, an SPD under these conditions results in permanent loss of secretory activity, apparently due to increased H+ permeability in the post-SPD state. Cl-, Rb+, and urea fluxes are unchanged by the SPD. Since gastric anoxia and mild serosal acidosis might be expected during strong sympathetic stimulation, it is notable that an SPD can be produced in vivo by anoxia or vasoconstrictive drugs under conditions apparently in agreement with the in vitro requirements. This might provide a model system for studies of stress ulcer production. An equivalent circuit model for the SPD is presented, which agrees satisfactorily with the observations.
先前在缺氧期间,当浆膜pH值略有下降时所观察到的伴有相关电阻下降的突然电位降(SPD),也可由底物剥夺产生,并可通过添加底物而逆转。在反应的关键部分,通过电流脉冲可选择交替稳定的高电位差和低电位差状态。浆膜溶液中高浓度的Ca2+可阻止SPD反应,任何阻止SPD反应的条件都会使SPD后的电位逆转。尽管pH值为1的黏膜溶液不会损伤组织,但在这些条件下的SPD会导致分泌活性永久性丧失,这显然是由于SPD后状态下H+通透性增加所致。SPD对Cl-、Rb+和尿素通量没有影响。由于在强烈交感神经刺激期间可能会出现胃缺氧和轻度浆膜酸中毒,值得注意的是,在体内,缺氧或血管收缩药物在明显符合体外条件的情况下可产生SPD。这可能为应激性溃疡产生的研究提供一个模型系统。本文提出了一个SPD的等效电路模型,该模型与观察结果令人满意地相符。