Analysis of calcium ion transition in the cochlear fluids under cochlear blood flow disturbance

耳蜗液中钙离子（Ca^<2+>）活性的动态平衡被认为是维持耳蜗功能所必需的。由于内耳局部缺血可破坏内耳稳态，我们在豚鼠压迫迷路动脉局部缺血期间和之后监测了淋巴周围和内淋巴Ca^<2+>的活性。局部缺血30分钟时，淋巴周围和淋巴内Ca^<2+>活性分别升高1.5倍和4倍。，分别为缺血前值。血流恢复后，活性呈指数型下降，接近缺血前值。局部缺血时淋巴周围和内淋巴明显可逆酸化，但对Ca^<2+>活性变化没有太大作用。另一方面，利用室模型和数学估计，揭示了电化学梯度驱动的被动扩散可以解释Ca^<2+>的转变。在此分析过程中，假设Ca^<2+>时血淋巴周围屏障（BPB）的表观透性表面积积（PS积）略大于血脑屏障（BBB），计算出淋巴周围周转率约为1.4 μ l/min。

Homeostasis of calcium ion (Ca^<2+>) activities in the cochlear fluids are considered to be essential to maintain the function of the cochlea. Since local ischemia in the inner ear could disrupt the homeostasis, Ca^<2+> activities in perilymph and endolymph were monitored during and after local ischemia induced by pressing a labyrinthine artery in the guinea pig. In 30-minute local ischemia, perilymph and endolymph Ca^<2+> activities increased approximately 1.5 and 4 times as much. as the preischemic values, respectively, After the blood flow was restored, the activities decreased close to the preischemic values in an exponential manner. An evident and reversible acidification of perilymph and endolymph was also noted during local ischemia but found not so contributory to the Ca^<2+> activity changes. On the other hand, utilizing compartment models and mathematical estimations, it was disclosed that Ca^<2+> transitions could be mostly explained by passive diffusion driven by electrochemical gradients. In this analytical procedure, the apparent permeability surface area product (PS product) of blood-perilymph barrier (BPB) for Ca^<2+> was assumed slightly larger than that of blood-brain barrier (BBB), and the perilymph turnover rate was computed to be about l.4mu l/min.