STROMAL LACTATE ACCUMULATION CAN ACCOUNT FOR CORNEAL EDEMA OSMOTICALLY FOLLOWING EPITHELIAL HYPOXIA IN THE RABBIT
STROMAL LACTATE ACCUMULATION CAN ACCOUNT FOR CORNEAL EDEMA OSMOTICALLY FOLLOWING EPITHELIAL HYPOXIA IN THE RABBIT
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DOI：
10.1113/jphysiol.1981.sp013971
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发表时间：
1981-01-01
影响因子：
5.5
通讯作者：
KLYCE, SD
中科院分区：
文献类型：
--
作者：
KLYCE, SD
在离体兔角膜中研究了上皮缺氧后基质水肿的机制。在整个角膜分离物和其中用硅油阻断流体穿过内皮的运动的制备物中，在泪液侧缺氧1小时后基质肿胀约20 μ m。在使用整个角膜的实验中，只要房水P[分压]O2> 40 mm Hg，基质厚度就与泪液侧O2张力无关。无论是上皮厚度，也不上皮电阻，总离子渗透性的措施，是显着影响阻塞呼吸。10度。C降低角膜温度显着降低缺氧肿胀的速度，这表明参与代谢依赖性水合过程，并暗示基质中的分解产物的积累。当CN-被用来模拟缺氧的效果，在隔离的整个角膜，被动36 Cl单向流量不受影响，但乳酸生产率和基质[乳酸]增加了一倍以上。这些测量结果与角膜水合动力学的数学模型一起使用，以检查缺氧性水肿的原因。上皮缺氧促进上皮乳酸产生和释放到间质。该过程导致基质乳酸盐浓度增加和基质NaCl浓度降低（主要通过稀释）。基质乳酸盐积累超过渗透负荷对[NaCl]的稀释作用，产生基质水肿。尽管缺氧导致角膜代谢性酸中毒，但不需要假设对HCO 3转运的内皮渗透性的影响来解释缺氧导致的基质水肿。
The mechanism underlying stromal edema subsequent to epithelial hypoxia was investigated in isolated rabbit corneas. Stromas swelled about 20 .mu.m following a 1-h period of tear side hypoxia in both whole corneal isolates and in preparations in which fluid movement across the endothelium was blocked with silicone oil. In the experiments using whole corneas, stromal thickness was independent of tear side O2 tension as long as aqueous humor P[partial pressure]O2 was > 40 mm Hg. Neither epithelial thickness nor epithelial electrical resistance, a measure of total ion permeability, was significantly affected by blocking respiration. A 10.degree. C reduction in corneal temperature markedly reduced the rate of hypoxic swelling, suggesting the involvement of a metabolism-dependent hydrating process and implicating the stromal accumulation of a catabolyte. When CN- was used to mimic the hypoxic effect in isolated whole corneas, the passive 36Cl unidirectional flux was unaffected, but lactate production rate and stromal [lactate] more than doubled. These measurements were used with a mathematical model for corneal hydration dynamics to examine the causes of hypoxic edema. Epithelial hypoxia enhances epithelial lactate production and release to the stroma. This process causes an increase in stromal lactate concentration and a decrease in stromal NaCl concentration (primarily through dilution). Stromal lactate accumulation exceeds in osmotic load the dilutional effect on [NaCl], producing stromal edema. Whereas hypoxia produces corneal metabolic acidosis, effects on endothelial permeability of HCO3- transport need not be postulated to explain the stromal edema that results from hypoxia.