| 摘要: | 本實驗主要是探討不同的抗青光眼藥，包括betaxolol， timolol，levobunolol，brimonidine，carteolol，dipivefrin，dorzolamide，brinzolamide，latanoprost，unoprostone，pilocarpine對牛角膜內皮細胞內鈣離子流動性的影響。不同的青光眼藥由原液稀釋成1/100，1/1,000及1/10,000三種濃度。細胞經fura-2-AM吸收後以螢光光度計測量細胞內鈣離子濃度的變化。結果發現timolol(58μM、5.8μM)，levobunolol（171μM、17.1μM及1.71μM），betaxolol（162μM、16.2μM及1.62μM），carteolol（680μM及68μM），dipivefrin（28μM及2.8μM），dorzolamide（616μM及61.6μM），brinzolamide(260μM)，latanoprost(1.1μM)，unoprostone（28.2μM、2.82μM及0.282μM）以及pilocarpine(408μM、40.8μM)都會明顯增加角膜內皮細胞內鈣離子的濃度，只有brimonidine(68μM 6.8μM)會明顯降低細胞內鈣離子的濃度，而Benzalkonium chloride防腐劑對細胞內鈣離子的流動性沒有影響。綜合以上的結果顯示所有的抗青光眼藥可能會改變角膜內皮細胞內鈣離子濃度而影響細胞的生理功能。
The aim of this study was to estimate the effects of various antiglaucoma drugs including betaxolol, timolol, levobunolol, brimonidine, carteolol, dipivefrin, dorzolamide, brinzolamide, latanoprost, unoprostone, and pilocarpine on intracellular free Ca(superscript 2+) ([Ca(superscript 2+)](subscript i)) mobility in cultured bovine corneal endothelial cells. Various antiglaucoma drugs were diluted from original concentrations to 1/100, 1/1,000, and 1/10,000. The [Ca(superscript 2+)](subscript i) mobility was studied by spectrofluorophotometry after loading with the ester of fura-2 (fura-2/AM). It was found that timolol (58 μM and 5.8 μM), levobunolol (171 μM, 17.1 μM, and 1.71 μM), betaxolol (162 μM, 16.2 μM, and 1.62 μM), carteolol (680 μM and 68 μM), dipivefrin (28 μM and 2.8 μM), dorzolamide (616 μM and 61.6 μM), brinzolamide (260 μM), latanoprost (1.1 μM), unoprostone (28.2 μM, 2.82 μM, and 0.282 μM), and pilocarpine (408 μM and 40.8 μM) induced a significant increase in [Ca(superscript 2+)](subscript i). Nevertheless, only brimonidine (68 μM and 6.8 μM) decreased [Ca(superscript 2+)](subscript i) concentration significantly. Benzalkonium chloride preservative did not affect [Ca(superscript 2+)](subscript i) after addition of 0.001, 0.0001 and 0.00001 mg/mL to cells. These results indicate that all antiglaucoma drugs may affect the physiologic function of corneal endothelial cells through change of [Ca(superscript 2+)](subscript i) mobility. |
