Delaey C, Boussery K, Van de Voorde J
Department of Physiology and Pathophysiology, Ghent University, Belgium.
Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3555-60.
To investigate the mechanisms involved in hypoxic vasodilation using an in vitro setup.
Retinal arteries with and without retinal tissue were mounted on a wire myograph. The segments were contracted with prostaglandin (PG)F(2alpha) (30 microM) or 120 mM K(+). Hypoxia was induced by replacement of O(2) by N(2) in the gas used to bubble the Krebs-Ringer bicarbonate organ bath solution.
Hypoxia induced complete relaxation of preparations with adherent retinal tissue contracted with PGF(2alpha). Preparations without retinal tissue were not affected by the change in oxygenation. When the retinal arteries were contracted with 120 mM K(+), hypoxia no longer induced relaxation of the preparation with adherent retinal tissue. The presence of an NO-synthase inhibitor (L-NA, 0.1 mM), a cyclooxygenase inhibitor (indomethacin, 50 microM), or an adenosine receptor antagonist (8-sulfophenyltheophylline, 1 mM) did not affect hypoxic vasodilation. Excitatory amino acids and lactate had no or only a limited effect on the PGF(2alpha)-induced contraction and are therefore unlikely mediators of hypoxic vasodilation. HCl (10 mM) reduced the pH to 6.1 +/- 0.08 (n = 4) and induced a pronounced but transient relaxation of the retinal artery contracted with PGF(2alpha) or 120 mM K(+), whereas hypoxia induced relaxation of the retinal artery contracted with PGF(2alpha) only in the presence of adherent retinal tissue.
Adherent retinal tissue mediates the hypoxic vasodilatation of bovine retinal arteries in vitro. Neither NO, prostanoids, adenosine, excitatory amino acids lactate or changes in pH seem to be involved in this hypoxic response.
使用体外实验装置研究低氧性血管舒张的相关机制。
将带有或不带有视网膜组织的视网膜动脉安装在钢丝肌动描记器上。这些节段用前列腺素（PG）F2α（30微摩尔）或120毫摩尔钾离子使其收缩。通过用氮气替换用于向克雷布斯 - 林格碳酸氢盐器官浴溶液中鼓泡的气体中的氧气来诱导低氧状态。
低氧状态可使因PGF2α收缩的带有附着视网膜组织的标本完全舒张。没有视网膜组织的标本不受氧合变化的影响。当视网膜动脉用120毫摩尔钾离子收缩时，低氧状态不再能使带有附着视网膜组织的标本舒张。一氧化氮合酶抑制剂（L - 硝基精氨酸，0.1毫摩尔）、环氧化酶抑制剂（吲哚美辛，50微摩尔）或腺苷受体拮抗剂（8 - 磺基苯基茶碱，1毫摩尔）的存在并不影响低氧性血管舒张。兴奋性氨基酸和乳酸对PGF2α诱导的收缩没有或仅有有限的影响，因此不太可能是低氧性血管舒张的介质。10毫摩尔盐酸将pH值降至6.1±0.08（n = 4），并使因PGF2α或120毫摩尔钾离子收缩的视网膜动脉出现明显但短暂的舒张，而低氧状态仅在存在附着视网膜组织时才会使因PGF2α收缩的视网膜动脉舒张。
附着的视网膜组织在体外介导了牛视网膜动脉的低氧性血管舒张。一氧化氮、前列腺素、腺苷、兴奋性氨基酸、乳酸或pH值变化似乎均不参与这种低氧反应。
