Physiology Programme, Department of Molecular Biosciences, University of Oslo, Oslo, Norway.
Am J Physiol Regul Integr Comp Physiol. 2010 May;298(5):R1225-39. doi: 10.1152/ajpregu.00521.2009. Epub 2010 Feb 17.
Systemic vascular resistance (R(sys)) of freshwater turtles increases substantially during anoxia, but the underlying mechanisms are not fully understood. We investigated whether hydrogen sulfide (H(2)S), an endogenously produced metabolite believed to be an O(2) sensor/transducer of vasomotor tone, contributes to the increased R(sys) of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H(2)S donor NaHS in anesthetized turtles at 21 degrees C and fully recovered normoxic turtles at 5 degrees C and 21 degrees C revealed H(2)S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H(2)S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21 degrees C; 14 days at 5 degrees C) when plasma H(2)S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by approximately 3- and 4-fold during anoxia at 21 degrees C, and 5 degrees C, respectively. Yet, blockade of endogenous H(2)S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (G(sys)) exhibited by 5 degrees C anoxic turtles. These findings suggest that the signal transduction pathway of H(2)S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent.
淡水龟的全身血管阻力（R(sys)）在缺氧期间会大幅增加，但其中的机制尚未完全明了。我们研究了内源性代谢产物硫化氢（H(2)S）是否有助于增加缺氧红耳滑龟（Trachemys scripta）的全身血管阻力。在 21°C 的麻醉龟和完全恢复到正常氧浓度的 5°C 和 21°C 的龟中，通过血管输注 H(2)S 供体 NaHS，结果表明 H(2)S 是全身循环的强烈血管收缩剂。同样，对离体龟肠系膜和肺动脉的电生理研究表明，H(2)S 介导缺氧引起的收缩。然而，有趣的是，当通过测量血浆酸不稳定硫氢化物浓度的比色法估计的血浆 H(2)S 浓度在 21°C 的缺氧期间可能增加约 3 倍，在 5°C 的缺氧期间增加约 4 倍时，NaHS 在 21°C 的缺氧（6 小时）和 5°C（14 天）时没有产生血管收缩作用。然而，用 DL-丙炔基甘氨酸或羟胺（0.44 mmol/kg）阻断内源性 H(2)S 的产生，部分逆转了 5°C 缺氧龟的全身传导性（G(sys)）降低。这些发现表明，H(2)S 介导的血管活性的信号转导途径在缺氧龟的全身循环中可能已经被最大程度地激活，或者它是依赖于氧气的。
