Söderström-Lauritzsen V, Nilsson G E, Lutz P L
Division of General Physiology, Department of Biology, University of Oslo, P.O.Box 1051, N-0316, Oslo, Norway.
Neurosci Lett. 2001 Sep 28;311(2):85-8. doi: 10.1016/s0304-3940(01)02136-x.
The effect of anoxia on cerebral blood velocity (CBV) on the dorsal surface of telencephalon was examined in the leopard frog, Rana pipiens, using a stereomicroscope. During exposure to anoxia, a transient 228% increase in CBV velocity was seen after 20 min, but CBV fell back to basal values after a further 20 min of anoxia. Topical application of 50 microM adenosine during normoxia caused a 52% increase in CBV, while 250 microM adenosine caused no further increase. At both concentrations, the effect was completely inhibited by the adenosine receptor blocker aminophylline (250 microM). Superfusing the brain with aminophylline during anoxia did not affect the anoxia-induced increase in CBV. We conclude that adenosine can stimulate CBV in R. pipiens. However, unlike in other anoxia-tolerant animals, adenosine seems not to be a main mediator of the anoxia induced increase in CBV in the frog.
使用体视显微镜,在豹蛙(北美豹蛙)中研究了缺氧对端脑背表面脑血流速度(CBV)的影响。在缺氧暴露期间,20分钟后CBV速度短暂增加了228%,但在进一步缺氧20分钟后,CBV又回到了基础值。在常氧状态下局部应用50微摩尔的腺苷会使CBV增加52%,而250微摩尔的腺苷则不会进一步增加。在这两种浓度下,腺苷受体阻滞剂氨茶碱(250微摩尔)完全抑制了这种作用。在缺氧期间用氨茶碱灌注大脑并不影响缺氧诱导的CBV增加。我们得出结论,腺苷可以刺激北美豹蛙的CBV。然而,与其他耐缺氧动物不同,腺苷似乎不是青蛙缺氧诱导CBV增加的主要介质。