Haller C, Kuschinsky W
Department of Physiology, University of Bonn, Federal Republic of Germany.
J Appl Physiol (1985). 1987 Dec;63(6):2208-15. doi: 10.1152/jappl.1987.63.6.2208.
The reactivity of pial arteries to the perivascular microapplication of artificial cerebrospinal fluids with mounting concentrations of adenosine (10(-11)-10(-3) M), K+ (0-10 mM), and H+ (pH 5.1-7.6) was determined in chloralose-anesthetized ventilated cats during normoxic control conditions and during moderate normocapnic arterial hypoxia (arterial Po2 47 Torr). Hypoxia induced a significant mean pial arterial dilatation of 18-29% in the various types of experiments. The pial arterial reactivity to each of the tested factors remained unchanged during hypoxia compared with normoxia. The hypoxic vasodilatation could not be reduced by the perivascular microapplication of theophylline (10(-5) and 5 X 10(-5) M). Systemic theophylline (50-75 mumol/kg, iv), regardless of whether given during or before hypoxia, did not attenuate the hypoxic vasodilatation, although it blocked dilatations induced by the perivascular microapplication of adenosine during normoxia. The present study shows that 1) local metabolic factors are vasoactive during moderate hypoxia; therefore they could mediate the hypoxic dilatation of brain vessels; 2) systemic theophylline can block vascular adenosine receptors; 3) since local theophylline had no effect on the hypoxic dilatation of pial arteries, adenosine may not be the main causative factor for the hypoxic hyperemia.
在氯醛糖麻醉、人工通气的猫中,于常氧对照条件下以及中度常碳酸血性动脉缺氧(动脉血氧分压47 Torr)期间,测定软脑膜动脉对人工脑脊液血管周围微量注射不同浓度腺苷(10⁻¹¹ - 10⁻³ M)、钾离子(0 - 10 mM)和氢离子(pH 5.1 - 7.6)的反应性。在各类实验中,缺氧导致软脑膜动脉显著平均扩张18 - 29%。与常氧相比,缺氧期间软脑膜动脉对每种测试因子的反应性保持不变。血管周围微量注射茶碱(10⁻⁵和5×10⁻⁵ M)不能减轻缺氧性血管扩张。全身给予茶碱(50 - 75 μmol/kg,静脉注射),无论在缺氧期间还是之前给予,均不能减弱缺氧性血管扩张,尽管它能阻断常氧期间血管周围微量注射腺苷所诱导的血管扩张。本研究表明:1)局部代谢因子在中度缺氧期间具有血管活性;因此它们可能介导脑血管的缺氧性扩张;2)全身给予茶碱可阻断血管腺苷受体;3)由于局部应用茶碱对软脑膜动脉的缺氧性扩张无影响,腺苷可能不是缺氧性充血的主要致病因素。