Dóra E, Kovách A G
Acta Physiol Hung. 1984;63(1):35-41.
In order to elucidate the importance of adrenergic beta receptors in the regulation of cerebral microcirculation during arterial hypoxia, chloralose anaesthetized cats were treated with propranolol hydrochloride. Arterial hypoxia, lasting for approximately 4 min, was induced by respiring the animals with a gas mixture containing 7% oxygen balanced in nitrogen gas. Arterial hypoxia was induced in the same animals before and during continuous infusion of propranolol (0.05 mg/kg/min into the lingual artery). Cerebrocortical vascular volume ( CVV ) and NADH fluorescence were measured through a cranial window with a microscope fluororeflectometer . Control arterial hypoxia (no treatment) increased CVV and NADH reduction by 22.2 +/- 2% and 20.4 +/- 2.1%, respectively. Following 1 mg/kg propranolol treatment arterial hypoxia of the same severity resulted in only approximately 2/3 of the CVV response obtained during the control arterial hypoxia. Since arterial hypoxia induced similar changes in arterial blood gases, arterial blood pressure, and intracranial pressure in both cases, our results indicate that the cortical vasodilatation occurring during arterial hypoxia is due, at least in part, to the activation of adrenergic beta receptors.
为了阐明肾上腺素能β受体在动脉缺氧期间对脑微循环调节中的重要性，用盐酸普萘洛尔处理水合氯醛麻醉的猫。通过用含7%氧气并以氮气平衡的混合气体让动物呼吸来诱导持续约4分钟的动脉缺氧。在持续输注普萘洛尔（0.05mg/kg/分钟，经舌动脉）之前和期间，在同一动物中诱导动脉缺氧。通过带有显微镜荧光反射计的颅窗测量大脑皮质血管容积（CVV）和NADH荧光。对照动脉缺氧（未处理）分别使CVV和NADH还原增加22.2±2%和20.4±2.1%。在1mg/kg普萘洛尔处理后，相同严重程度的动脉缺氧仅导致对照动脉缺氧期间所获得的CVV反应的约2/3。由于在两种情况下动脉缺氧均引起动脉血气、动脉血压和颅内压的相似变化，我们的结果表明，动脉缺氧期间发生的皮质血管舒张至少部分归因于肾上腺素能β受体的激活。
