Kalsner S
Br J Pharmacol. 1974 Sep;52(1):5-12. doi: 10.1111/j.1476-5381.1974.tb09680.x.
1 The possibility of a vasodilator innervation to the isolated and perfused central artery of the rabbit ear was examined.2 Stimulation of the periarterial nerves in the presence of noradrenaline or other agonist used to maintain a partial constriction of the ear artery, led to a decrease in intraluminal flow followed after the cessation of stimulation by an increase in flow beyond the pre-stimulation level.3 After blockade of adrenergic transmission with bretylium or guanethidine or of the alpha- and beta-adrenoceptors with phentolamine and propranolol, stimulation of the periarterial nerves in the presence of a background tone, led to a clearly detectable vasodilation. This dilatation was not blocked by treatment with atropine or mepyramine; nor was it enhanced by physostigmine.4 Pretreatment of rabbits with reserpine (2 mg/kg) to deplete catecholamine stores, eliminated both the vasoconstrictor and vasodilator responses to nerve stimulation. However, a lower dose of reserpine (0.2 to 0.5 mg/kg) selectively eliminated the vasoconstrictor component of periarterial nerve activation.5 The ear artery dilated in response to low concentrations of prostaglandin E(1), and E(2), in the presence of noradrenaline, but treatment with inhibitors of prostaglandin synthesis, indomethacin, aspirin or eicosa-5,8,11,14-tetraynoic acid did not reduce the vasodilator response. Attempts to extract a prostaglandin in the bathing medium were unsuccessful.6 The involvement of a purine nucleotide appeared unlikely since the ear artery dilated only in response to fairly high concentrations of adenosine 5'-triphosphate (ATP), adenosine 5'-diphosphate (ADP) and adenosine 5'-monophosphate (AMP). Furthermore, dipyridamole, an inhibitor of adenosine uptake, enhanced dilation due to exogenous ATP but not to periarterial nerve stimulation.7 It is concluded that the central artery of the rabbit ear has a vasodilator innervation but the identity of the transmitter remains to be established.
对兔耳离体灌注中央动脉是否存在血管舒张神经支配进行了研究。
在去甲肾上腺素或其他用于维持耳动脉部分收缩的激动剂存在的情况下,刺激动脉周围神经,导致管腔内血流减少,刺激停止后血流增加,超过刺激前水平。
用溴苄铵或胍乙啶阻断肾上腺素能传递,或用酚妥拉明和普萘洛尔阻断α和β肾上腺素能受体后,在有背景张力的情况下刺激动脉周围神经,可导致明显可检测到的血管舒张。这种舒张不受阿托品或美吡拉敏处理的阻断;毒扁豆碱也不能增强它。
用利血平(2mg/kg)预处理兔子以耗尽儿茶酚胺储备,消除了对神经刺激的血管收缩和血管舒张反应。然而,较低剂量的利血平(0.2至0.5mg/kg)选择性地消除了动脉周围神经激活的血管收缩成分。
在去甲肾上腺素存在的情况下,兔耳动脉对低浓度的前列腺素E(1)和E(2)有舒张反应,但用前列腺素合成抑制剂吲哚美辛、阿司匹林或5,8,11,14-二十碳四炔酸处理并没有降低血管舒张反应。在浴液中提取前列腺素的尝试未成功。
嘌呤核苷酸参与的可能性不大,因为兔耳动脉仅对相当高浓度的5'-三磷酸腺苷(ATP)、5'-二磷酸腺苷(ADP)和5'-单磷酸腺苷(AMP)有舒张反应。此外,腺苷摄取抑制剂双嘧达莫增强了外源性ATP引起的舒张,但对动脉周围神经刺激引起的舒张没有增强作用。
得出的结论是,兔耳中央动脉有血管舒张神经支配,但递质的身份仍有待确定。