Tobin J R, Breslow M J, Traystman R J
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287.
Am J Physiol. 1993 Sep;265(3 Pt 2):H966-72. doi: 10.1152/ajpheart.1993.265.3.H966.
To evaluate effects of cholinergic receptor stimulation on regional adrenal blood flow (Q, radiolabeled microspheres) and catecholamine secretion, acetylcholine (ACh) was infused into pentobarbital-anesthetized, ventilated dogs. Unilateral adrenal denervation and placement of lumboadrenal catheters preceded intra-aortic infusion of 1) ACh alone (n = 6), 2) ACh plus hexamethonium (Hex) 20 mg/kg (n = 6), or 3) ACh plus atropine (Atr) (0.5 mg/kg) and Hex. ACh alone and in combination with Hex elicited similar dose-related (2, 20, and 100 mumol/min) increases in catecholamine secretion (181 +/- 61 to 1,055 +/- 229, 31,644 +/- 9,411, and 179,181 +/- 69,659 ng.min-1 x g medulla-1), whereas Hex and Atr together inhibited ACh-induced secretion by 95%. ACh caused marked medullary vasodilation (0.71 +/- 0.05 to 0.14 +/- 0.03 mmHg.ml-1 x min.100 g) in all three groups. To determine whether medullary vasodilation was due to incomplete muscarinic blockade, Hex-pretreated animals (n = 4) received ACh (100 mumol/min) and three increasing doses of Atr (0.5, 5, and 25 mg/kg). Catecholamine secretion was inhibited by all doses of Atr; however, vasodilation was blocked only by the two higher doses of Atr. These data suggest possible different mechanisms of muscarinic receptor-mediated catecholamine secretion and vasodilation.
为评估胆碱能受体刺激对局部肾上腺血流（Q，放射性微球）和儿茶酚胺分泌的影响，将乙酰胆碱（ACh）注入戊巴比妥麻醉、通气的犬体内。在主动脉内输注以下物质之前，先进行单侧肾上腺去神经支配并放置腰肾上腺导管：1）单独使用ACh（n = 6），2）ACh加六甲铵（Hex）20 mg/kg（n = 6），或3）ACh加阿托品（Atr）（0.5 mg/kg）和Hex。单独使用ACh以及与Hex联合使用时，儿茶酚胺分泌均出现类似的剂量相关（2、20和100 μmol/min）增加（分别为181±61至1,055±229、31,644±9,411和179,181±69,659 ng·min⁻¹·g髓质⁻¹），而Hex和Atr共同作用时可将ACh诱导的分泌抑制95%。ACh在所有三组中均引起明显的髓质血管舒张（从0.71±0.05至0.14±0.03 mmHg·ml⁻¹·min·100 g）。为确定髓质血管舒张是否由于毒蕈碱阻断不完全所致对用Hex预处理的动物（n = 4）给予ACh（100 μmol/min）和三个递增剂量的Atr（0.5、5和25 mg/kg）。所有剂量的Atr均抑制儿茶酚胺分泌；然而，仅较高剂量的Atr可阻断血管舒张。这些数据提示毒蕈碱受体介导的儿茶酚胺分泌和血管舒张可能存在不同机制。
