White S R, Stimler-Gerard N P, Munoz N M, Popovich K J, Murphy T M, Blake J S, Mack M M, Leff A R
Section of Pulmonary and Critical Care Medicine, University of Chicago, Illinois.
Am Rev Respir Dis. 1989 Jan;139(1):73-9. doi: 10.1164/ajrccm/139.1.73.
We examined the effect of beta-adrenoceptor blockade and residual alpha-adrenoceptor effects during sympathetic stimulation on mast cell secretion of histamine in 12 natively allergic mongrel dogs. Bronchial mast cell response was measured as the arteriovenous difference (AVd) in plasma histamine concentration [H] across the bronchus. Plasma [H] was determined simultaneously from the azygos outflow tract and femoral artery as a marker of mast cell response prior to and for 90 s after intra-arterial injection of sham diluent and 1:100 and 1:30 dilutions of Ascaris suum antigen. Sympathetic (alpha-adrenergic) stimulation was elicited with continuous infusion of the nicotinic agonist, dimethylphenylpiperazinium (DMPP) under conditions of muscarinic blockade with atropine and beta-adrenoceptor blockade with propranolol. Plasma epinephrine (EPI) increased from 315 +/- 106 to 34,127 +/- 10,711 pg/ml (p less than 0.02). Control animals receiving sham infusion in place of sympathetic stimulation additionally had neural blockade with hexamethonium and alpha-adrenoceptor blockade with phentolamine. Plasma EPI was 90 +/- 58 pg/ml and did not change significantly during mast cell degranulation. Significant AVd in [H] was elicited after 1:30 A. suum antigen in both control (72.9 +/- 12.5 ng/ml versus 2.8 +/- 10.1 ng/ml at baseline; p = 0.031) and beta-adrenergically blocked (alpha-stimulated) (106.1 +/- 20.1 versus -1.5 +/- 35.9 ng/ml at baseline; p = 0.031) animals. However, alpha-adrenoceptor stimulation did not elicit significantly augmented secretion of [H]. We demonstrate that beta-adrenoceptor blockade blocks completely the inhibition of mast cell secretion caused by sympathetic stimulation with DMPP. However, alpha-adrenoceptor stimulation does not cause significant augmentation of mast cell secretion in the large airways of the dog.
我们在12只天然过敏的杂种犬中研究了β-肾上腺素能受体阻断以及交感神经刺激期间残余α-肾上腺素能受体效应对肥大细胞组胺分泌的影响。支气管肥大细胞反应通过支气管血浆组胺浓度[H]的动静脉差值（AVd）来衡量。在动脉内注射假稀释剂以及1:100和1:30稀释的猪蛔虫抗原之前及之后90秒，同时从奇静脉流出道和股动脉测定血浆[H]，作为肥大细胞反应的标志物。在使用阿托品进行毒蕈碱阻断以及使用普萘洛尔进行β-肾上腺素能受体阻断的条件下，通过持续输注烟碱激动剂二甲基苯基哌嗪鎓（DMPP）引发交感神经（α-肾上腺素能）刺激。血浆肾上腺素（EPI）从315±106 pg/ml增加至34,127±10,711 pg/ml（p<0.02）。接受假输注以代替交感神经刺激的对照动物另外还用六甲铵进行神经阻断并用酚妥拉明进行α-肾上腺素能受体阻断。血浆EPI为90±58 pg/ml，在肥大细胞脱颗粒期间无显著变化。在对照动物（72.9±12.5 ng/ml对基线时的2.8±10.1 ng/ml；p = 0.031）和β-肾上腺素能阻断（α-刺激）动物（106.1±20.1对基线时的-1.5±35.9 ng/ml；p =0.031）中，1:30猪蛔虫抗原注射后均引发了显著的[H] AVd。然而，α-肾上腺素能受体刺激并未引发[H]分泌的显著增加。我们证明，β-肾上腺素能受体阻断完全阻断了由DMPP交感神经刺激引起的肥大细胞分泌抑制。然而，α-肾上腺素能受体刺激在犬的大气道中并未引起肥大细胞分泌的显著增加。
