Leff A R, Munoz N M
J Appl Physiol Respir Environ Exerc Physiol. 1981 Aug;51(2):428-37. doi: 10.1152/jappl.1981.51.2.428.
The response of canine tracheal muscle to autonomic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) was studied isometrically in 39 dogs in vivo. Intra-arterial (ia) DMPP (2.5 X 10(-4) to 2.5 X 10(-2) mg/kg) caused selective dose related contraction [maximum 30.1 +/- 6.5 gram-force (gf)/cm] due to regional stimulation of parasympathetic ganglia. This contraction was blocked by regional administration of atropine 10(-3) mg/kg ia and hexamethonium 5 X 10(-2) mg/kg ia. Nonselective intravenous (iv) administration of DMPP 2.5 X 10(-2) mg/kg caused parasympathetic tracheal contraction [+13.4 +/- 1.64 gf/cm] followed by later sympathetic relaxation [-11.8 +/- 2.3 gf/cm]; 0.5 mg/kg iv atropine abolished contraction but did not affect relaxation. The role of the adrenal gland vs. direct sympathetic innervation in producing tracheal relaxation after sympathetic stimulation was also studied. Tracheal relaxation to 2.5 X 10(-2) mg/kg iv DMPP was -18.2 +/- 4.0 gf/cm before adrenalectomy (ADX) and -4.3 +/- 0.9 gf/cm afterward (P less than 0.001). In contrast, tracheal contraction resulting from alpha-adrenergic stimulation after 2.5 X 10(-2) mg/kg iv DMPP in beta-blocked (BB) dogs was not significantly altered by ADX. At 2.5 X 10(-1) mg/kg iv DMPP, the alpha-adrenergic contractile response was still 70% of the response prior to ADX. We conclude that sympathetic tracheal relaxation in dogs is predominantly mediated by circulating catecholamine from the adrenal gland, but that alpha-adrenergic contraction after BB results predominantly from direct sympathetic innervation and is not greatly augmented by adrenal secretion. We also report a new method for selective stimulation of airway cholinergic nerves in vivo without systemic effects.
在39只活体犬中,采用等长测定法研究了犬气管肌肉对用碘化1,1 - 二甲基 - 4 - 苯基哌嗪(DMPP)进行自主神经刺激的反应。动脉内(ia)注射DMPP(2.5×10⁻⁴至2.5×10⁻²mg/kg)由于副交感神经节的局部刺激引起与剂量相关的选择性收缩[最大30.1±6.5克力(gf)/厘米]。这种收缩可被局部给予10⁻³mg/kg ia的阿托品和5×10⁻²mg/kg ia的六甲铵阻断。非选择性静脉内(iv)注射2.5×10⁻²mg/kg的DMPP会引起副交感神经介导的气管收缩[+13.4±1.64 gf/厘米],随后是交感神经介导的舒张[-11.8±2.3 gf/厘米];静脉注射0.5mg/kg阿托品可消除收缩,但不影响舒张。还研究了交感神经刺激后肾上腺与直接交感神经支配在产生气管舒张中的作用。肾上腺切除(ADX)前,静脉注射2.5×10⁻²mg/kg DMPP引起的气管舒张为-18.2±4.0 gf/厘米,术后为-4.3±0.9 gf/厘米(P<0.001)。相反,在β受体阻断(BB)的犬中,静脉注射2.5×10⁻²mg/kg DMPP后由α肾上腺素能刺激引起的气管收缩,ADX后无明显改变。静脉注射2.5×10⁻¹mg/kg DMPP时,α肾上腺素能收缩反应仍为ADX前反应的70%。我们得出结论,犬的交感神经介导的气管舒张主要由肾上腺分泌的循环儿茶酚胺介导,但β受体阻断后α肾上腺素能收缩主要由直接交感神经支配引起,且肾上腺分泌并未使其显著增强。我们还报告了一种在体内选择性刺激气道胆碱能神经而无全身效应的新方法。