| pubmed-article:7118633 | pubmed:abstractText | The effect of sympathetic stimulation on histamine-induced tracheal contraction was studied in 42 dogs in situ. After cholinergic blockade with atropine, dose-response curves to intra-arterial (ia) histamine (10(-10)-10(-6) mol) were performed in 11 adrenal-intact (ADi) and 5 adrenalectomized (ADx) dogs receiving steady-state sympathetic stimulation from continuous intravenous infusion (62.5-312 micrograms . kg-1 . min-1) of 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). In ADi dogs receiving maximal sympathetic prestimulation (312 micrograms . kg-1 . min-1 DMPP), tracheal tension barely exceeded base-line resting tension after 10(-6) mol ia histamine. In five dogs, tracheal tension after maximal sympathetic prestimulation exceeded base line for greater than or equal to 10(-8) mol ia histamine. In 12 other dogs, reversal of histamine-induced contraction by maximal sympathetic prestimulation was studied. Tracheal tension decreased 45.6 +/- 4.4 g/cm in four ADi dogs (P less than 0.001), 12.4 +/- 2.8 g/cm in four ADx dogs (P less than 0.02), and 2.2 +/- 2.5 g/cm in four control dogs receiving sham infusions (P greater than 0.90). No evidence was found for nonadrenergic relaxation of canine airway smooth muscle. We conclude that tracheal sympathetic nerves cause significant antagonism of histamine-induced contraction, which is augmented by adrenal secretion. We also report a pharmacological method for dose-related steady-state sympathetic stimulation of canine airways. | lld:pubmed |
