Modulation of bronchoconstrictor responses to histamine in pithed guinea-pigs by sympathetic nerve stimulation.
1 Electrical stimulation (40V, 0.5-8 Hz, pulse width 0.5 ms) of the thoracic spinal outflow for between 10 and 120 s inhibited histamine-induced bronchoconstriction in pithed guinea-pigs. 2 The degree of this bronchodilatation varied with the position of the stimulating electrode within the spinal canal. Two maxima were identified. The first, at the level of the 9th and 10th thoracic vertebrae, was abolished by adrenalectomy. The second, at the level of the 3rd and 4th thoracic vertebrae, was associated with tachycardia and was unchanged by adrenalectomy. 3 The magnitude of this second bronchodilator effect varied with the frequency of stimulation. It was abolished by pretreatment with reserpine (5 mg/kg i.p. 48 and 24 h beforehand) and was competitively blocked by propranolol (0.01-1.0 mg/kg). 4 These observations are consistent with the view that bronchodilator tone is derived from neuronally-released noradrenaline within the lung. The noradrenaline probably overflows from well-innervated vasculature adjacent to sparsely innervated airways.
D000403:Airway Resistance; D000818:Animals; D001980:Bronchi / Q000187:drug effects / Q000294:innervation*; D004558:Electric Stimulation; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D012110:Reserpine / Q000494:pharmacology; D013116:Spinal Cord / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*
D006632:Histamine; D012110:Reserpine