Bronchial vasodilation by histamine in sheep: Characterization of receptor subtype

G. H. Parsons, Amparo C Villablanca, J. M. Brock, R. S. Howard, S. R. Colbert, G. M. Nichol, K. F. Chung

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Abstract

Histamine has been shown to mediate features of pulmonary allergic reactions including increased tracheobronchial blood flow. To determine whether the increase in blood flow was due to stimulation of H1- or H2- histamine receptors, we gave histamine base (0.1 μg/kg iv) or histamine dihydrochloride as an aerosol (10 breaths of 0.5% 'low dose' or 5% 'high dose') before and after H1- or H2-receptor antagonists. Blood velocity in the common bronchial branch of the bronchoesophageal artery (V(br)) was continuously measured using a chronically implanted Doppler flow probe. Pretreatment with H2-receptor antagonists cimetidine, ranitidine, or metiamide did not affect the increase in V(br) induced by intravenous histamine [106 ± 45% (SD)]. Addition of the H1-receptor antagonists diphenhydramine or chlorpheniramine, however, reduced the V(br) response to 16 ± 22, 21 ± 28, 23 ± 23, and 37 ± 32% of the unblocked responses (P < 0.05) when intravenous histamine was given at 3, 10, 20, and 30 min, respectively, after the H1 antagonist. At 40, 50, and 60 min the H1- receptor blockade appeared to attenuate, but subsequent continuous infusion of chlorpheniramine (2 mg · kg-1 · min-1) then blocked the histamine response for 60 min. Low-dose histamine aerosol did not change mean arterial or pulmonary arterial pressures, cardiac output, or arterial blood gases but increased V(br) transiently from 15.2 ± 3.4 to 37.6 ± 8.4 (SE) cm/s. After chlorpheniramine, the V(br) response to histamine, 16.3 ± 2.2 to 22.6 ± 3.6 cm/s, was significantly reduced (P < 0.05). High-dose histamine aerosol increased V(br) from 15.1 ± 4.2 to 56.9 ± 4.9 cm/s, an effect not blocked by chlorpheniramine, but after H2-receptor blockade the V(br) response to histamine, 12.6 ± 1.5 to 28.4 ± 3.3 cm/s, was significantly reduced (P < 0.05). We conclude that the histamine receptor subtype mediating an increase in V(br) depends on the dose of agonist. We postulate that the bronchovascular H1 receptor has a greater affinity for histamine than the H2 receptor and is therefore preferentially stimulated at a lower dose of histamine.

Original languageEnglish (US)
Pages (from-to)2090-2098
Number of pages9
JournalJournal of Applied Physiology
Volume72
Issue number6
StatePublished - 1992

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Keywords

  • aerosol
  • airway blood flow
  • bronchial blood flow
  • chlorpheniramine
  • cimetidine
  • diphenhydramine
  • Doppler
  • metiamide
  • ranitidine
  • sheep

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Parsons, G. H., Villablanca, A. C., Brock, J. M., Howard, R. S., Colbert, S. R., Nichol, G. M., & Chung, K. F. (1992). Bronchial vasodilation by histamine in sheep: Characterization of receptor subtype. Journal of Applied Physiology, 72(6), 2090-2098.