Histamine H1 and H2 receptor-mediated vasoreactivity of human internal thoracic and radial arteries.


Journal Article

BACKGROUND: Although internal thoracic arteries (ITAs) and radial arteries (RAs) have been shown to have similar patency, RAs tend to be more vasospastic postoperatively compared with ITAs. Therefore, the purpose of this study was to examine the effect of histamine subclass 1 (H1) receptors and histamine subclass 2 (H2) receptors on vasoreactivity in human ITAs and RAs. METHODS: Vessels were obtained from coronary artery bypass grafting patients. Human arterial rings (2 mm) were mounted in tissue baths, and baseline contractility was determined. Histamine concentration response curves (10(-9)-10(-3) mol/L) were performed in the absence or presence of diphenhydramine (H1 antagonist, 10(-4) mol/L) or famotidine (H2 antagonist, 10(-4) mol/L). Comparison of curves was performed by 2-way analysis of variance with repeated measures and a Bonferroni post-t test. RESULTS: Maximal contraction to histamine was significantly greater in RA (8.3 +/- 0.8 g, n = 6) than in ITA (2.9 +/- 0.3, n = 6), (P < .05). However, there was no difference in sensitivity. Histamine-mediated responses of both RA and ITA were blocked by pre-exposure to H1 antagonist, whereas an H2 antagonist only partially inhibited RA responses while blocking most of the ITA response to histamine. CONCLUSION: These studies suggest that H1 receptors alone cause contraction in RA but not in ITA, which may have potential linkage to patency and vasospasm. Further studies are necessary to identify the exact role of H2 receptors in ITA.

Full Text

Cited Authors

  • Daneshmand, MA; Keller, RS; Canver, MC; Canver, AC; Canver, CC

Published Date

  • August 2004

Published In

Volume / Issue

  • 136 / 2

Start / End Page

  • 458 - 463

PubMed ID

  • 15300215

Pubmed Central ID

  • 15300215

Electronic International Standard Serial Number (EISSN)

  • 1532-7361

International Standard Serial Number (ISSN)

  • 0039-6060

Digital Object Identifier (DOI)

  • 10.1016/j.surg.2004.05.025


  • eng