Effects of sodium glycocholate and protease inhibitors on permeability of TRH and insulin across rabbit trachea

Pharm Acta Helv. 2000 Apr;74(4):411-5. doi: 10.1016/s0031-6865(00)00024-8.

Abstract

The permeabilities of thyrotropin-releasing hormone (TRH) and insulin as model peptides were examined to characterize the tracheal epithelial barrier in in vitro experiments using excised rabbit trachea. TRH was not metabolized during 150 min duration of tracheal permeation and the apparent permeability coefficient (Papp) for TRH was about 3 x 10(-7) cm/s. The tracheal permeability of TRH was increased about three times by 10 mM glycocholate as a permeation enhancer. Insulin showed a slight degradation during 150 min duration of tracheal permeation, the Papp for insulin was 7 x 10(-9) cm/s. The tracheal permeability of insulin was significantly increased by 10 mM glycocholate, 1 mM bestatin (aminopeptidase B and leucine aminopeptidase inhibitor), and 10,000 KIU/ml aprotinin (trypsin and chymotrypsin inhibitor). The peptidase activities of rabbit tracheal epithelium were found to be the following; di-peptidyl-aminopeptidase IV (DPP IV) > Leu-aminopeptidase > cathepsin-B > trypsin. These activities were significantly lower than those of jejunal mucosal tissues. These results suggest that the tracheal absorption of peptide drugs through the respiratory tract may contribute to the systemic delivery of these drugs following the pulmonary administration of these drugs by intratracheal insufflation and instillation.

MeSH terms

  • Animals
  • Glycocholic Acid / pharmacology*
  • Insulin / metabolism*
  • Protease Inhibitors / pharmacology*
  • Rabbits
  • Rats
  • Thyrotropin-Releasing Hormone / pharmacokinetics*
  • Trachea / drug effects
  • Trachea / metabolism*

Substances

  • Insulin
  • Protease Inhibitors
  • Thyrotropin-Releasing Hormone
  • Glycocholic Acid