Contraction Of Parenchymal Strips Research Articles

Antigen-induced contraction of guinea pig isolated pulmonary arteries and lung parenchyma

We characterized the kinetics of and determined the mediators involved in antigen-induced contraction of pulmonary arteries (PA) and lung parenchyma isolated from actively sensitized guinea pigs. Ovalbumin (10(-2) mg/ml) induced contractions of PA rings, which reached maximum amplitude by 2 min and decayed to 50% of maximum by 4-6 min. Pyrilamine (10(-6) M) delayed the onset of contraction and decreased the peak of the response by > 50%. Metiamide (10(-4) M) partially reversed this effect. The addition of indomethacin (10(-6) M) to the combination of pyrilamine and metiamide had no significant effect. The further addition of the leukotriene (LT) D4/LTE4 receptor antagonist SKF 104353 (10(-5) M) reduced the contraction by > 80%. The maximum amplitude of antigen-induced contraction of parenchymal strips was reached by 15 min and was sustained for > 60 min. In these tissues, SKF 104353 inhibited the contraction by approximately 35%, but the histamine receptor antagonists and indomethacin had no significant effect. These results suggest that both histamine and sulfidopeptide LTs mediate antigen-induced contraction of PA, whereas sulfidopeptide LTs, but not histamine, are involved in the parenchymal response.

Parainfluenza-3 infection of the guinea pig airways induces respiratory airway hyperreactivityin vitro

Guinea pigs were inoculated intra-tracheally with bovine parainfluenza type 3 virus (PI-3) to investigate airway responsiveness to histamine and arecoline in vitro. Two days after saline or PI-3 inoculation no difference in the reactivity of the tracheal spirals was observed after cumulative concentration/response curves with both drugs. Similarly, contractions of parenchymal strips, induced by histamine, did not differ between both groups. However, 4 days after PI-3 inoculation the histamine induced contraction of the tracheal spirals was increased by 47% and the arecoline induced contractions by 32% as compared to the control group. Further, the contractions induced by histamine in parenchymal strips were significantly enhanced (p less than 0.01) in the PI-3 treated group. In conclusion, PI-3 infection of guinea pig respiratory tract induces hyperreactivity of the central and peripheral airways in vitro.

Inhibition of bronchoconstriction in the guinea pig by a calcium channel blocker, nifedipine.

We investigated the inhibitory effects of nifedipine, a calcium channel blocker, on airway smooth muscle constriction in the guinea pig. In vitro, nifedipine (0.003 to 3.0 microM) caused significant dose-dependent reversal of intrinsically existing tone in both tracheal spirals and parenchymal strips. Nifedipine also inhibited the constriction of tracheal spirals and parenchymal strips induced by two different agonists, histamine and carbachol. At a concentration of 3.0 microM, nifedipine increased by 48-fold the concentration of carbachol required to produce a 50% of maximal contraction of parenchymal strips, and by 5-fold the concentration of histamine. Increasing extracellular calcium ion concentration in the tissue baths significantly diminished the inhibitory action of nifedipine. In vivo, nifedipine (30 micrograms/kg body weight given intravenously) did not alter pulmonary resistance or dynamic compliance. It did, however, attenuate histamine-induced bronchoconstriction in 3 of 5 animals studied. In response to the maximal dose of histamine infused, mean pulmonary resistance rose 40 +/- 16% (SEM) after nifedipine versus 182 +/- 65% in the control animals (p less than 0.025) and mean dynamic compliance decreased 35 +/- 8% after nifedipine versus 58 +/- 6% in the control animals (p less than 0.01). Thus, this calcium channel blocker inhibits mediator-induced constriction of both central and peripheral airway contractile tissues, a finding of potential clinical applicability.