Vanda B, Montaño L M, Segura P, Rubio H, Selman M, Vargas M H
Instituto Nacional de Enfermedades Respiratorias, Unidad de Investigación, México, DF.
Arch Int Pharmacodyn Ther. 1992 Sep-Oct;319:101-13.
In vivo and in vitro studies have demonstrated that beta-adrenoceptor blockers enhance the airway smooth muscle contraction to antigen, but the mechanisms are not fully understood. In the present work, we corroborated that propranolol (3.9 x 10(-6) M, 30 min incubation) induces hyperreactivity to antigenic challenge (cumulative concentration-response curve to ovalbumin, 0.01 to 100 micrograms/ml) in lung parenchyma strips from sensitized guinea-pigs. This hyperreactivity was enhanced by indomethacin (3.2 x 10(-5) M) and was unaffected by the lipoxygenase/cyclooxygenase inhibitor phenidone (1 x 10(-4) M). However, the histamine H1 receptor antagonist pyrilamine (1 x 10(-6) M) reduced the potentiation effect of propranolol. These results suggest that bronchoconstrictor prostaglandins, thromboxane A2 and leukotrienes, are not involved in the propranolol-induced lung parenchyma strips hyperreactivity to antigen in vitro, and that histamine may account, at least in part, for such propranolol effect.
体内和体外研究均表明，β-肾上腺素受体阻滞剂可增强气道平滑肌对抗原的收缩反应，但其机制尚未完全明确。在本研究中，我们证实普萘洛尔（3.9×10⁻⁶ M，孵育30分钟）可使致敏豚鼠肺实质条带对抗原刺激产生高反应性（对卵清蛋白的累积浓度-反应曲线，0.01至100微克/毫升）。吲哚美辛（3.2×10⁻⁵ M）可增强这种高反应性，而脂氧合酶/环氧化酶抑制剂非那吡啶（1×10⁻⁴ M）对其无影响。然而，组胺H1受体拮抗剂吡苄明（1×10⁻⁶ M）可降低普萘洛尔的增强作用。这些结果表明，支气管收缩性前列腺素、血栓素A2和白三烯不参与普萘洛尔诱导的肺实质条带体外对抗原的高反应性，且组胺可能至少部分地介导了普萘洛尔的这种作用。
