Perpiña M, Palau M, Cortijo J, Fornas E, Ortiz J L, Morcillo E
Service of Pneumology and Research Center, Hospital ia Fe, Valencia, Spain.
Respiration. 1989;55(2):105-12. doi: 10.1159/000195712.
Active sensitization of guinea pigs resulted in an increase in the responsiveness and sensitivity of tracheal strips to CaCl2 in K+-depolarized tissue (Emax 0.81 +/- 0.22 g/mm2 and pD2 2.35 +/- 0.10 in normal vs. 0.98 +/- 0.01 g/mm2 and 3.10 +/- 0.08 in sensitized tissue; p less than 0.05), KCl (Emax 0.62 +/- 0.08 g/mm2 and pD2 1.71 +/- 0.03 in normal vs. 0.91 +/- 0.04 g/mm2 and 2.00 +/- 0.01 in sensitized tissue; p less than 0.05) and histamine (Emax 0.70 +/- 0.06 g/mm2 and pD2 5.08 +/- 0.06 in normal vs. 0.94 +/- 0.09 g/mm2 and 5.80 +/- 0.16 in sensitized tissue; p less than 0.05) but not to caffeine 10 mM (20 degrees C, indomethacin 2.8 microM). Generation of responses to these agonists in nonsensitized tissues bathed in a Ca2+-free medium resulted in the abolition of KCl-induced contraction and partial inhibition of the responses to histamine (60% inhibition) and caffeine (40% inhibition). The contraction of sensitized tracheal strips in response to histamine in 0 calcium was greater than that obtained in nonsensitized tissues (0.48 +/- 0.02 g/mm2 vs. 0.28 +/- 0.04 g/mm2, respectively; p less than 0.05). The caffeine-induced contraction of sensitized tracheae was independent of extracellular calcium. These results suggest that a greater calcium entry and/or intracellular calcium release may be an alteration underlying hyperreactivity of sensitized tissues to spasmogens.
豚鼠的主动致敏导致气管条对钾离子去极化组织中氯化钙的反应性和敏感性增加（正常组织中Emax为0.81±0.22 g/mm²，pD2为2.35±0.10，致敏组织中分别为0.98±0.01 g/mm²和3.10±0.08；p<0.05），对氯化钾（正常组织中Emax为0.62±0.08 g/mm²，pD2为1.71±0.03，致敏组织中分别为0.91±0.04 g/mm²和2.00±0.01；p<0.05）和组胺（正常组织中Emax为0.70±0.06 g/mm²，pD2为5.08±0.06，致敏组织中分别为0.94±0.09 g/mm²和5.80±0.16；p<0.05）的反应性增加，但对10 mM咖啡因（20℃，吲哚美辛2.8 μM）无反应。在无钙培养基中孵育的未致敏组织中，这些激动剂引发的反应导致氯化钾诱导的收缩消失，对组胺（60%抑制）和咖啡因（40%抑制）的反应部分受到抑制。在0钙条件下，致敏气管条对组胺的收缩反应大于未致敏组织（分别为0.48±0.02 g/mm²和0.28±0.04 g/mm²；p<0.05）。咖啡因诱导的致敏气管收缩与细胞外钙无关。这些结果表明，更多的钙内流和/或细胞内钙释放可能是致敏组织对致痉剂反应性增强的潜在改变。
