Souhrada M, Souhrada J F
Respir Physiol. 1981 Oct;46(1):17-27. doi: 10.1016/0034-5687(81)90065-7.
Airway smooth muscle preparations were isolated from control guinea pigs, from animals sensitized to albumin and Pertussis vaccine, from sensitized animals which had been resensitized and from animals that had been sensitized and exposed to an inhalation challenge of albumin for 14 days. The resting membrane potential, its changes and contractile response of airway smooth muscle were measured during in vitro antigen challenge, administration of histamine dihydrochloride (10(-3) M), or isoproterenol (10(-3) M). We have found that: (1) The resting membrane potential of normal airway smooth muscle of guinea pig was -61.3 +/- 0.2 mV (+/- SE); (2) Resting membrane potential of airway smooth muscle from sensitized animals was significantly increased (P less than 0.05) to -72.9 +/- 0.3 mV (+/- SE); (3) One week after resensitization of animals a further significant increase (P less than 0.05) in resting membrane potential to -76.2 +/- 0.2 mV (+/- SE) was observed; (4) Resting membrane potential of airway smooth muscle isolated from animals repeatedly exposed to inhalation challenge of antigen significantly decreased (P less than 0.01) to -50.6 +/- 0.5 mV (+/- SE) as compared to controls; (5) After histamine, isoproterenol or antigen administration, the airway smooth muscle from sensitized animals repeatedly exposed to inhalation challenge showed attenuated response (P less than 0.01) as measured by both membrane potential and isometric force. In contrast, the response to antigen and histamine in preparations from sensitized animals is potentiated. It is concluded that both acute sensitization and resensitization on one hand and repeated exposure of sensitized animals to inhaled albumin on the other will alter cellular mechanism(s) responsible for the maintenance of membrane potential and the regulation of excitation-contraction coupling in airway smooth muscle.
气道平滑肌标本取自对照豚鼠、对白蛋白和百日咳疫苗致敏的动物、再次致敏的致敏动物以及致敏并接受白蛋白吸入激发14天的动物。在体外抗原激发、给予盐酸组胺(10⁻³ M)或异丙肾上腺素(10⁻³ M)期间,测量气道平滑肌的静息膜电位、其变化和收缩反应。我们发现:(1)豚鼠正常气道平滑肌的静息膜电位为-61.3±0.2 mV(±标准误);(2)致敏动物气道平滑肌的静息膜电位显著升高(P<0.05)至-72.9±0.3 mV(±标准误);(3)动物再次致敏1周后,静息膜电位进一步显著升高(P<0.05)至-76.2±0.2 mV(±标准误);(4)与对照组相比,反复接受抗原吸入激发的动物分离出的气道平滑肌静息膜电位显著降低(P<0.01)至-50.6±0.5 mV(±标准误);(5)给予组胺、异丙肾上腺素或抗原后,反复接受吸入激发的致敏动物的气道平滑肌,无论是通过膜电位还是等长力测量,其反应均减弱(P<0.01)。相比之下,致敏动物标本对抗原和组胺的反应增强。结论是,一方面急性致敏和再次致敏以及另一方面致敏动物反复接触吸入的白蛋白,都会改变负责维持膜电位和调节气道平滑肌兴奋-收缩偶联的细胞机制。