Bonham A C, Kott K S, Joad J P
Department of Internal Medicine and Pharmacology, University of California, Davis 95616, USA.
J Appl Physiol (1985). 1996 Oct;81(4):1715-22. doi: 10.1152/jappl.1996.81.4.1715.
We determined the effect of sidestream tobacco smoke (SS) exposure on responses of lung rapidly adapting receptors (RARs), peak tracheal pressure (Ptr), and arterial blood pressure (ABP) to substance P in young guinea pigs. Guinea pigs were exposed to SS or filtered air from day 8 to days 41-45 of life. They were then anesthetized and given three doses of intravenous substance P (1.56-4.94 nmol/kg). SS exposure augmented substance P-evoked increases in RAR activity (P = 0.029 by analysis of variance) but not substance P-evoked increases in peak Ptr or decreases in ABP. Neurokinin 1-receptor blockade (CP-96345, 400 nmol/kg) attenuated substance P-evoked increases in RAR activity (P = 0.001) and ABP (P = 0.009) but not in peak Ptr (P = 0.06). This chronic exposure to SS in young guinea pigs exaggerates RAR responsiveness to substance P. The findings may help explain the increased incidence of airway hyperresponsiveness and cough in children chronically exposed to environmental tobacco smoke.
我们确定了侧流烟草烟雾(SS)暴露对幼龄豚鼠肺快速适应性感受器(RARs)、气管峰值压力(Ptr)以及动脉血压(ABP)对P物质反应的影响。从出生第8天至41 - 45天,将豚鼠暴露于SS或过滤空气中。然后对它们进行麻醉,并给予三剂静脉注射P物质(1.56 - 4.94 nmol/kg)。SS暴露增强了P物质诱发的RAR活性增加(方差分析P = 0.029),但未增强P物质诱发的Ptr峰值增加或ABP降低。神经激肽1受体阻断(CP - 96345,400 nmol/kg)减弱了P物质诱发的RAR活性增加(P = 0.001)和ABP降低(P = 0.009),但未减弱Ptr峰值增加(P = 0.06)。幼龄豚鼠长期暴露于SS会夸大RAR对P物质的反应性。这些发现可能有助于解释长期暴露于环境烟草烟雾的儿童气道高反应性和咳嗽发病率增加的原因。