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哮喘中的肺血小板动力学

Pulmonary platelet kinetics in asthma.

作者信息

Ind P W, Peters A M, Malik F, Lavender J P, Dollery C T

出版信息

Thorax. 1985 Jun;40(6):412-7. doi: 10.1136/thx.40.6.412.

Abstract

Platelets produce a range of bronchoconstrictor mediators. Measurements of plasma factors have implicated platelet activation in allergic asthma, and sensitised guinea pigs challenged with ovalbumin show pulmonary platelet aggregation accompanying bronchoconstriction. To investigate this further we injected autologous platelets labelled with indium 111 and red cells labelled with technetium 99m into three young volunteers with atopic asthma and three non-asthmatic volunteers and, after equilibration of platelets between blood and splenic pool, monitored lung 99mTc and 111In activities continuously. Comparison with the corresponding activities in blood samples allowed calculation of pulmonary platelet to red cell transit time ratio (tp/tr). This ratio was 0.9, 1.02, and 0.98 in the non-asthmatic subjects compared with 1.04, 0.97, and 1.17 in the asthmatic subjects. This argues against the existence of an intrapulmonary platelet pool in normal subjects; transpulmonary transit time was slightly prolonged in one asthmatic subject. Bronchial challenge with Dermatophagoides pteronyssinus was performed in the asthmatic subjects and monitoring continued for a further 30 minutes. Antigen induced falls in FEV1 of 20-50% were accompanied by small decreases in the 111In but not in the 99mTc lung signal. In line with this tp/tr fell to 0.89, 0.89, and 1.05. Antigen induced bronchoconstriction was therefore not accompanied by intrapulmonary platelet accumulation. Platelet survival was normal at 10.2 days in both groups of subjects.

摘要

血小板会产生一系列支气管收缩介质。血浆因子的测量表明血小板激活与过敏性哮喘有关,用卵清蛋白攻击致敏的豚鼠会出现支气管收缩伴随肺血小板聚集。为了进一步研究这一现象,我们将用铟111标记的自体血小板和用锝99m标记的红细胞注入三名患有特应性哮喘的年轻志愿者和三名非哮喘志愿者体内,在血小板在血液和脾池之间达到平衡后,持续监测肺部锝99m和铟111的活性。将其与血样中的相应活性进行比较,可计算出肺血小板与红细胞的转运时间比(tp/tr)。非哮喘受试者的该比值分别为0.9、1.02和0.98,而哮喘受试者的该比值分别为1.04、0.97和1.17。这表明正常受试者不存在肺内血小板池;一名哮喘受试者的经肺转运时间略有延长。对哮喘受试者进行了粉尘螨支气管激发试验,并继续监测30分钟。抗原诱导第一秒用力呼气量下降20%-50%,同时铟111肺部信号略有下降,但锝99m肺部信号未下降。与此一致,tp/tr降至0.89、0.89和1.05。因此,抗原诱导的支气管收缩并未伴随肺内血小板积聚。两组受试者的血小板生存期均正常,为10.2天。

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