The effect of in vivo hyperoxic exposure on the release of endogenous histamine from the rat isolated perfused lung.
The effect of in vivo hyperoxic exposure on the release of endogenous histamine from the rat isolated perfused lung.
复制标题
体内高氧暴露对大鼠离体灌注肺释放内源性组胺的影响。
DOI：
10.1016/0041-008x(84)90257-6
复制
发表时间：
1984
影响因子：
3.8
通讯作者：
Faiman,MD
中科院分区：
文献类型：
--
作者：
Januszkiewicz,AJ;Faiman,MD
将雌性大鼠暴露于1atm空气或100%O2中12、24或48小时，处死大鼠，取出肺，制备离体灌注肺（IPL）系统。在再循环系统中用改良的Krebs-Henseleit缓冲液灌注离体肺标本，并测定O2暴露对IPL释放组胺的影响。还检查了这些O2暴露对IPL中丙二醛形成的影响。组胺的最大释放发生在灌注20分钟后。灌流液中释放的最大组胺浓度与大鼠暴露于常压高氧的时间长度呈线性关系。肺灌流液中丙二醛含量也随氧暴露时间的延长呈线性增加。另外的H1受体拮抗剂，d-氯苯那敏，灌注液完全抑制基础组胺释放IPL的空气和O2暴露的大鼠，而另外的H2受体拮抗剂，metamide，增强释放过程。当在灌注液中加入等摩尔浓度的阿托品时，没有显示出显著的效果。动脉血浆组胺暴露于100%O224小时的大鼠增加40%时相比，暴露于空气中的控制，而从强脉冲光组胺释放增加75%。总之，大鼠暴露于常压高氧引起组胺释放和丙二醛形成。组胺释放可能是自由基诱导的含组胺肥大细胞脂质膜过氧化的结果。强脉冲光中组胺的释放可能是O2损伤的早期生化标志物。
Female rats were exposed to either 1 atm air or 100% O2for 12, 24, or 48 hr. The rats were killed, the lungs were removed, and an isolated perfused lung (IPL) system was prepared. The isolated lung preparation was perfused with a modified Krebs-Henseleit buffer in a recirculating system, and the effect of the O2exposures on histamine release from the IPL was determined. The effect of these O2exposures on malondialdehyde formation in the IPL also was examined. Maximal release of histamine occurred after 20 min of perfusion. A linear relationship was found between the maximal histamine concentration released into the perfusate and the length of time the rats were exposed to normobaric hyperoxia. Malondialdehyde in lung perfusate also increased in a linear manner with increasing O2exposure time. Addition of the H1-receptor antagonist, d-chlorpheniramine, to the perfusate completely inhibited basal histamine release from the IPL of both air- and O2-exposed rats, while addition of the H2-receptor antagonist, metamide, potentiated the release process. There was no significant effect demonstrated when an equimolar concentration of atropine was added to the perfusate. Arterial plasma histamine from rats exposed to 100% O2for 24 hr increased 40% when compared to air-exposed controls, while histamine release from the IPL increased 75%. In conclusion, exposure of rats to normobaric hyperoxia caused both histamine release and malondialdehyde formation. Histamine release probably occurred as a result of a free radical-induced peroxidation of the lipid membrane of histamine-containing mast cells. Release of histamine from the IPL may be an early biochemical marker of damage by O2.