磷脂酶A2阻断剂对再灌注损伤后肺β肾上腺素能受体的影响及其意义

The effects and significance of phospholipase A2 inhibitors on beta adrenergic receptor in lung tissue after reperfusion injuries

  • 摘要: 目的:探讨失血性休克再灌注损伤(S/R)过程中肺组织β受体及其效应系统的变化同局部磷脂酶(PLA2)激活的关系。方法:采用放射受体结合分析和放射免疫分析测定了失血性休克再灌注损伤(S/R)肺组织中β肾上腺素能受体和第二信使cAMP、cGMP,同时还观察了损伤前后血液pH值和二氧化碳结合力(tCO2)的改变。结果:发现S/R损伤后β受体数量和cAMP/cGMP比值下降。使用磷脂酶A2(PLA2)阻断剂及抗氧化剂黄芪酮,可以显著提高肺β受体数量和损伤后cAMP和cGMP的比值。伴随β受体及第二信使的下调,S/R后血液pH值和tCO2也下降,表现为明显的酸中毒,使用上述药物可以明显减轻损伤后的酸中毒状态。结论:S/R损伤造成的肺组织β受体及其效应系统失敏可能同局部PLA2激活有关,PLA2阻断剂和抗氧化剂可能通过提高β受体的传导能力而改善肺通气功能。

     

    Abstract: Objective:To demonstrate the relationship between the changes of lung tissue beta receptors as well as its messenger conduction system and local phospholipaseA2 activation after hemorrhagic shock and reperfusion injuries (S/R).Methods:The beta adrenergic receptor and second messenger cAMP and cGMP in rabbit lung tissue after hemorrhagic shock and reperfusion injuries(S/R) were tested by radioreceptor binding assay and radioimmunoassay. The blood pH values and tCO2 before or after S/R inury also were observed. Results:The number of beta receptor decreased and the receptor affinity increased after S/R injury. Although both cAMP and cGMP were increased, the ratio of cAMP/cGMP was decreased due to the more increase of cGMP than that of cAMP at the same time. Otherwise, beta receptor Bamx was significantly increased and its affinity was decreased by the use of phospholipase A2 inhibitors chloroquine compounds and antioxidant (TFA) after shock before reperfusion. In addition, cAMP/cGMP after S/R injury was also increased by the use of the above drugs consisting with the increase of beta receptor numbers. Furthermore, following the down regulation of beta receptor and its second messenger, the blood pH value and tCO2 were decreased, which represented typical acidosis in body but it was attenuated by the above drugs. Conclusion:All those results indicate that the improvement of air exchange and the attenuation of acidosis may be accomplished by the use of phospholipse A2 inhibitors and antioxdant.

     

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