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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。
Objective: To investigate the relationship between the change of β receptor and its effector system in lung tissue and the activation of local phospholipase (PLA2) during hemorrhagic shock and reperfusion injury (S / R). Methods: Radioimmunoassay and radioimmunoassay were used to determine the cAMP and cGMP levels of β-adrenergic receptor and second messenger RNA in hemorrhagic shock-reperfusion injury (S / R) lung tissue. The blood pH before and after injury Changes in values and carbon dioxide binding (tCO2). Results: The number of β receptors and the cAMP / cGMP ratio decreased after S / R injury. Using phospholipase A2 (PLA2) blocker and anti-oxidant astragalus can significantly increase the ratio of lung β receptor and cAMP and cGMP after injury. With the downregulation of beta receptors and second messengers, blood pH and tCO2 also decreased after S / R, showing obvious acidosis. Using these drugs can obviously reduce the acidosis after injury. CONCLUSIONS: S / R injury induced systemic ß-receptor and its effector system desensitization may be related to local PLA2 activation. PLA2 blockers and antioxidants may improve pulmonary ventilation by increasing β-adrenergic conduction.