一氧化氮对急、慢性缺氧大鼠血流动力学及缺氧性肺血管收缩反应的影响

观察了吸入０．００４％的一氧化氮（ＮＯ）对急、慢性缺氧大鼠血流动力学、缺氧性肺血管收缩反应（ＨＰＶ）、血气及高铁血红蛋白（ＭｅｔＨｂ）的影响。结果表明：（１）常氧吸入ＮＯ时能明显降低慢性缺氧大鼠肺动脉平均压（Ｐｐａ）和肺血管阻力（ＰＶＲ），但对正常大鼠的Ｐｐａ和ＰＶＲ无明显影响；（２）慢性缺氧大鼠急性缺氧时ＨＰＶ较正常大鼠弱，吸入ＮＯ不但降低两者的急性缺氧肺动脉高压，且完全逆转两者的ＨＰＶ；（３）吸入ＮＯ对急、慢性缺氧大鼠体循环血流动力学、血气及ＭｅｔＨｂ含量无明显影响。提示吸入ＮＯ能选择性降低，急、慢性缺氧性肺动脉高血压，且逆转ＨＰＶ。     

Wirkung der Lipoxygenase- und Cyclooxygenase-Metaboliten auf die akute hypoxische pulmonale Vasokonstriktion beim Schweinchen

The role of lipoxygenase and cyclooxygeriase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets, it has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstrion, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. indomethacin potentiated mar kedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vsaoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.     

慢性缺氧对大鼠肺血管反应性的影响及其与组胺的关系

作者研究了慢性间断低压缺氧对大鼠肺血管反应性的影响及其与组胺的关系。动物经慢性缺氧后发生慢性肺动脉高压,其肺血管对急性缺氧的反应性降低。联合使用扑尔敏和甲氰咪胍阻断组胺受体后,对照大鼠肺血管反应性明显增强,慢性肺动脉高压大鼠肺血管反应性无明显改变。结果表明组胺可能参与大鼠肺血管反应的调节,慢性肺动脉高压大鼠由于对急性缺氧的肺血管收缩反应较弱,因而组胺的调节作用也较弱。     

Comparative study between the effects of total intravenous anesthesia with propofol and balanced anesthesia with halothane on the alveolar-arterial oxygen tension difference and on the pulmonary shunt.

Inhalation anesthesia with halothane, inhibiting hypoxic pulmonary vasoconstriction, causes an increase in intrapulmonary shunt development as well as an increase of alveolar-arterial oxygen tension difference. In contrast, total intravenous anesthesia with propofol, as with other intravenous anesthetics, should not alter pulmonary gas exchange. The present study was carried out using two groups of patients of similar age, sex and weight, who were subjected to neurosurgical procedures. One group was under general inhalational anesthesia with halothane and the other group under total intravenous anesthesia with propofol. In a simple clinical manner and applying established formulae, the determination of intrapulmonary shunt and alveolar-arterial oxygen tension difference showed a significant increase after 120 min in the halothane group, whereas the group that received propofol did not show any significant variation. We therefore conclude that propofol, different from halothane, does not affect the pulmonary gas exchange.     

电压依赖性钾通道与Miconazole在低氧性肺血管收缩中的作用

目的观察大鼠肺动脉平滑肌细胞(PaSMCs)膜上电压依赖性钾通道(Kv)与细胞色素P450氧化酶抑制剂Miconazole在低氧性肺血管收缩中的作用。方法采用急性酶分离法分离出大鼠肺动脉平滑肌细胞(PaSMCs),利用全细胞膜片钳技术记录PaSMCs的Kv通道的电流特性;用低氧液体灌流PaSMCs造成急性低氧模型,记录低氧作用前后Kv通道的电流变化;用不同浓度的Miconazole作用于PaSMCs,记录加药前后的电流变化。结果低氧液体灌流以及不同浓度的Miconazole对Kv均有明显的抑制作用,且Miconazole的抑制作用具有一定的浓度依赖性,在加用Kv的特异性的阻断剂4氨基吡啶(4AP)后再加用该药不能进一步抑制Kv电流。结论低氧和Miconazole均作用于Kv通道的同一部位,支持PaSMCs膜上的Kv通道在低氧性肺血管收缩中起重要作用,而细胞色素P450氧化酶可调节细胞内的氧化还原状态,可能系一重要的氧感受器。     

肺心营养合剂抑制吸烟引起的缺氧性肺血管收缩反应增强

20名健康男大学生 ,随机分为两组 ,分别服肺心营养合剂 (PX)和安慰剂 1个月 ,用肺阻抗血流图测定由吸烟引起的肺血管反应性的变化。结果表明 :吸烟可增强缺氧性肺血管收缩反应 (HPV) ,营养合剂则可抑制吸烟引起的 HPV增加。     

PI3K/Akt信号通路在缺氧性肺血管收缩中的机制

目的：探讨15-羟基二十碳四烯酸（15-HETE）致大鼠肺动脉收缩的信号转导途径,阐明15-HETE引起慢性缺氧性肺动脉收缩作用的可能机制。方法：采用组织浴槽血管环方法观察15-HETE对缺氧和正常组大鼠血管收缩的作用,同时观察PI3K/Akt抑制剂LY294002对肺动脉环收缩强度的改变,明确PI3K/Akt信号转导途径在15-HETE收缩肺动脉中的作用。结果：15-HETE对正常组和缺氧模型组大鼠血管环均有收缩作用,加入AKT抑制剂LY294002可明显阻断15-HETE对缺氧大鼠肺动脉的收缩作用（P〈0.05）。结论：15-HETE通过AKT信号转导途径收缩慢性缺氧性大鼠肺动脉。     

PAF受体拮抗剂对缺氧性肺血管收缩和PAF舒血管反应的影响

用SRI63-441和BN52021两种结构不同的血小板活化因子(PAF)受体拮抗剂,研究其对整体大鼠缺氧性肺血管收缩反应(HPV)的影响及对PAF舒血管反应的抑制作用。结果两种PAF受体拮抗剂均可抑制由PAF诱导的舒血管反应,并增加基础状态下肺动脉压、肺血管阻力,但对HPV无明显影响。提示PAF的舒血管反应通过受体起作用,内源性PAF在维持肺动脉低张状态中可能起一定的作用,而在HPV中不起主要作用。     

用肺组织条作缺氧性肺血管收缩反应研究的探索

目的　探索由急性缺氧所致肺组织条张力变化与肺动脉和气管张力变化的关系 ,以探讨用肺组织条研究缺氧性肺血管反应的可行性。方法　因为肺组织条中可收缩的部分主要是血管和气管 ,所以分别做肺组织条、肺动脉、气管的张力实验。纵向剪取Wistar大鼠肺组织条以及肺动脉环 (肺动脉三级分支制成的肺动脉环 )和肺内段气管条悬挂于张力传感器上 ,记录张力变化。结果　急性缺氧使肺组织条及肺动脉环张力增加 ,而气管条张力下降 ,在加入消炎痛阻断前列腺素生成后 ,肺组织条缺氧性收缩反应增强 ,肺血管环缺氧反应也增加 ,而对肺内气管条的缺氧反应无明显影响 ;在加入L -NAME阻断一氧化氮生成后 ,肺组织条和肺血管环缺氧性收缩反应均增强 ,而对肺内气管条的缺氧反应无明显影响 ;在加入 4-AP阻断电压门控钾通道后 ,肺组织条与肺血管环缺氧性收缩反应均下降 ,气管缺氧性舒张反应减弱。结论　必要时可用肺组织条作缺氧性肺血管反应性研究     

Der Einfluß des Rauchens auf die hypoxische pulmonale Vasokonstriktion in der isolierten Lunge der Ratte — die Rolle der Prostaglandine und Leukotriene

Isolated rat lungs perfused with blood were used to determine the effects of cigarette smoke, delivered into the lung by a ventilator, on the pulmonary vascular resistance (PVR), and on the hypoxic pulmonary vasoconstriction (HPV), and to explore the role the prostsglandines (PG) and leukotrienes (LT) play in. that effect. The results showed that PVR did not change, while HPV was significantly enhanced by smoking. Indomethacin, an inhibitor of PG biosynthesis, administered in the perfusing blood (20 μg/ml) increased HPV in non-smoking lungs, but not in lungs after smoking. Diethylcarbamazine citrate (DEC, l mg/ml),an inhibitor of LT biosynthesis, decreased HPV before and after smoking. After perfusion with both indomethacin and DEC, HPV also decreased. It is suggested that LT act as mediators whereas PG as modulators in HPV, and PG and LT might play an important role in the increase of HPV by cigarette smoking.