Acetyl glyceryl ether phosphorylcholine-stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2.
Acetyl glyceryl ether phosphorylcholine-stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2.
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乙酰甘油醚磷酸胆碱刺激的人血小板引起离体兔肺肺动脉高压和水肿。
DOI：
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发表时间：
1983
影响因子：
15.9
通讯作者：
J. Repine
中科院分区：
文献类型：
--
作者：
J. Heffner;S. Shoemaker;E. Canham;M. Patel;I. McMurtry;H. G. Morris;J. Repine
巨噬细胞、中性粒细胞和血小板可能在急性水肿性肺损伤中发挥作用，如在成人呼吸窘迫综合征（ARDS）中所见，但它们的潜在作用和相互作用尚不清楚。由于刺激的人巨噬细胞和中性粒细胞可以释放乙酰甘油醚磷酸胆碱（AGEPC），一种有效的血小板激活剂，我们假设在ARDS中，白细胞释放的AGEPC可能刺激血小板释放血栓素A2（TXA 2），然后产生肺动脉高压和肺水肿。在支持这一前提，我们发现，肺动脉高压和水肿发生在离体兔肺灌注人血小板和AGEPC，但不与血小板或AGEPC单独。输注血管扩张剂（硝酸甘油），以维持基线肺动脉压与血小板和AGEPC灌注肺防止肺水肿的发展，这表明血小板和AGEPC诱导的水肿是流体静力学性质。另外的实验表明，压力增加是由AGEPC刺激血小板释放TXA 2的结果。具体来说，在输注AGEPC之前，将血小板与咪唑（一种血栓烷合成酶阻断剂）预孵育，可显著降低肺动脉高压并预防肺水肿。此外，在输注AGEPC和未处理的血小板之前，用TXA 2拮抗剂13-氮杂丙烷酸预处理肺制剂也降低了肺动脉高压并阻断了肺水肿。当输注血小板和AGEPC的肺灌注液产生高水平的TXA 2时，TXA 2的作用得到进一步提示，而对照组的灌注液则没有。这些结果表明，AGEPC诱导的血小板聚集可能通过释放TXA 2而导致ARDS，TXA 2升高微血管压力并增加水肿形成，特别是当存在潜在的渗透性缺陷时。
Macrophages, neutrophils, and platelets may play a role in acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), but their potential actions and interactions are unclear. Because stimulated human macrophages and neutrophils can release acetyl glyceryl ether phosphorylcholine (AGEPC), a potent platelet activator, we hypothesized that in ARDS, leukocyte release of AGEPC might stimulate platelets to release thromboxane A2 (TXA2), which then produces pulmonary hypertension and lung edema. In support of this premise, we found that pulmonary hypertension and edema occurred in isolated rabbit lungs perfused with human platelets and AGEPC, but not with platelets or AGEPC alone. Infusion of a vasodilator (nitroglycerin) to maintain base-line pulmonary artery pressures in lungs perfused with platelets and AGEPC prevented the development of lung edema suggesting that platelet and AGEPC-induced edema was hydrostatic in nature. Additional experiments suggested that the increased pressure was a result of TXA2 release from platelets stimulated by AGEPC. Specifically, preincubation of platelets with imidazole, a thromboxane synthetase blocker, prior to infusion with AGEPC significantly diminished pulmonary hypertension and prevented lung edema. Furthermore, pretreating lung preparations with 13-azaprostanoic acid, a TXA2 antagonist, before infusion of AGEPC and untreated platelets also reduced the pulmonary hypertension and blocked the lung edema. The role of TXA2 was further suggested when perfusates from lungs infused with platelets and AGEPC developed high levels of TXA2, whereas perfusates from controls did not. These results suggest that platelet aggregation induced by AGEPC may contribute to ARDS by releasing TXA2, which raises microvascular pressure and increases edema formation, especially when an underlying permeability defect is present.
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血小板耗竭对家兔 IgE 过敏反应和乙酰甘油醚磷酰胆碱输注生理变化的不同影响。
DOI：
10.1164/arrd.1981.124.4.416
发表时间：
1981
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Halonen,M;Palmer,JD;Lohman,IC;McManus,LM;Pinckard,RN
通讯作者：
Pinckard,RN
硝酸甘油刺激培养的人内皮细胞合成前列环素。
DOI：
10.1172/jci110093
发表时间：
1981
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Levin,RI;Jaffe,EA;Weksler,BB;Tack-Goldman,K
通讯作者：
Tack-Goldman,K
乙酰甘油醚磷酸胆碱（兔子 IgE 过敏反应的介体）诱导的呼吸和循环改变。
DOI：
10.1164/arrd.1980.122.6.915
发表时间：
1980
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Halonen,M;Palmer,JD;Lohman,IC;McManus,LM;Pinckard,RN
通讯作者：
Pinckard,RN
1-O-十六烷基/十八烷基-2-乙酰基-sn-甘油基-3-磷酸胆碱（血小板激活因子）激活兔血小板磷脂酶和血栓素合成。
DOI：
10.1016/0005-2760(81)90208-3
发表时间：
1981
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Shaw,JO;Klusick,SJ;Hanahan,DJ
通讯作者：
Hanahan,DJ
DOI：
10.1172/jci110108
发表时间：
1981
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
McManus,LM;Hanahan,DJ;Pinckard,RN
通讯作者：
Pinckard,RN