Platelet-activating factor raises airway and vascular pressures and induces edema in lungs perfused with platelet-free solution.
Platelet-activating factor raises airway and vascular pressures and induces edema in lungs perfused with platelet-free solution.
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血小板激活因子会升高气道和血管压力，并在灌注无血小板溶液的肺部引起水肿。
DOI：
10.1164/arrd.1984.129.5.742
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Said,SI
中科院分区：
文献类型：
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作者：
Hamasaki,Y;Mojarad,M;Saga,T;Tai,HH;Said,SI
用无血小板Krebs-Ringer液灌流豚鼠肺，观察合成血小板激活因子(PAF)对豚鼠肺的作用。当PAF(1µg)注入肺动脉(PA)时，可显著增加气道压力(最大增加84.7%)和中度增加(最大增加22.8%)。同样的剂量还可引起TXA2的稳定代谢产物血栓素B2(TXB2)大量(29倍)释放到灌流液中，开始于呼吸道和PA压力增加之前。前列环素的稳定代谢产物6-酮-前列腺素F1-α的浓度在血栓素B_2峰值释放后也增加了约70 S(达到对照水平的5倍)。消炎痛完全阻断TXB2释放，使气道压力升高幅度降低79%，并缩短其持续时间和PA压力升高的持续时间。较大浓度的PAF(3和10微克)在呼吸道和PA压力上产生更大的增加，但这些仅被吲哚美辛适度减弱。此外，PAF还增加了血管外肺水，表现为肺湿重/干重和肺/体重比的增加。在0.1ug浓度下，PAF对气道压和PA压无影响，也不刺激TXB2或6-keto-PGF_1α的释放。溶血型PAF同样无效。我们得出结论：PAF不依赖于血小板而引起豚鼠肺的气道收缩、肺动脉高压和肺水肿。这些作用与刺激合成TXA2有关，但其产生机制尚不清楚。
The effects of synthetic platelet-activating factor (PAF) on guinea pig lung were examined in isolated lungs perfused with platelet-free Krebs-Ringer solution. When PAF (1µg)was injected into the pulmonary artery (PA), it markedly increased airway pressure (maximal increase, 84.7%) and moderately raised PA pressure (maximal increase, 22.8%). The same dose also provoked a massive (29-fold) release of thromboxane B2(TXB2), the stable metabolite of TXA2, into the perfusate, beginning before the increases in airway and PA pressures. The concentration of 6 keto-PGF1α, the stable metabolite of prostacyclin, also increased (to 5 times control levels) about 70 s after peak release of TXB2. Indomethacin completely blocked TXB2release, reduced the magnitude of airway pressure increase by 79%, and shortened its duration, as well as the duration of the PA pressure rise. Larger concentrations of PAF (3 and 10 µg) produced even greater increments in airway and PA pressures, but these were only moderately attenuated by indomethacin. Also, PAF increased extravascular lung water, as evidenced by increases in wet/dry lung weight and lung/body weight ratios. In a concentration of 0.1 µg, PAF had no effects on airway or PA pressures, nor did it stimulate TXB2or 6-keto-PGF1αrelease. Lyso-PAF was similarly ineffective.We conclude that PAF induces airway constriction, pulmonary hypertension, and pulmonary edema in guinea pig lung independently of platelets. These effects are associated with stimulated synthesis of TXA2, but the mechanisms of their production remain to be determined.