Importance of vasoconstriction in lipid mediator-induced pulmonary edema.
Importance of vasoconstriction in lipid mediator-induced pulmonary edema.
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血管收缩在脂质介质引起的肺水肿中的重要性。
DOI：
10.1152/jappl.1989.66.6.2667
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Voelkel,NF
中科院分区：
文献类型：
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作者：
Sakai,A;Chang,SW;Voelkel,NF
炎症的脂质介质导致肺水肿，但目前尚不清楚血液动力学改变或血管通透性增加在多大程度上有助于肺水肿的形成。采用大鼠离体肺标本，观察白三烯C4(LTC4)和血小板活化因子(PAF)对大鼠肺动脉压(PPA)、肺微血管压(PMV)、肺湿干重比和125I-白蛋白逃逸指数的影响。我们首先通过提高肺流出压来确定用无蛋白盐溶液灌流的大鼠离体肺对流体动力应激的反应。持续升高的肺排出压低于5.5cmH2O(4.01毫米汞柱)引起的PPA和湿/干肺重量比的增加可以忽略不计。高于7.5cmH2O(5.4毫米汞柱)的流出压力增加血管白蛋白逃逸指数比增加肺湿/干重量比更多。二丁酰腺苷3‘，5’-环磷酸腺苷(db-cAMP)可抑制肺流出压升高引起的白蛋白逃逸指数的增加，提示db-cAMP可能具有非压力依赖性的微血管膜效应。LTC4(2微克丸)和PAF(2-2000 ng/ml灌流液)均增加白蛋白逃逸指数，并伴随PPA和PMV的增加。由于注射LTC4或PAF后白蛋白逃逸指数的增加在很大程度上是由于血管压力的增加以及db-cAMP和罂粟碱抑制血管压力的升高和白蛋白逃逸指数的增加，我们得出结论：血管收缩是LTC4和PAF诱导的大鼠肺水肿形成的重要因素。
Lipid mediators of inflammation cause pulmonary edema, yet it is unclear to what degree hemodynamic alterations or increased vascular permeability contribute to lung edema formation. The isolated rat lung preparation was used to examine the effect of leukotriene C4 (LTC4) and platelet-activating factor (PAF) on pulmonary arterial pressure (Ppa), lung microvascular pressure (Pmv), lung wet-to-dry weight ratio, and the 125I-albumin escape index. We first defined the response of the isolated rat lung perfused with protein-free salt solution to hydrodynamic stress by raising the lung outflow pressure. Sustained elevation of the lung outflow pressure less than 5.5 cmH2O (4.01 mmHg) caused a negligible increase in Ppa and wet-to-dry lung weight ratio. Elevation of outflow pressures greater than 7.5 cmH2O (5.4 mmHg) increased the vascular albumin escape index more than the lung wet-to-dry weight ratio. Dibutyryl adenosine 3′,5′-cyclic monophosphate (db-cAMP) inhibited the increase in albumin escape index because of increased lung outflow pressure, suggesting perhaps a pressure-independent microvascular membrane effect of db-cAMP. Both LTC4 (2-micrograms bolus) and PAF (2–2,000 ng/ml perfusate) increased the albumin escape index in association with increases in Ppa and Pmv. Because the increased albumin escape index after LTC4 or PAF injection was largely accounted for by the increased vascular pressures and because db-cAMP and papaverine inhibited the rise in vascular pressures and in the albumin escape index, we conclude that vasoconstriction is an important contributor to LTC4- and PAF-induced edema formation in rat lungs.