首页> 外文期刊>Intensive care medicine >Soluble selectins in the pulmonary and systemic circulation in acute cardiogenic and non-cardiogenic pulmonary failure.
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Soluble selectins in the pulmonary and systemic circulation in acute cardiogenic and non-cardiogenic pulmonary failure.

机译:可溶性选择素在急性心源性和非心源性肺衰竭的肺和全身循环中。

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OBJECTIVE: Pulmonary endothelial activation caused by high pulmonary capillary pressures may be involved in the pathogenesis of cardiogenic pulmonary edema (CPE). We studied soluble selectins and soluble ICAM-1 as markers of cell activation in the systemic and pulmonary circulation of patients with respiratory failure (RF) due to CPE (RFCPE) as compared to patients with RF due to pulmonary infection (RFPI). SETTING: Cardiovascular Intensive Care Unit at a university hospital. PATIENTS: Twenty patients with RFCPE, 20 patients with RFPI and 17 critically ill patients without RF. INTERVENTIONS: Blood samples were obtained from the arterial and the pulmonary capillary circulation and sE-, sL-, and sP-selectin as well as sICAM-1 were determined. To distinguish between systemic and pulmonary endothelial activation, transpulmonary gradients (concentrationarterial blood - concentrationpulmonary capillary blood) were calculated. RESULTS: Systemic concentration of sL-selectin was lower in patients with RFCPE and RFPI than in patients without RF (RFCPE: 719.0 +/- 243.9 ng/ml, RFPI: 528.5 +/- 220.8 ng/ml, no RF: 882.4 +/- 222.6 ng/ml; P < 0.001). Systemic concentrations of ICAM-1, sE- and sP-selectin were not significantly different between the three groups. Transpulmonary gradients in sE- and sL-selectin were predominantly negative in patients with RFCPE (-3.2 +/- 7.8 ng/ml and -55.4 +/- 116.1 ng/ml, respectively) and RFPI (-2.3 +/- 5.8 ng/ml and -17.6 +/- 40.3 ng/ml, respectively) but were predominantly positive in patients without RF (11.6 +/- 7.2 ng/ml and 66.6 +/- 69.6 ng/ml, respectively), which suggests trapping of sE- and sL-selectin in the pulmonary circulation in the majority of patients with RFPI as well as in the majority of patients with RFCPE. CONCLUSION: Pulmonary endothelial activation occurs during both RFCPE and RFPI. This adds evidence that, besides hydrostatic mechanisms, cell activation occurs during CPE.
机译:目的:高肺毛细血管压力引起的肺血管内皮活化可能与心源性肺水肿(CPE)的发病机制有关。我们研究了可溶性选择素和可溶性ICAM-1作为与CPE(RFCPE)相关的呼吸衰竭(RF)与由于肺部感染(RFPI)引起的RF患者的全身和肺循环中细胞活化的标志物。地点:大学医院的心血管重症监护室。患者:20例RFCPE患者,20例RFPI患者和17例无RF的危重患者。干预措施:从动脉和肺毛细血管循环中获取血样,并测定sE-,sL-和sP-选择素以及sICAM-1。为了区分全身和肺内皮激活,计算了经肺的梯度(浓度动脉血-浓度肺毛细血管血)。结果:RFCL和RFPI患者的sL-选择素系统浓度低于无RF患者(RFCPE:719.0 +/- 243.9 ng / ml,RFPI:528.5 +/- 220.8 ng / ml,无RF:882.4 + / -222.6 ng / ml; P <0.001)。三组间ICAM-1,sE-和sP-选择素的全身浓度无显着差异。 RFCE(分别为-3.2 +/- 7.8 ng / ml和-55.4 +/- 116.1 ng / ml)和RFPI(-2.3 +/- 5.8 ng / ml)患者的sE-和sL-selectin跨肺梯度主要为阴性ml和-17.6 +/- 40.3 ng / ml),但在无RF的患者中主要呈阳性(分别为11.6 +/- 7.2 ng / ml和66.6 +/- 69.6 ng / ml),这表明sE-大部分RFPI患者以及大多数RFCPE患者的肺循环中使用sL和sL-选择素。结论:RFCPE和RFPI均发生肺血管内皮激活。这增加了证据,除了静水机制外,在CPE期间还会发生细胞活化。

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