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心源休克患者的血浆腺苷水平和 A2A 受体表达。

Adenosine Plasma Level and A2A Receptor Expression in Patients With Cardiogenic Shock.

机构信息

Department of Cardiology, Assistance Publique-Hôpitaux de Marseille, Hôpital Nord, Marseille, France.

Mediterranean Academic Association for Research and Studies in Cardiology (MARS Cardio), Marseille, France.

出版信息

Crit Care Med. 2018 Sep;46(9):e874-e880. doi: 10.1097/CCM.0000000000003252.

Abstract

OBJECTIVES

To investigate whether adenosine A2A receptors lead to vasodilation and positive inotropic function under stimulation and whether they play a role in the control of blood pressure in patients with cardiogenic shock.

DESIGN

Prospective observational study.

SETTING

Monocentric, Hopital Nord, Marseille, France.

SUBJECTS

Patients with cardiogenic shock (n = 16), acute heart failure (n = 16), and acute myocardial infarction (n = 16).

INTERVENTIONS

None.

MEASUREMENTS AND MAIN RESULTS

Arterial adenosine plasma level and A2A receptor expression on peripheral blood mononuclear cells were evaluated by mass spectrometry and Western blot, respectively, at admission and after 24 hours. Hemodynamic parameters, including systemic vascular resistance, were also assessed. Mean adenosine plasma level at admission was significantly higher in patients with cardiogenic shock (2.74 ± 1.03 µM) versus acute heart failure (1.33 ± 0.27) or acute myocardial infarction (1.19 ± 0.27) (normal range, 0.4-0.8 µM) (p < 0.0001). No significant correlation was found between adenosine plasma level and systemic vascular resistance. Mean adenosine plasma level decreased significantly by 24 hours after admission in patients with cardiogenic shock (2.74 ± 1.03 to 1.53 ± 0.68; p < 0.001). Mean A2A receptor expression was significantly lower in patients with cardiogenic shock (1.18 ± 0.11) versus acute heart failure (1.18 ± 0.11 vs 1.39 ± 0.08) (p = 0.005).

CONCLUSIONS

We observed high adenosine plasma level and low A2A receptor expression at admission in patients with cardiogenic shock versus acute heart failure or acute myocardial infarction. This may contribute to the physiopathology of cardiogenic shock.

摘要

目的

探讨腺苷 A2A 受体在刺激下是否导致血管扩张和正性肌力作用,以及它们在心源性休克患者的血压控制中是否发挥作用。

设计

前瞻性观察性研究。

地点

法国马赛 Nord 医院单中心。

对象

心源性休克患者(n=16)、急性心力衰竭患者(n=16)和急性心肌梗死患者(n=16)。

干预

无。

测量和主要结果

通过质谱和 Western blot 分别评估入院时和 24 小时后外周血单核细胞的动脉腺苷血浆水平和 A2A 受体表达。还评估了血流动力学参数,包括全身血管阻力。心源性休克患者入院时的平均腺苷血浆水平(2.74±1.03µM)显著高于急性心力衰竭患者(1.33±0.27µM)或急性心肌梗死患者(1.19±0.27µM)(正常范围,0.4-0.8µM)(p<0.0001)。未发现腺苷血浆水平与全身血管阻力之间存在显著相关性。心源性休克患者入院 24 小时后,平均腺苷血浆水平显著下降(2.74±1.03 至 1.53±0.68;p<0.001)。心源性休克患者的平均 A2A 受体表达(1.18±0.11)显著低于急性心力衰竭患者(1.18±0.11 vs 1.39±0.08)(p=0.005)。

结论

与急性心力衰竭或急性心肌梗死患者相比,我们观察到心源性休克患者入院时的腺苷血浆水平较高和 A2A 受体表达较低。这可能有助于心源性休克的病理生理学。

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