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原发性肺动脉高压患者血浆血清素增加。

Increased plasma serotonin in primary pulmonary hypertension.

作者信息

Hervé P, Launay J M, Scrobohaci M L, Brenot F, Simonneau G, Petitpretz P, Poubeau P, Cerrina J, Duroux P, Drouet L

机构信息

Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine Béclère, Université Paris Sud, Clamart, France.

出版信息

Am J Med. 1995 Sep;99(3):249-54. doi: 10.1016/s0002-9343(99)80156-9.

Abstract

PURPOSE

Pulmonary hypertension can occur in patients who have disorders associated with altered platelet serotonin storage, including collagen vascular disease and platelet storage pool disease. We tested the hypothesis that primary pulmonary hypertension (PPH) may be also associated with impaired handling of serotonin by platelets, resulting in increased plasma serotonin levels.

PATIENTS AND METHODS

We used radioenzymatic assays to measure serotonin in platelets and plasma and serotonin released during in vitro platelet aggregation in 16 patients with PPH, and in 16 normal controls matched for age and sex. Six patients were restudied after heart-lung transplantation to determine whether serotonin abnormalities persisted after pulmonary arterial pressure returned to normal.

RESULTS

Patients had decreased platelet serotonin concentration (1.8 +/- 0.6 x 10(-18) mol/platelet versus 3.2 +/- 0.2 x 10(-18) mol/platelet in controls; P < 0.01) and increased plasma serotonin concentration (30.1 +/- 9.2 x 10(-9) mol/L versus 0.6 +/- 0.1 x 10(-9) mol/L in controls; P < 0.001). Serotonin released during in vitro platelet aggregation was higher in patients than in controls. After heart-lung transplantation, platelet serotonin concentrations remained decreased and plasma levels remained increased.

CONCLUSIONS

Abnormal handling of serotonin by platelets leading to an increase in plasma serotonin occurs in PPH. The persistent decrease in platelet storage of serotonin after heart-lung transplantation suggests that this platelet abnormality is not secondary to PPH.

摘要

目的

肺动脉高压可发生于患有与血小板5-羟色胺储存改变相关疾病的患者,包括胶原血管病和血小板储存池病。我们检验了以下假设:原发性肺动脉高压(PPH)可能也与血小板对5-羟色胺的处理受损有关,从而导致血浆5-羟色胺水平升高。

患者与方法

我们使用放射酶法测定了16例PPH患者以及16例年龄和性别相匹配的正常对照者血小板和血浆中的5-羟色胺,以及体外血小板聚集过程中释放的5-羟色胺。6例患者在心肺移植后再次接受研究,以确定肺动脉压恢复正常后5-羟色胺异常是否持续存在。

结果

患者的血小板5-羟色胺浓度降低(1.8±0.6×10⁻¹⁸摩尔/血小板,而对照组为3.2±0.2×10⁻¹⁸摩尔/血小板;P<0.01),血浆5-羟色胺浓度升高(30.1±9.2×10⁻⁹摩尔/升,而对照组为0.6±0.1×10⁻⁹摩尔/升;P<0.001)。患者体外血小板聚集过程中释放的5-羟色胺高于对照组。心肺移植后,血小板5-羟色胺浓度仍降低,血浆水平仍升高。

结论

PPH患者存在血小板对5-羟色胺的异常处理,导致血浆5-羟色胺增加。心肺移植后血小板5-羟色胺储存持续降低表明这种血小板异常并非PPH的继发表现。

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