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肺血清素代谢

Lung serotonin metabolism.

作者信息

Hart C M, Block E R

机构信息

Department of Medicine, University of Florida College of Medicine, Gainesville.

出版信息

Clin Chest Med. 1989 Mar;10(1):59-70.

PMID:2650964
Abstract

The pulmonary vascular endothelium, a metabolically active tissue, serves as an important site of injury in many types of clinical and experimental lung disease. Removal of 5-HT from the circulation constitutes one of the endothelial metabolic functions that is depressed early in the course of lung injury. Experimental evidence confirms that measuring 5-HT uptake detects alterations in endothelial cell function that precede the abnormalities detected by more conventional diagnostic tests such as radiographs, pulmonary function tests, and arterial blood gases. In addition, depression of 5-HT uptake can lead to increased concentrations of 5-HT in the pulmonary vasculature, which may contribute to the pathogenesis of lung injury. The development of an ideal method for measuring 5-HT uptake accurately in the lungs of critically ill patients has just begun. As yet, numerous variables reviewed in this article confound clinical measurements of 5-HT uptake. However, if investigators can continue to refine and develop the techniques for measuring 5-HT uptake in human patients, clinicians can look forward to the addition of a sensitive tool to their diagnostic armamentarium. Hopefully, the ability to detect diffuse lung injury earlier in its course will enable future clinicians to institute therapy that will prevent the pathologic progression to morbidity and death seen all too frequently in current medical practice.

摘要

肺血管内皮是一种具有代谢活性的组织,在许多类型的临床和实验性肺部疾病中是重要的损伤部位。从循环中清除5-羟色胺(5-HT)是内皮代谢功能之一,在肺损伤过程早期会受到抑制。实验证据证实,测量5-HT摄取可检测到内皮细胞功能的改变,这些改变早于通过更传统的诊断测试(如X光片、肺功能测试和动脉血气分析)检测到的异常。此外,5-HT摄取受抑制会导致肺血管中5-HT浓度升高,这可能有助于肺损伤的发病机制。准确测量重症患者肺部5-HT摄取的理想方法的开发才刚刚开始。到目前为止,本文中所讨论的众多变量使5-HT摄取的临床测量变得复杂。然而,如果研究人员能够继续完善和开发在人类患者中测量5-HT摄取的技术,临床医生有望在其诊断手段中增加一种敏感工具。希望能够在弥漫性肺损伤病程的早期进行检测,这将使未来的临床医生能够采取治疗措施,防止目前医疗实践中经常出现的病理进展,导致发病和死亡。

相似文献

1
Lung serotonin metabolism.肺血清素代谢
Clin Chest Med. 1989 Mar;10(1):59-70.
2
Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies?成人呼吸窘迫综合征的病理生理学。我们从人体研究中学到了什么?
Crit Care Clin. 1986 Jul;2(3):429-53.
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Depression of serotonin uptake by rat lungs exposed to paraquat.
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Xanthine oxidase-induced lung injury inhibits removal of 5-hydroxytryptamine from the pulmonary circulation.黄嘌呤氧化酶诱导的肺损伤会抑制肺循环中5-羟色胺的清除。
Anesth Analg. 1982 Aug;61(8):666-70.
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Early metabolic changes in response to lung injury: extrapolation from animals to humans.肺损伤早期的代谢变化:从动物到人类的推断
J Toxicol Environ Health. 1984;13(2-3):369-86. doi: 10.1080/15287398409530504.
6
Pulmonary endothelial cell injury and altered lung metabolic function. Early detection of the adult respiratory distress syndrome and possible functional significance.肺内皮细胞损伤与肺代谢功能改变。成人呼吸窘迫综合征的早期检测及其可能的功能意义。
Clin Chest Med. 1990 Dec;11(4):723-36.
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Depressed prostaglandin E1 and 5-hydroxytryptamine removal in patients with adult respiratory distress syndrome.
Am Rev Respir Dis. 1986 Oct;134(4):739-44. doi: 10.1164/arrd.1986.134.4.739.
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Enflurane, halothane, and isoflurane inhibit removal of 5-hydroxytryptamine from the pulmonary circulation.
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Altered metabolic function of the pulmonary microcirculation. Early detection of lung injury and possible functional significance.肺微循环代谢功能改变。肺损伤的早期检测及其可能的功能意义。
Crit Care Clin. 1986 Jul;2(3):497-509.
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Pulmonary sequelae and lung repair in survivors of the adult respiratory distress syndrome.成人呼吸窘迫综合征幸存者的肺部后遗症与肺修复
Crit Care Clin. 1986 Jul;2(3):629-65.

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