Role of serotonin in the pathogenesis of acute and chronic pulmonary hypertension

Egermayer, Paul; Town, G. Ian; Peacock, AJ

doi:10.1136/thx.54.2.161

Cited by 101 publications

(74 citation statements)

References 152 publications

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“…Examples include rats [68], poultry [69,70], cattle [71,72], pigs [73] and horses [74]. Many stimuli that provoke PH in man, such as altitude, hypoxia, parasitic infections, patent ductus arteriosus, endotoxins, anorexient and other drugs have also been shown to provoke similar responses in several other mammalian species, suggesting more interspecies similarities than differences [75]. The fact that chronic PH was not provoked by repeated injections of thrombotic material in any of the animal species previously discussed, is indirect evidence that such a mechanism may also not be operative in humans.…”

Section: Chronic Pulmonary Hypertension In Animalsmentioning

confidence: 99%

“…Interaction of platelets with arteriosclerotic plaques also leads to the release of vasoactive substances [75].…”

Section: Are Venous Thromboembolism and Chronic Thromboembolic Pulmonmentioning

confidence: 99%

“…Numerous influences such as hypoxia, endogenous vasoconstrictors, and inflammatory cytokines could help to sustain this process [75]. PE could be one such traumatic influence resulting in endothelial damage, but other influences may be more prevalent and more important.…”

Section: Are Venous Thromboembolism and Chronic Thromboembolic Pulmonmentioning

confidence: 99%

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Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis

Egermayer¹,

Peacock²

2000

Eur Respir J

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148

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Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis. P Egermayer, A.J. Peacock. #ERS Journals Ltd 2000. ABSTRACT: The hypothesis that chronic thromboembolic pulmonary hypertension results from unresolved pulmonary embolism has strongly influenced the diagnosis and management of this disease since the 1960s. However, it is nearly impossible to induce chronic pulmonary hypertension in any animal species by means of repeated embolization of thrombotic material. The haemodynamic effects of thrombotic pulmonary embolism of different degrees of magnitude have also been studied in humans and there is little to suggest that chronic pulmonary hypertension is a likely long term outcome. Furthermore many conditions which predispose to venous thromboembolism do not appear to cause thromboembolic pulmonary hypertension. Other arteriopathic and atherosclerotic risk factors, are found in patients with chronic thromboembolic pulmonary hypertension, but not in those with venous thrombosis, suggesting that these may be unrelated conditions.Thrombosis in situ of the pulmonary arteries is common in severe pulmonary hypertension of any cause. Such thrombosis cannot usually be distinguished from pulmonary embolism. It is hypothesized that in situ thrombosis and pulmonary arteriopathy are common causes of vascular occlusion which is usually diagnosed as "chronic thromboembolic pulmonary hypertension" and that venous thromboembolism is unlikely to be a common cause of chronic pulmonary hypertension. It is further hypothesized that pulmonary embolism is seldom the sole cause of "chronic thromboembolic pulmonary hypertension". Eur Respir J 2000; 15: 440±448.

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Section: Chronic Pulmonary Hypertension In Animalsmentioning

confidence: 99%

“…Interaction of platelets with arteriosclerotic plaques also leads to the release of vasoactive substances [75].…”

Section: Are Venous Thromboembolism and Chronic Thromboembolic Pulmonmentioning

confidence: 99%

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Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis

Egermayer¹,

Peacock²

2000

Eur Respir J

Self Cite

148

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“…The action of serotonin in pulmonary circulation is wide and also includes vasoconstriction, for instance, in response to hypoxia 17 . Increased plasmatic levels of serotonin are observed in some forms of PAH 18 . Besides, the increased expression of its transporter could be related to accumulation of intracellular serotonin 19 .…”

Section: Cellular Proliferation and Matrix Changes In Pulmonary Vascumentioning

confidence: 99%

Hipertensão arterial pulmonar: fisiopatologia, aspectos genéticos e resposta ao uso crônico do sildenafil

Barreto¹,

Franchi²,

Pereira³

et al. 2005

Arq. Bras. Cardiol.

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“…They are omnipresent in the lung, along with their receptors, 136,137 and are thought to be the key mediators in many forms of vascular lung injury, such as adult respiratory distress syndrome, 138 146,147 and APTE. 121,148,149 Because of their potency and universal nature in regulating vascular smooth muscle tone, some have asserted that other mediators implicated in APTE, including thromboxane 150 and serotonin, 151 manifest their vasoconstriction via the endothelin pathway. [152][153][154] Lee et al 121 showed that endothelin-1 was expressed in situ in the embolized lung and that its antagonist mitigated the subsequent PH.…”

Section: Pulmonary Hypertension (Ph) In Aptementioning

confidence: 99%

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Tsang

Hogg

2014

Pulm. circ.

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Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/ perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin-mediated vasoconstriction also persisted at significant level during the early phase. More than 30 years ago, Eugene Robin commented on the problems of diagnosing acute pulmonary thromboembolism (APTE) by referring the physicians' attitudes to the emperor's vanity in Hans Christian Andersen's fable. 1,2 Although significant advances have occurred over the years, 3-5 some aspects of its pathophysiology remain puzzling. 6 This report provides an updated review of the literature, published mostly from 1980 onward, specifically addressing the mechanisms of hypoxemia and pulmonary hypertension (PH) after APTE. The emphasis is on the elucidation of the underlying pathophysiological principles and bringing them to the bedside, rather than on presenting meta-analysis or clinical trials. It also allows for occasional personal perspectives but has excluded recent works at the molecular level. GAS EXCHANGE IN APTEHypoxemia is a common and nonspecific feature of APTE. 7,8 It remains mysterious because the patient's arterial oxygen tension (PaO 2 ) is often unpredictable and correlates poorly with embolic load. [9][10][11] It is also associated with very different V/Q (ventilation/perfusion ratio) patterns measured by the multiple inert gas elimination technique (MIGET) among similar subjects 12 or in the same subject over time. 12,13 The roles of anatomical shunts may be important among a minority of patients but are questionable in the rest. These variations in gas exchange are clinically relevant in a negative way, because blood gas results do not contribute to defining pretest probabilities in the interpretation of nuclear scans. 1,14,15 The major purpose of this communication is to discuss the key factors that determine the degree of hypoxemia after APTE and their relevance to 5 commonly asked questions:1. Why do patients with APTE present with such a wide range of hypoxemia? 2. Why do many patients with APTE have relatively clear chest X-rays while severely hypoxic? 3. Can patients with significant APTE present with relatively normal PaO 2 ? 4. Why does hypoxemia worsen when cardiac output is increased? 5. Why do some patients with APTE have pulmonary infarcts and the others do not?

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Role of serotonin in the pathogenesis of acute and chronic pulmonary hypertension

Cited by 101 publications

References 152 publications

Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis

Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis

Hipertensão arterial pulmonar: fisiopatologia, aspectos genéticos e resposta ao uso crônico do sildenafil

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

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