![]() Moreover, the effects of serotonin are intensified under hypoxemic conditions and the administration of catecholamines. The different effects of serotonin on the two circulatory systems are similar to those observed under hypoxemia. Serotonin is a potent pulmonary vasoconstrictor but causes profound vasodilation in the systemic vasculature. These anorexigens (fenfluramine, D-fenfluramine and aminorex) have been shown to increase the levels of circulating serotonin (5-hydroxytryptamine, 5-HTT) by inhibiting its reuptake in neurons and platelets, inducing platelet release of serotonin, and by blocking its degradation through interaction with the monoamine oxidase enzymes. In the 1980s, fenfluramine was the second anorexigen linked to PH. In the 1960s, an association between PH and the anorexigen aminorex was identified, leading to the withdrawal of aminorex from the market in 1972. The serotonin system seems to be involved in the pathogenesis of PH. Nevertheless, the major part of the etiopathogenesis of PH is still incompletely understood. These progresses are also reflected in newer PH classifications and evolving therapies. In the last decade, major advances in the pathogenetic understanding of pulmonary vascular diseases have led to better treatment options and prognosis. Pulmonary hypertension (PH) comprises a group of relatively rare disorders with a consistently progressive course and a dismal prognosis. The negative transpulmonary platelet serotonin gradient and the strong negative correlation of arterial blood platelet serotonin with pulmonary hemodynamics might indicate increased serotonin uptake in the lungs of PH patients. Conclusion: The lower platelet serotonin concentration in PH patients compared with unaffected controls is an unprecedented finding. Plasmatic serotonin levels did not differ between the PH and control groups. An inverse correlation was found between the arterial blood platelet serotonin content and pulmonary hemodynamics. The mean transpulmonary gradient (arterial-mixed venous) was negative in the PH group and positive in the controls. Platelet serotonin content was significantly lower in the PH patients than in the controls. Results: PH was classified as arterial in 4 and chronic thromboembolic in 9 patients with a mean pulmonary artery pressure of 37 (interquartile range: 32–43) mm Hg. After careful thawing, plasmatic and platelet serotonin levels were determined by ELISA. Arterial and mixed venous blood samples were immediately centrifuged to obtain plasma and platelets and thereafter frozen at –20☌. ![]() Patients and Methods: Catheters were placed in the radial and pulmonary artery in patients with PH (n = 13) for diagnosis and in age-matched controls (n = 6) undergoing percutaneous closure of the patent foramen ovale. Objective: To comparatively analyze plasmatic and intrathrombocytic serotonin levels in arterial and mixed venous blood of patients with PH and unaffected controls to elucidate pulmonary serotonin metabolisms. The DPG is superior to the TPG for the diagnosis of "out of proportion" pulmonary hypertension.Background: The serotonin system has repeatedly been associated with the pathogenesis of pulmonary hypertension (PH). The measurement of a diastolic P(pa)/P(pcw) gradient (DPG) combined with systemic blood pressure and cardiac output allows for a step-by-step differential diagnosis between pulmonary vascular disease, high output or high left-heart filling pressure state, and sepsis. It may, therefore, be preferable to rely on a gradient between diastolic P(pa) and P(pcw). Furthermore, pulmonary blood flow is pulsatile, with systolic P(pa) and mean P(pa) determined by stroke volume and arterial compliance. This value is arbitrary, because the gradient is sensitive to changes in cardiac output and both recruitment and distension of the pulmonary vessels, which decrease the upstream transmission of P(la). In these patients, a TPG of >12 mmHg would result in a diagnosis of "out of proportion" pulmonary hypertension. ![]() The transpulmonary pressure gradient (TPG), defined by the difference between mean pulmonary arterial pressure (P(pa)) and left atrial pressure (P(la) commonly estimated by pulmonary capillary wedge pressure: P(pcw)) has been recommended for the detection of intrinsic pulmonary vascular disease in left-heart conditions associated with increased pulmonary venous pressure.
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