Liver disease and pulmonary hypertension

Ss, Salvi

doi:10.1136/gut.47.4.595

Gut

2000

DOI: 10.1136/gut.47.4.595

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Liver disease and pulmonary hypertension

Salvi Ss¹

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Cited by 4 publications

(2 citation statements)

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“…Hypoxia also increases expression of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine synthesis (36), and increases expression of ␣ 1 -adrenoceptors (ARs) in VSMCs in vitro and in aorta in vivo (9). The incidence of PH is increased by certain appetite suppressants (aminorex and fenfluramine), cocaine, and liver disease, which all increase plasma catecholamines (36,37). Although adrenergic innervation of PAs is less dense than most other vascular beds (25), the contractile sensitivity of medium-sized PAs to NE, which is ␣ 1 -AR dependent (28), is the highest among 12 rabbit arteries and veins studied in vitro (up to 200-fold greater) (3).…”

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“…Chronic alveolar hypoxia is thought to cause hypoxic-metabolic and/or hemodynamic "injury" to the endothelium and vascular wall, including enhanced production of reactive oxidative species (for a review, see Refs. 6,14,19,33,36,37,and 40). Induction of multiple intracellular and autocrine and paracrine signals leads to proliferation of endothelial cells, vascular smooth muscle cells (VSMCs), fibroblasts, intermediate cells, and pericytes.…”

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Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

Faber

Szymeczek²,

Salvi³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Enhanced ␣1-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats. Am J Physiol Heart Circ Physiol 291: H2272-H2281, 2006. First published June 23, 2006 doi:10.1152/ajpheart.00404.2006.-Mechanisms that induce the excessive proliferation of vascular wall cells in hypoxic pulmonary hypertension (PH) are not fully understood. Alveolar hypoxia causes sympathoexcitation, and norepinephrine can stimulate ␣1-adrenoceptor (␣1-AR)-dependent hypertrophy/hyperplasia of smooth muscle cells and adventitial fibroblasts. Adrenergic trophic activity is augmented in systemic arteries by injury and altered shear stress, which are key pathogenic stimuli in hypoxic PH, and contributes to neointimal formation and flow-mediated hypertrophic remodeling. Here we examined whether norepinephrine stimulates growth of the pulmonary artery (PA) and whether this is augmented in PH. PA from normoxic and hypoxic rats [9 days of 0.1 fraction of inspired O2 (FIO 2 )] was studied in organ culture, where wall tension, PO2, and PCO2 were maintained at values present in normal and hypoxic PH rats. Norepinephrine treatment for 72 h increased DNA and protein content modestly in normoxic PA (ϩ10%, P Ͻ 0.05). In hypoxic PA, these effects were augmented threefold (P Ͻ 0.05), and protein synthesis was increased 34-fold (P Ͻ 0.05). Inferior thoracic vena cava from normoxic or hypoxic rats was unaffected. Norepinephrine-induced growth in hypoxic PA was dose dependent, had efficacy greater than or equal to endothelin-1, required the presence of wall tension, and was inhibited by ␣1A-AR antagonist. In hypoxic pulmonary vasculature, ␣1A-AR was downregulated the least among ␣1-AR subtypes. These data demonstrate that norepinephrine has trophic activity in the PA that is augmented by PH. If evident in vivo in the pulmonary vasculature, adrenergic-induced growth may contribute to the vascular hyperplasia that participates in hypoxic PH. vascular smooth muscle; hypertrophy; catecholamines; adrenergic receptors; hypoxia CHRONIC OBSTRUCTIVE DISEASES, hypoventilatory disorders, and extended exposure to high altitude lead to hypoxic pulmonary hypertension (PH), the most common type of PH not arising from left ventricular dysfunction. Chronic alveolar hypoxia is thought to cause hypoxic-metabolic and/or hemodynamic "injury" to the endothelium and vascular wall, including enhanced production of reactive oxidative species (for a review, see Refs. 6,14,19,33,36,37,and 40). Induction of multiple intracellular and autocrine and paracrine signals leads to proliferation of endothelial cells, vascular smooth muscle cells (VSMCs), fibroblasts, intermediate cells, and pericytes. Proliferation, migration, and matrix accumulation elicit wall hypertrophy, fibrosis, and distal muscularization in the pulmonary arterial circulation. These changes cause structural lumen loss, enhanced VSMC tone, and reduced compliance, which, together with polycythemia, increase pulmonary vascular resistance, right heart hypertrophy, and risk of right heart failure....

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confidence: 99%

mentioning

confidence: 99%

Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

Faber

Szymeczek²,

Salvi³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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α₁-Adrenoceptor-dependent vascular hypertrophy and remodeling in murine hypoxic pulmonary hypertension

Faber

Szymeczek²,

Cotecchia

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Excessive proliferation of vascular wall cells underlies the development of elevated vascular resistance in hypoxic pulmonary hypertension (PH), but the responsible mechanisms remain unclear. Growth-promoting effects of catecholamines may contribute. Hypoxemia causes sympathoexcitation, and prolonged stimulation of alpha(1)-adrenoceptors (alpha(1)-ARs) induces hypertrophy and hyperplasia of arterial smooth muscle cells and adventitial fibroblasts. Catecholamine trophic actions in arteries are enhanced when other conditions favoring growth or remodeling are present, e.g., injury or altered shear stress, in isolated pulmonary arteries from rats with hypoxic PH. The present study examined the hypothesis that catecholamines contribute to pulmonary vascular remodeling in vivo in hypoxic PH. Mice genetically deficient in norepinephrine and epinephrine production [dopamine beta-hydroxylase(-/-) (DBH(-/-))] or alpha(1)-ARs were examined for alterations in PH, cardiac hypertrophy, and vascular remodeling after 21 days exposure to normobaric 0.1 inspired oxygen fraction (Fi(O(2))). A decrease in the lumen area and an increase in the wall thickness of arteries were strongly inhibited in knockout mice (order of extent of inhibition: DBH(-/-) = alpha(1D)-AR(-/-) > alpha(1B)-AR(-/-)). Distal muscularization of small arterioles was also reduced (DBH(-/-) > alpha(1D)-AR(-/-) > alpha(1B)-AR(-/-) mice). Despite these reductions, increases in right ventricular pressure and hypertrophy were not attenuated in DBH(-/-) and alpha(1B)-AR(-/-) mice. However, hematocrit increased more in these mice, possibly as a consequence of impaired cardiovascular activation that occurs during reduction of Fi(O(2)). In contrast, in alpha(1D)-AR(-/-) mice, where hematocrit increased the same as in wild-type mice, right ventricular pressure was reduced. These data suggest that catecholamine stimulation of alpha(1B)- and alpha(1D)-ARs contributes significantly to vascular remodeling in hypoxic PH.

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Doppler-defined pulmonary hypertension in β-thalassemia major in Kurdistan, Iraq

Mohammad

Dawad²,

Kashmoola³

et al. 2020

PLoS ONE

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Cardiopulmonary complications are among the most important complications of thalassemia major. Pulmonary hypertension is among these complications and studies addressing its frequency and associations in the latter disorder are sparse from Iraq. For this purpose a total 100 thalassemia major patients (≥ 8 years old) were enrolled from a main thalassemia center in Kurdistan, Northern Iraq. All patients had a full history and clinical examination. Full blood count, biochemical tests and viral screen including hepatitis B surface antigen and hepatitis C virus antibody, in addition to transthoracic Doppler echocardiography for tricuspid regurgitation jet velocity (TRV). The enrolled patients had a mean (SD) age of 17.6 (5.5) years, and included 52 males and 48 females. Pulmonary hypertension as defined by TRV> 2.8 m/s coupled with both exertional dyspnea and an absence of left sided heart failure, was identified in nine patients (9%). The latter subgroup of patients had significantly higher reticulocyte counts, S. LDH, S. ferritin, and hepatitis C sero-positivity compared to those without this complication by univariate analysis. While by multivariate logistic regression only reticulocytes and hepatitis C sero-positivity remained significant. Furthermore, TRV as a continuous variable was positively correlated with reticulocytes, S. bilirubin and LDH (p<0.001, p = 0.002 and p<0.001 respectively), but not with age or S. ferritin (p = 0.77, and p = 0.93 respectively). In conclusion, pulmonary hypertension is not uncommon in Iraqi patients with thalassemia major, and it appears to be linked to chronic hemolysis rather than iron overload.

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Liver disease and pulmonary hypertension

Cited by 4 publications

References 12 publications

Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

α₁-Adrenoceptor-dependent vascular hypertrophy and remodeling in murine hypoxic pulmonary hypertension

Doppler-defined pulmonary hypertension in β-thalassemia major in Kurdistan, Iraq

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Liver disease and pulmonary hypertension

Cited by 4 publications

References 12 publications

Enhanced α1-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

Enhanced α1-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

α1-Adrenoceptor-dependent vascular hypertrophy and remodeling in murine hypoxic pulmonary hypertension

Doppler-defined pulmonary hypertension in β-thalassemia major in Kurdistan, Iraq

Contact Info

Product

Resources

About

Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

Enhanced α₁-adrenergic trophic activity in pulmonary artery of hypoxic pulmonary hypertensive rats

α₁-Adrenoceptor-dependent vascular hypertrophy and remodeling in murine hypoxic pulmonary hypertension