The Physics of Hypoxic Pulmonary Hypertension and Its Connection with Gene Actions

2006 ◽  
pp. 35-50
Author(s):  
Yuan-Cheng Fung ◽  
Wei Huang
Keyword(s):  
Pulmonary Hypertension ◽  
Hypoxic Pulmonary Hypertension

Inhibition of mTOR by rapamycin does not improve hypoxic pulmonary hypertension-induced right heart failure in old mice

2021 ◽  
pp. 111395
Author(s):  
Benjamin D. McNair ◽  
Jacob A. Schlatter ◽  
Ross F. Cook ◽  
Musharraf Yusifova ◽  
Danielle R. Bruns
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Right Heart ◽  
Hypoxic Pulmonary Hypertension ◽  
Old Mice

scholarly journals The Y Chromosome Plays a Protective Role in Experimental Hypoxic Pulmonary Hypertension

2018 ◽  
Vol 197 (7) ◽  
pp. 952-955 ◽  
Author(s):  
Soban Umar ◽  
Christine M. Cunningham ◽  
Yuichiro Itoh ◽  
Shayan Moazeni ◽  
Mylene Vaillancourt ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Y Chromosome ◽  
Protective Role ◽  
Hypoxic Pulmonary Hypertension

Chronic EDRF inhibition and hypoxia: effects on pulmonary circulation and systemic blood pressure

1993 ◽  
Vol 75 (4) ◽  
pp. 1748-1757 ◽  
Author(s):  
V. Hampl ◽  
S. L. Archer ◽  
D. P. Nelson ◽  
E. K. Weir
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Systemic Blood Pressure ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Hypoxic Pulmonary Hypertension ◽  
Basal Tone ◽  
Isolated Lungs

It has been suggested that chronic hypoxic pulmonary hypertension results from chronic hypoxic inhibition of endothelium-derived relaxing factor (EDRF) synthesis. We tested this hypothesis by studying whether chronic EDRF inhibition by N omega-nitro-L-arginine methyl ester (L-NAME) would induce pulmonary hypertension similar to that found in chronic hypoxia. L-NAME (1.85 mM) was given for 3 wk in drinking water to rats living in normoxia or hypoxia. Unlike chronic hypoxia, chronic L-NAME treatment did not increase pulmonary arterial pressure. Cardiac output was reduced and mean systemic arterial pressure was increased by chronic L-NAME treatment. The vascular pressure-flow relationship in isolated lungs was shifted toward higher pressures by chronic hypoxia and, to a lesser degree, by L-NAME intake. In isolated lungs, vasoconstriction in response to angiotensin II and acute hypoxia and vasodilation in response to sodium nitroprusside were increased by chronic L-NAME treatment in normoxia and chronic hypoxia. Chronic hypoxia, but not L-NAME, induced hypertensive pulmonary vascular remodeling. Chronic supplementation with the EDRF precursor L-arginine did not have any significant effect on chronic hypoxic pulmonary hypertension. We conclude that the chronic EDRF deficiency state, induced by L-NAME, does not mimic chronic hypoxic pulmonary hypertension in our model. In addition, EDRF proved to be less important for basal tone regulation in the pulmonary than in the systemic circulation.

scholarly journals The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes

2015 ◽  
Vol 308 (3) ◽  
pp. L229-L252 ◽  
Author(s):  
Steven C. Pugliese ◽  
Jens M. Poth ◽  
Mehdi A. Fini ◽  
Andrea Olschewski ◽  
Karim C. El Kasmi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Signaling Pathways ◽  
Vascular Remodeling ◽  
Mesenchymal Cells ◽  
World Health ◽  
Small Subset ◽  
Cellular Interactions ◽  
Pulmonary Vascular Remodeling ◽  
Hypoxic Pulmonary Hypertension ◽  
Group I

Hypoxic pulmonary hypertension (PH) comprises a heterogeneous group of diseases sharing the common feature of chronic hypoxia-induced pulmonary vascular remodeling. The disease is usually characterized by mild to moderate pulmonary vascular remodeling that is largely thought to be reversible compared with the progressive irreversible disease seen in World Health Organization (WHO) group I disease. However, in these patients, the presence of PH significantly worsens morbidity and mortality. In addition, a small subset of patients with hypoxic PH develop “out-of-proportion” severe pulmonary hypertension characterized by pulmonary vascular remodeling that is irreversible and similar to that in WHO group I disease. In all cases of hypoxia-related vascular remodeling and PH, inflammation, particularly persistent inflammation, is thought to play a role. This review focuses on the effects of hypoxia on pulmonary vascular cells and the signaling pathways involved in the initiation and perpetuation of vascular inflammation, especially as they relate to vascular remodeling and transition to chronic irreversible PH. We hypothesize that the combination of hypoxia and local tissue factors/cytokines (“second hit”) antagonizes tissue homeostatic cellular interactions between mesenchymal cells (fibroblasts and/or smooth muscle cells) and macrophages and arrests these cells in an epigenetically locked and permanently activated proremodeling and proinflammatory phenotype. This aberrant cellular cross-talk between mesenchymal cells and macrophages promotes transition to chronic nonresolving inflammation and vascular remodeling, perpetuating PH. A better understanding of these signaling pathways may lead to the development of specific therapeutic targets, as none are currently available for WHO group III disease.

scholarly journals A Time- and Compartment-Specific Activation of Lung Macrophages in Hypoxic Pulmonary Hypertension

2017 ◽  
Vol 198 (12) ◽  
pp. 4802-4812 ◽  
Author(s):  
Steven C. Pugliese ◽  
Sushil Kumar ◽  
William J. Janssen ◽  
Brian B. Graham ◽  
Maria G. Frid ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Hypoxic Pulmonary Hypertension ◽  
Lung Macrophages
Sign in / Sign up

Export Citation Format

Share Document