scholarly journals Role Of Inhaled Nitric Oxides In Pregnancy With Eisenmenger Syndrome

2020 ◽  
Vol 4 (1) ◽  
pp. 11
Author(s):  
Muhammad Anas ◽  
Nenny Triastuti ◽  
Muhammad Perdana Airlangga
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Vascular Tissue ◽  
Pulmonary Arteries ◽  
Right Heart Failure ◽  
Relative Increase ◽  
Nitric Oxides ◽  
Eisenmenger Syndrome ◽  
High Concentrations

ABSTRACTEisenmenger Syndrome (ES) is congenital heart disease with pulmonary hypertension and shunting turning from right to left. The resistance of pulmonary vascular more than 7.5 mmHg/L/min. The right ventricle and pulmonary artery always enlarge. During pregnancy, there will be hemodynamic changes that will affect the ES. It can be understood the possible dangers that can occur, like right heart failure; an increase in pulmonary arteries or the aggravation of pulmonary hypertension because there is no decrease in pulmonary resistance; A sudden decrease in venous return in supine hypotension syndrome can cause a relative increase in pulmonary arterial pressure so as to aggravate pulmonary hypertension and reverse shunting.Physiological effects of inhaled nitric oxide (INO) therapy cause selective pulmonary vasodilation: Hypoxia alveoli causes reversible vasoconstriction, thereby increasing pulmonary wedge pressure. INO can lower it. Moderate cardiac output and systematic arterial pressure are not affected; Selective in pulmonary because it is activated by hemoglobin; Selective vasodilation in the ventilated area, local hypoxia alveoli constricts the surrounding vascular tissue and redistributes blood flow to the ventilated lungs better and higher intraalveolar oxygen pressure. INO enhances this mechanism by increasing blood flow through a well-ventilated lung; Bronchodilators; Pulmonary surfactant, The combination of high concentrations of inspired oxygen and high concentrations of INO reduces the minimum surfactant surface tension.Keywords: Inhalation Nitric Oxides, Pregnancy, Eisenmenger Syndrome

scholarly journals Usage of Inhaled Nitric Oxides in Cases of Eisenmenger Syndrome

2020 ◽  
Vol 1 (1) ◽  
pp. 13-19
Author(s):  
Nenny Triastuti ◽  
Muhammad Perdana Airlangga ◽  
Muhammad Anas
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vascular Tissue ◽  
Inhaled Nitric Oxide ◽  
Nitric Oxides ◽  
Eisenmenger Syndrome ◽  
Pulmonary Vasodilation ◽  
High Concentrations ◽  
The Right ◽  
Nitric Oxide Therapy

Eisenmenger Syndrome is congenital heart disease with pulmonary hypertension and shunting turning from right to left. The resistance of pulmonary vascular more than 7.5 mmHg/L/min. The right ventricle and pulmonary artery always enlarge. Physiological effects of inhaled nitric oxide therapy cause selective pulmonary vasodilation: Hypoxia alveoli causes reversible vasoconstriction, thereby increasing pulmonary wedge pressure. Inhaled nitric oxide can lower it. Moderate cardiac output and systematic arterial pressure are not affected; Selective in pulmonary because it is activated by hemoglobin; Selective vasodilation in the ventilated area, local hypoxia alveoli constricts the surrounding vascular tissue and redistributes blood flow to the ventilated lungs better and higher intraalveolar oxygen pressure. Inhaled nitric oxide enhances this mechanism by increasing blood flow through a well-ventilated lung; Bronchodilators; Pulmonary surfactant, The combination of high concentrations of inspired oxygen and high concentrations of Inhaled nitric oxide reduces the minimum surfactant surface tension.

Cold-induced pulmonary hypertension in cattle

1978 ◽  
Vol 45 (3) ◽  
pp. 469-473 ◽  
Author(s):  
D. H. Will ◽  
I. F. McMurtry ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Right Heart Failure ◽  
Early Spring ◽  
Oxygen Breathing ◽  
Pulmonary Arterial ◽  
Lung Vessels

The frequency with which cattle develop right-heart failure during the winter at high altitude suggested that cold might contribute to hypoxic pulmonary hypertension. Indeed in a preliminary study conducted out-of-doors during early Spring, two calves with known hyperreactive pulmonary vessels showed elevated pulmonary arterial pressures attributed to their prior exposure to nighttime cold (-5 degrees C). In a second study five hyperreactive calves had increases in mean pulmonary arterial pressure from 29 to 45 Torr (+ 55%) during 48 h of exposure to cold (0 to -5 degrees C) in a climatic chamber. Three calves with less reactive lung vessels increased their pressures from 25 to 36 Torr (+ 44%). In a more complete study, six calves selected as potential hyperresponders showed increases in pulmonary arterial pressure (+ 60%), blood flow (+ 18%), and vascular resistance (+ 38%) during 48 h of cold exposure. Arterial PO2 decreased (-10 Torr) and PCO2 rose (+6 Torr) suggesting hypoventilation. Oxygen breathing returned pulmonary pressures and resistance to near control values, suggesting that cold had induced a hypoxic pulmonary vasoconstriction and an increased blood flow. Thus, a cold produced pulmonary hypertension in cattle at the modest altitude of 1,524 m and the pressor responses were greater in calves with more reactive lung vessels.

Vasoconstrictor Responses to Vasopressor Agents in Human Pulmonary and Radial Arteries

2014 ◽  
Vol 121 (5) ◽  
pp. 930-936 ◽  
Author(s):  
Dale A. Currigan ◽  
Richard J. A. Hughes ◽  
Christine E. Wright ◽  
James A. Angus ◽  
Paul F. Soeding
Keyword(s):  
Pulmonary Hypertension ◽  
Radial Artery ◽  
Vascular Tone ◽  
Pulmonary Arteries ◽  
Right Heart Failure ◽  
Response Curves ◽  
Vasopressor Agent ◽  
Vasopressor Agents ◽  
Vascular Beds ◽  
Potent Vasoconstrictor

Abstract Background: Vasopressor drugs, commonly used to treat systemic hypotension and maintain organ perfusion, may also induce regional vasoconstriction in specialized vascular beds such as the lung. An increase in pulmonary vascular tone may adversely affect patients with pulmonary hypertension or right heart failure. While sympathomimetics constrict pulmonary vessels, and vasopressin does not, a direct comparison between these drugs has not been made. This study investigated the effects of clinically used vasopressor agents on human isolated pulmonary and radial arteries. Methods: Isolated pulmonary and radial artery ring segments, mounted in organ baths, were used to study the contractile responses of each vasopressor agent. Concentration–response curves to norepinephrine, phenylephrine, metaraminol, and vasopressin were constructed. Results: The sympathomimetics norepinephrine, phenylephrine, and metaraminol caused concentration-dependent vasoconstriction in the radial (pEC50: 6.99 ± 0.06, 6.14 ± 0.09, and 5.56 ± 0.07, respectively, n = 4 to 5) and pulmonary arteries (pEC50: 6.86 ± 0.11, 5.94 ± 0.05 and 5.56 ± 0.09, respectively, n = 3 to 4). Vasopressin was a potent vasoconstrictor of the radial artery (pEC50 9.13 ± 0.20, n = 3), whereas in the pulmonary artery, it had no significant effect. Conclusions: Sympathomimetic-based vasopressor agents constrict both human radial and pulmonary arteries with similar potency in each. In contrast, vasopressin, although a potent vasoconstrictor of radial vessels, had no effect on pulmonary vascular tone. These findings provide some support for the use of vasopressin in patients with pulmonary hypertension.

scholarly journals Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension

2021 ◽  
Vol 118 (17) ◽  
pp. e2023130118
Author(s):  
Zdravka Daneva ◽  
Corina Marziano ◽  
Matteo Ottolini ◽  
Yen-Lin Chen ◽  
Thomas M. Baker ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Endothelial Cell ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Lung Edema ◽  
Structural Protein ◽  
Caveolin 1 ◽  
Pulmonary Arterial ◽  
Trpv4 Channel

Recent studies have focused on the contribution of capillary endothelial TRPV4 channels to pulmonary pathologies, including lung edema and lung injury. However, in pulmonary hypertension (PH), small pulmonary arteries are the focus of the pathology, and endothelial TRPV4 channels in this crucial anatomy remain unexplored in PH. Here, we provide evidence that TRPV4 channels in endothelial cell caveolae maintain a low pulmonary arterial pressure under normal conditions. Moreover, the activity of caveolar TRPV4 channels is impaired in pulmonary arteries from mouse models of PH and PH patients. In PH, up-regulation of iNOS and NOX1 enzymes at endothelial cell caveolae results in the formation of the oxidant molecule peroxynitrite. Peroxynitrite, in turn, targets the structural protein caveolin-1 to reduce the activity of TRPV4 channels. These results suggest that endothelial caveolin-1–TRPV4 channel signaling lowers pulmonary arterial pressure, and impairment of endothelial caveolin-1–TRPV4 channel signaling contributes to elevated pulmonary arterial pressure in PH. Thus, inhibiting NOX1 or iNOS activity, or lowering endothelial peroxynitrite levels, may represent strategies for restoring vasodilation and pulmonary arterial pressure in PH.

Chronic O2 exposure in the newborn rat results in decreased pulmonary arterial nitric oxide release and altered smooth muscle response to isoprostane

2004 ◽  
Vol 96 (2) ◽  
pp. 725-730 ◽  
Author(s):  
J. Belik ◽  
R. P. Jankov ◽  
J. Pan ◽  
M. Yi ◽  
I. Chaudhry ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Protein Content ◽  
Vascular Tissue ◽  
Ex Vivo ◽  
Pulmonary Arteries ◽  
Newborn Rat ◽  
Nitric Oxide Release ◽  
Pulmonary Arterial

Chronic oxygen exposure in the newborn rat results in lung isoprostane formation, which may contribute to the pulmonary hypertension evident in this animal model. The purpose of this study was to investigate the pulmonary arterial smooth muscle responses to 8-iso-prostaglandin F2α (8-iso-PGF2a) in newborn rats exposed to 60% O2 for 14 days. Because, in the adult rat, 8-iso-PGF2α may have a relaxant effect, mediated by nitric oxide (NO), we also sought to evaluate the pulmonary arterial NO synthase (NOS) protein content and NO release in the newborn exposed to chronic hyperoxia. Compared with air-exposed control animals, 8-iso-PGF2a induced a significantly greater force ( P < 0.01) and reduced ( P < 0.01) relaxation of precontracted pulmonary arteries in the 60% O2-treated animals. These changes were reproduced in control pulmonary arteries by NOS blockade by using NG-nitro-l-arginine methyl ester. Pulmonary arterial endothelial NOS was unaltered, but the inducible NOS protein content was significantly decreased ( P < 0.01) in the experimental group. Pulmonary ( P < 0.05) and aortic ( P < 0.01) tissue ex vivo NO accumulation was significantly reduced in the 60% O2-treated animals. We speculate that impaired pulmonary vascular tissue NO metabolism after chronic O2 exposure potentiates 8-iso-PGF2α-induced vasoconstriction in the newborn rat, thus contributing to pulmonary hypertension.

Repeated inhalation of adrenomedullin ameliorates pulmonary hypertension and survival in monocrotaline rats

2003 ◽  
Vol 285 (5) ◽  
pp. H2125-H2131 ◽  
Author(s):  
Noritoshi Nagaya ◽  
Hiroyuki Okumura ◽  
Masaaki Uematsu ◽  
Wataru Shimizu ◽  
Fumiaki Ono ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Systemic Arterial Pressure ◽  
Inhalation Therapy ◽  
Rank Test ◽  
Pulmonary Resistance ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Adrenomedullin (AM) is a potent vasodilator peptide. We investigated whether inhalation of aerosolized AM ameliorates monocrotaline (MCT)-induced pulmonary hypertension in rats. Male Wistar rats given MCT (MCT rats) were assigned to receive repeated inhalation of AM ( n = 8) or 0.9% saline ( n = 8). AM (5 μg/kg) or saline was inhaled as an aerosol using an ultrasonic nebulizer for 30 min four times a day. After 3 wk of inhalation therapy, mean pulmonary arterial pressure and total pulmonary resistance were markedly lower in rats treated with AM than in those given saline [mean pulmonary arterial pressure: 22 ± 2 vs. 35 ± 1 mmHg (–37%); total pulmonary resistance: 0.048 ± 0.004 vs. 0.104 ± 0.006 mmHg · ml–1 · min–1 · kg–1 (–54%), both P < 0.01]. Neither systemic arterial pressure nor heart rate was altered. Inhalation of AM significantly attenuated the increase in medial wall thickness of peripheral pulmonary arteries in MCT rats. Kaplan-Meier survival curves demonstrated that MCT rats treated with aerosolized AM had a significantly higher survival rate than those given saline (70% vs. 10% 6-wk survival, log-rank test, P < 0.01). In conclusion, repeated inhalation of AM inhibited MCT-induced pulmonary hypertension without systemic hypotension and thereby improved survival in MCT rats.

scholarly journals Chronic thromboembolic pulmonary hypertension – still evolving

2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Mario Gerges ◽  
Magdi Yacoub
Keyword(s):  
Pulmonary Hypertension ◽  
Medical Therapy ◽  
Treatment Options ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Pulmonary Vasculature ◽  
Pulmonary Hemodynamics ◽  
Thromboembolic Pulmonary Hypertension ◽  
Multiple Treatments

Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the leading causes of severe pulmonary hypertension (PH). The disease is still underdiagnosed, and the true prevalence is unknown. CTEPH is characterized by intraluminal non-resolving thrombus organization and fibrous stenosis, or complete obliteration of pulmonary arteries, promoted by progressive remodeling of the pulmonary vasculature. One consequence of this is an increase in pulmonary vascular resistance and pressure, resulting in PH and progressive right heart failure, leading to death if left untreated.Endovascular disobliteration by pulmonary endarterectomy (PEA) is the preferred treatment for CTEPH patients. PEA surgery is the only technique that can potentially cure CTEPH disease, especially in patients with fresh or organized thrombi of the proximal branches of pulmonary arteries. However, not all patients are eligible for PEA surgery. Recent research has provided evidence suggesting balloon pulmonary angioplasty (BPA) and targeted medical therapy as additional promising available treatments options for inoperable CTEPH and recurrent/persistent PH after PEA surgery.Studies on BPA have shown it to improve pulmonary hemodynamics, symptoms, exercise capacity and RV function in inoperable CTEPH. Subsequently, BPA has developed into an essential component of the modern era of CTEPH treatment. Large randomized controlled trials have demonstrated varying significant improvements with targeted medical therapy in technically inoperable CTEPH patients. Thus, treatment of CTEPH requires a comprehensive multidisciplinary assessment, including an experienced PEA surgeon, PH specialist, BPA interventionist and CTEPH-trained radiologist at expert centers. In this comprehensive review, we address the latest developments in the fast-evolving field of CTEPH. These include advancements in imaging modalities and developments in operative and interventional techniques, which have widened the range of patients who may benefit from these procedures. The efficacy and safety of targeted medical therapies in CTEPH patients are also discussed. As the treatment options for CTEPH improve, hybrid management involving multiple treatments in the same patient may become a viable option in the near future.

scholarly journals Role of the Purinergic P2Y2 Receptor in Pulmonary Hypertension

2021 ◽  
Vol 18 (21) ◽  
pp. 11009
Author(s):  
Mazen Shihan ◽  
Tatyana Novoyatleva ◽  
Thilo Lehmeyer ◽  
Akylbek Sydykov ◽  
Ralph T. Schermuly
Keyword(s):  
Pulmonary Hypertension ◽  
Drug Targets ◽  
Vascular Tone ◽  
Fluid Shear Stress ◽  
Purinergic Signaling ◽  
Pulmonary Arteries ◽  
Right Heart Failure ◽  
Systemic Circulation ◽  
P2y2 Receptor

Pulmonary arterial hypertension (PAH), group 1 pulmonary hypertension (PH), is a fatal disease that is characterized by vasoconstriction, increased pressure in the pulmonary arteries, and right heart failure. PAH can be described by abnormal vascular remodeling, hyperproliferation in the vasculature, endothelial cell dysfunction, and vascular tone dysregulation. The disease pathomechanisms, however, are as yet not fully understood at the molecular level. Purinergic receptors P2Y within the G-protein-coupled receptor family play a major role in fluid shear stress transduction, proliferation, migration, and vascular tone regulation in systemic circulation, but less is known about their contribution in PAH. Hence, studies that focus on purinergic signaling are of great importance for the identification of new therapeutic targets in PAH. Interestingly, the role of P2Y2 receptors has not yet been sufficiently studied in PAH, whereas the relevance of other P2Ys as drug targets for PAH was shown using specific agonists or antagonists. In this review, we will shed light on P2Y receptors and focus more on the P2Y2 receptor as a potential novel player in PAH and as a new therapeutic target for disease management.

scholarly journals From pulmonary embolism to chronic thromboembolic pulmonary hypertension: risk factors

2021 ◽  
Vol 25 (3) ◽  
pp. 11
Author(s):  
O. Ya. Vasiltseva ◽  
A. G. Edemskiy ◽  
D. S. Grankin ◽  
E. N. Kliver ◽  
A. M. Chernyavskiy
Keyword(s):  
Risk Factors ◽  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Recurrence Risk ◽  
National Guidelines ◽  
Thromboembolic Pulmonary Hypertension

<p>Chronic thromboembolic pulmonary hypertension is a long-term consequence of acute pulmonary embolism. Gradual obstruction of the pulmonary arteries and secondary changes in the pulmonary microcirculation over time cause progressive increases in pulmonary vascular resistance and pulmonary artery pressure that can result in severe right heart failure. This article provides an overview of pulmonary embolism and chronic thromboembolic pulmonary hypertension scientific literature and national guidelines. We focus on disease and recurrence risk factors and outline future directions of research to improve short- and long-term patient outcomes.</p><p>Received 17 January 2021. Revised 1 March 2021. Accepted 19 April 2021.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> The authors declare no conflicts of interests.</p><p><strong>Contribution of the authors</strong><br />Conception and study design: A.M. Chernyavskiy, A.G. Edemskiy, D.S. Grankin, E.N. Kliver<br />Drafting the article: O.Ya. Vasiltseva<br />Critical revision of the article: E.N. Kliver<br />Final approval of the version to be published: O.Ya. Vasiltseva, A.G. Edemskiy, D.S. Grankin, E.N. Kliver, A.M. Chernyavskiy</p>

scholarly journals Chronic Thromboembolic Pulmonary Hypertension

2018 ◽  
Vol 35 (02) ◽  
pp. 136-142 ◽  
Author(s):  
G. Pretorius ◽  
Stuart Jamieson
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Scar Tissue ◽  
Right Heart ◽  
Fibrotic Scar ◽  
Thromboembolic Pulmonary Hypertension

AbstractChronic thromboembolic pulmonary hypertension occurs when acute thromboemboli fail to dissolve completely. The resulting fibrotic scar tissue within the pulmonary arteries is obstructive and eventually leads to right heart failure. Medical therapy for this condition is supportive, but surgery with pulmonary artery endarterectomy is curative, and carries a low mortality at experienced centers.

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