scholarly journals High-fat diet attenuates the improvement of hypoxia-induced pulmonary hypertension in mice during reoxygenation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Koichi Sugimoto ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Takashi Kaneshiro ◽  
Akiomi Yoshihisa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
High Fat Diet ◽  
Metabolic Disorder ◽  
Pulmonary Arteries ◽  
Reverse Remodeling ◽  
High Fat ◽  
Artery Pressure

Abstract Background It is widely recognized that metabolic disorder is associated with pulmonary hypertension (PH). It is known that hypoxia-induced elevated pulmonary artery pressure in mice returns to normal pressure during reoxygenation. However, it is still unclear how metabolic disorder affects the reverse remodeling of pulmonary arteries. In this study, we investigated the effects of high-fat diet (HFD) on the decrease in pulmonary artery pressure and reverse remodeling of pulmonary arteries in mice with hypoxia-induced PH. Methods We used female C57BL/6 mice aged 8 weeks. After being exposed to hypoxia (10% oxygen for four weeks) to induce PH, the mice were returned to normoxic conditions and randomized into a normal diet (ND) group and HFD group. Both groups were fed with their respective diets for 12 weeks. Results The Fulton index and right ventricular systolic pressure measured by a micro-manometer catheter were significantly higher in the HFD group than in the ND group at 12 weeks after reoxygenation. The medial smooth muscle area was larger in the HFD group. Caspase-3 activity in the lung tissue of the HFD group was decreased, and the apoptosis of pulmonary smooth muscle cells was suppressed after reoxygenation. Moreover, the expression levels of peroxisome proliferator-activated receptor-γ and apelin were lower in the HFD group than in the ND group. Conclusions The results suggest that metabolic disorder may suppress pulmonary artery reverse remodeling in mice with hypoxia-induced PH during reoxygenation.

High-Fat Diet Attenuates the Improvement of Hypoxia-induced Pulmonary Artery Hypertension in Mice During Reoxygenation.

2021 ◽  
Author(s):  
Koichi Sugimoto ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Takashi Kaneshiro ◽  
Akiomi Yoshihisa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
High Fat Diet ◽  
Metabolic Disorder ◽  
Pulmonary Arteries ◽  
Reverse Remodeling ◽  
High Fat ◽  
Artery Pressure

Abstract Background: It has been widely recognized that metabolic disorder is associated with pulmonary hypertension. It is known that elevated pulmonary artery pressure induced by hypoxia in mice returns to normal pressure under reoxygenation. However, it is still unclear how metabolic disorder affects the reverse remodeling of pulmonary arteries. In this study, we investigated the effects of a high-fat diet (HFD) on the decrease of pulmonary artery pressure and reverse remodeling of pulmonary arteries in mice with hypoxia-induced pulmonary hypertension.Methods: We used female C57/Bl6 mice aged 8 weeks. After the mice were exposed to hypoxia (10% oxygen for 4 weeks) for induction of pulmonary hypertension. Then, they were returned to normoxic conditions and randomized into a normal diet (ND) group and a HFD group. Both groups were fed their respective diets for 12 weeks.Results: The right ventricular systolic pressure measured by a micro-manometer catheter and the Fulton index were significantly higher in the HFD group than in the ND group at 12 weeks after reoxygenation. The medial smooth muscle area was larger in the HFD group. Caspase 3 activity in lung tissue of the HFD group was decreased, and an apoptosis of pulmonary smooth muscle cells was suppressed after reoxygenation. Moreover, the expression levels of peroxisome proliferator-activated receptor-γ and apelin were lower in the HFD group than in the LFD group.Conclusion: Our results suggest the metabolic disorder may suppress pulmonary artery reverse remodeling in mice with hypoxia-induced pulmonary hypertension under reoxygenation.

Abstract 12990: High Fat Diet Delays Reverse Remodeling of Pulmonary Artery in Hypoxia-induced Pulmonary Hypertension Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Koichi Sugimoto ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Sayoko Yokokawa ◽  
Kazuhiko Nakazato ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
High Fat Diet ◽  
Metabolic Disorder ◽  
Density Lipoprotein ◽  
Reverse Remodeling ◽  
High Fat ◽  
Pulmonary Artery Smooth Muscle

Background: Previous studies suggest the association of metabolic disorder with pulmonary hypertension. Elevated pulmonary artery pressure induced by hypoxia in mice returns to normal when they are placed back in normoxia. In this study, we investigated the effect of high-fat diet (HFD) on pulmonary artery pressure and reverse remodeling of pulmonary artery in mouse model of hypoxia-induced pulmonary hypertension. Methods: We used the female C57/Bl6 mice at the age of 8 weeks. After exposed to hypoxia (10% oxygen for 4 weeks) for induction of pulmonary hypertension, mice were returned to normoxic condition and fed HFD or low-fat diet (LFD) for 12 weeks. Results: The body weight (BW), glucose, low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C), but not triglyceride (TG) were significantly increased in HFD group (36.9±5.1 vs. 24.0±1.4 g [BW], P<0.05; 404.2±55.1 vs. 326.5±8.7 mg/dl [glucose], P<0.05; 10.2±3.6 vs. 7.5±0.9 mg/dl [LDL-C], P<0.05; 47.2±10.0 vs. 30.9±8.7 mg/dl [HDL-C], P<0.05 and 40.0±21.1 vs. 53.4±12.9 mg/dl [TG], P=0.09). The right ventricular systolic pressure (RVSP) measured by a micro-manometer catheter and the Fulton index in HFD group were significantly higher than those in LFD group (23.8±2.3 vs. 19.3±2.9 mmHg [RVSP], P<0.05; 0.30±0.06 vs. 0.25±0.04 [Fulton index], P<0.05, respectively). The medial smooth muscle area (expressed as a percentage of the external area of the vessel) was larger in HFD group (40.1±5.3 vs. 34.5±3.1%, P<0.05). In addition, the levels of active caspase-3 detected by Western blotting was lower in HFD group than in LFD group. TUNEL staining revealed that the apoptosis of pulmonary artery smooth muscle cells was suppressed in HFD group. Conclusion: Our results suggest that metabolic disorder attenuates pulmonary artery reverse remodeling, at least in part, by suppressing apoptosis of pulmonary artery smooth muscle cells when hypoxia-induced pulmonary hypertension mice were returned to normoxia.

scholarly journals Parameters of acute vasoreactivity testing after balloon pulmonary angioplasty in patients with chronic thromboembolic pulmonary hypertension

2020 ◽  
Vol 17 (3) ◽  
pp. 53-58
Author(s):  
Sergey Y. Yarovoy ◽  
Irina E. Chazova ◽  
Yuri G. Matchin ◽  
Nikolay M. Danilov
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Structural Parameters ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Hemodynamic Parameters ◽  
Artery Pressure ◽  
Balloon Pulmonary Angioplasty ◽  
Thromboembolic Pulmonary Hypertension

Aim.To study the effect of balloon pulmonary angioplasty (BPA) on the changes of pulmonary artery pressure, cardiac output and structural parameters of pulmonary arteries after acute vasoreactivity testing (AVT) in inoperable patients with chronic thromboembolic pulmonary hypertension (CTEPH). Materials and methods.The prospective study included 22 patients with inoperable CTEPH. 11 patients underwent intravascular ultrasound (IVUS) of the pulmonary arteries. The assessment of clinical and hemodynamic parameters, vasoreactivity, structural parameters of the pulmonary arteries according to IVUS data was performed at 2 visits before the first BPA and after a series of BPA. Results.The patients underwent 2.31.4 stages of BPA. The follow up was 160 (85; 248) days. Positive changes after a series of BPA were revealed in clinical (functional class, distance in the 6-minute walk test, level of brain natriuretic peptide) and hemodynamic (systolic and mean pulmonary artery pressure, right atrium pressure, etc.) parameters. The results of the AVT after BPA demonstrated a decrease in the portion of non-responders from 63.6 to 55.5%, and a group of responders (16.7%) has appeared. According to IVUS before and after AVT, the response to iloprost administration was observed basically in branches of subsegmental pulmonary arteries and initially corresponded to the process of vasodilation. However, after a series of BPA there was noted a paradoxical reaction in the middle section after the AVT a decrease in the vessel lumen and an increase in the thickness and area of the vessel wall. This effect is probably associated with the response to the test at the level of the microvasculature, as in pulmonary arterial hypertension before the onset of its pronounced structural changes. The data obtained confirm the reverse remodeling of the pulmonary vessels and the restoration of vasoreactivity after a series of BPA. Conclusion.BPA improves clinical and hemodynamic parameters, as well as pulmonary vasoreactivity, in inoperable patients with CTEPH. AVT may be included in the recommendations for the examination of patients with CTEPH to assess the effectiveness of BPA and determine the disease prognosis.

Comparison of pulmonary vascular function and structure in early and established hypoxic pulmonary hypertension in rats

2001 ◽  
Vol 79 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Trina K Jeffery ◽  
Janet C Wanstall
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Contractile Function ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Hypoxic Pulmonary Hypertension ◽  
Artery Pressure

In pulmonary hypertension, changes in pulmonary vascular structure and function contribute to the elevation in pulmonary artery pressure. The time-courses for changes in function, unlike structure, are not well characterised. Medial hypertrophy and neomuscularisation and reactivity to vasoactive agents were examined in parallel in main and intralobar pulmonary arteries and salt-perfused lungs from rats exposed to hypoxia (10% O2) for 1 and 4 weeks (early and established pulmonary hypertension, respectively). After 1 week of hypoxia, in isolated main and intralobar arteries, contractions to 5-hydroxytryptamine and U46619 (thromboxane-mimetic) were increased whereas contractions to angiotensins I and II and relaxations to acetylcholine were reduced. These alterations varied quantitatively between main and intralobar arteries and, in many instances, regressed between 1 and 4 weeks. The alterations in reactivity did not necessarily link chronologically with alterations in structure. In perfused lungs, constrictor responses to acute alveolar hypoxia were unchanged after 1 week but were increased after 4 weeks, in conjunction with the neomuscularisation of distal alveolar arteries. The data suggest that in hypoxic pulmonary hypertension, the contribution of altered pulmonary vascular reactivity to the increase in pulmonary artery pressure may be particularly important in the early stages of the disease.Key words: pulmonary vasculature, hypoxic pulmonary hypertension, contractile function, endothelial function, remodelling.

Pulmonary Endarterectomy: Assessment of Operability, Surgical Description, and Post-op Care

2014 ◽  
Vol 12 (4) ◽  
pp. 186-192 ◽  
Author(s):  
David Poch ◽  
Victor Pretorius
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Endarterectomy ◽  
Pulmonary Thromboendarterectomy ◽  
Thromboembolic Pulmonary Hypertension ◽  
Wedge Pressure

Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as a mean pulmonary artery pressure ≥25 mm Hg and pulmonary artery wedge pressure ≤15 mm Hg in the presence of occlusive thrombi within the pulmonary arteries. Surgical pulmonary thromboendarterectomy (PTE) is considered the best treatment option for CTEPH.

scholarly journals The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021 ◽  
Vol 22 (9) ◽  
pp. 4980
Author(s):  
Inés Roger ◽  
Javier Milara ◽  
Paula Montero ◽  
Julio Cortijo
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Clinical Manifestations ◽  
Different Types ◽  
Artery Remodeling ◽  
Stat Pathway ◽  
Pulmonary Artery Remodeling

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular, and cellular processes involved in PH. Chronic inflammation contributes to pulmonary artery remodeling and PH, among other vascular disorders, and many inflammatory mediators signal through the JAK/STAT pathway. Recent evidence indicates that the JAK/STAT pathway is overactivated in the pulmonary arteries of patients with PH of different types. In addition, different profibrotic cytokines such as IL-6, IL-13, and IL-11 and growth factors such as PDGF, VEGF, and TGFβ1 are activators of the JAK/STAT pathway and inducers of pulmonary remodeling, thus participating in the development of PH. The understanding of the participation and modulation of the JAK/STAT pathway in PH could be an attractive strategy for developing future treatments. There have been no studies to date focused on the JAK/STAT pathway and PH. In this review, we focus on the analysis of the expression and distribution of different JAK/STAT isoforms in the pulmonary arteries of patients with different types of PH. Furthermore, molecular canonical and noncanonical JAK/STAT pathway transactivation will be discussed in the context of vascular remodeling and PH. The consequences of JAK/STAT activation for endothelial cells and pulmonary artery smooth muscle cells’ proliferation, migration, senescence, and transformation into mesenchymal/myofibroblast cells will be described and discussed, together with different promising drugs targeting the JAK/STAT pathway in vitro and in vivo.

scholarly journals Evaluation of the morphology and mechanics of the right ventricle using echocardiography before and after transcatheter balloon pulmonary angioplasty in patients with chronic thromboembolic pulmonary

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
KIRILL Malikov ◽  
MARINA Kirichkova ◽  
MARIA Simakova ◽  
NARECK Marukyan ◽  
OLGA Moiseeva
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Pulmonary Artery Pressure ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Reverse Remodeling ◽  
Free Wall ◽  
Artery Pressure ◽  
Balloon Pulmonary Angioplasty ◽  
Before And After ◽  
The Right

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Chronic thromboembolic pulmonary hypertension (CTEPH) leads to a progressive increase in pulmonary vascular resistance (PVR) and pulmonary artery pressure (PAP) with the development of severe dysfunction of the right heart and heart failure. Mortality for three years with an average pressure in the pulmonary artery (PA) of more than 50 mmHg is more than 90%. Balloon pulmonary angioplasty (BPA) has a significant advantage over other methods of surgical treatment, but it requires the determination of additional non-invasive markers of effectiveness. Transthoracic echocardiography (TTE) remains the main method for assessing the morphology and function of the heart. Purpose Compare different indicators reflecting the severity of CTEPH with TTE indicators before and after BPA. To evaluate the effectiveness of using BPA for the treatment of patients with CTEPH using routine TTE and speckle tracking mode. Materials and methods For 18 months 30 patients without concomitant cardiovascular pathology were subjected to several BPA sessions. Before treatment, 50% of patients belonged to the 3 CTEPH functional class (FC), 40% to 2 FC, 10% to 1 FC. The average number of sessions was 4.7 ± 1.3. Before the first BPA and after the last, all the patients were performed: six-minute walk test (6MWT, metres), Borg scale (in points), test for NT-proBNP (pg/ml); TTE with assessment of the right ventricle (RV) and left ventricle (LV) including areas of the right atrium (aRA, cm2), mean pulmonary artery pressure (PUPM,mmHg),RV free wall strain (GLSFW, %), RV free wall strain rate (GLSRFW, sm/sec), RV free wall postsystolic shortening (PSSFW, %), tricuspid annular plane systolic excursion (TAPSE, sm), tricuspid annulus systolic velocity (TASV, sm/sec). Results. Before the first BPA session, the 6MWT in the patient group averaged 315.9 ± 9.08 metres, after - 439.5 ± 11.45 m; the Borg from 5.4 ± 0.94 points decreased to 4 ± 1.01 points; NT-proBNP before the treatment was 1513 ± 13.01 pg/ml, after - 171 ± 6.09; according to TTE the ratio of RV/ LV before and after treatment was 1.31 ± 0.02 and 0.97 ± 0.04; aRA was 29.3 ± 4.87 and 22.3 ± 3.53 cm2; basal RV - 52 ± 5.11 and 44 ± 7.26 mm; PUPM decreased from 76.6 ± 7.65 to 31.3 ± 3.78 mmHg; GLSFW from -14.69 ± 2.33 came to 17.5 ± 3.45 %; GLSRFW with -0.9 ± 0.09 to -1.7 ± 0.11 cm/sec; TAPSE from 16.7 ± 1.87 to 18.2 ± 2.34 cm; TASV from 10.11 ± 1.45 to 12.25 ± 1.98 cm/s, PSSFW before treatment was -18.4 ± 1.2%, after treatment in 66% of patients disappeared, in 34% became an average of 17.4 ± 0.9% The distribution of STEPH FC has also changed. Conclusion. BPA leads to an improvement in the tolerance of physical activity, clinical indicators, and parameters of central hemodynamics in the pulmonary circulation, evaluated according to direct manometry, and leads to reverse remodeling of the RV in the long term. Performing a staged BPA leads to an improvement in the functional parameters of contractility of the RV.

scholarly journals Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1212
Author(s):  
Fabian Mueller-Graf ◽  
Jonas Merz ◽  
Tim Bandorf ◽  
Chiara Albus ◽  
Maike Henkel ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Transit Time ◽  
Pulse Wave ◽  
Correlation Coefficients ◽  
Physiological Basis ◽  
Artery Pressure ◽  
Hypoxic Vasoconstriction ◽  
Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

scholarly journals The Relationship between Vitamin D Deficiency and Pulmonary Hypertension

2013 ◽  
Vol 114 (3) ◽  
pp. 154-161 ◽  
Author(s):  
Mehmet Demir ◽  
U. Uyan ◽  
S. Keçeoçlu ◽  
C. Demir
Keyword(s):  
Vitamin D ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vitamin D Deficiency ◽  
Pulmonary Artery Pressure ◽  
Control Group ◽  
Systolic Pulmonary Artery Pressure ◽  
Control Groups ◽  
Artery Pressure ◽  
Vitamin D Levels

Vitamin D deficiency actives renin-angiotensin-aldosterone system (RAAS) which affects cardiovascular system. Activation of RAAS is associated with pulmonary hypertension (PHT). Relation between vitamin D deficiency and PHT could be therefore suggested. In  our study we compared pulmonary artery pressure between vitamin D deficiency and control groups. 115 consecutive patients (average age: 61.86 ± 5.86) who have detected very low vitamin D (vitamin D levels < 10 ng/ml) were enrolled. 117 age matched persons (average age: 61.74 ± 5.99) were selected as the control group. All groups underwent transthoracic echocardiography. Routine biochemical measurement of 25-OH vitamin D and parathormon (PTH) levels were performed. Baseline characteristics of the study groups were comparable. Systolic pulmonary artery pressure (SPAP) of patients in  the low vitamin D group was higher than the control groups. As a  result our study, a  relation between vitamin D deficiency and pulmonary artery hypertension was revealed.

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