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.

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.

Angiotensin II prevents hypoxic pulmonary hypertension and vascular changes in rat

1988 ◽  
Vol 254 (3) ◽  
pp. H500-H508 ◽  
Author(s):  
M. Rabinovitch ◽  
M. Mullen ◽  
H. C. Rosenberg ◽  
K. Maruyama ◽  
H. O'Brodovich ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Angiotensin Ii ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Vascular Changes ◽  
Hypoxic Pulmonary Hypertension ◽  
Artery Pressure

Angiotensin II, a vasoconstrictor, has been previously demonstrated to produce a secondary vasodilatation due to release of prostaglandins. Because of this effect, we investigated whether infusion of exogenous angiotensin II via miniosmopumps in rats during a 1-wk exposure to chronic hypobaric hypoxia might prevent pulmonary hypertension, right ventricular hypertrophy, and vascular changes. We instrumented the rats with indwelling cardiovascular catheters and compared the hemo-dynamic and structural response in animals given angiotensin II, indomethacin in addition to angiotensin II (to block prostaglandin production), or saline with or without indomethacin. We then determined whether angiotensin II infusion also prevents acute hypoxic pulmonary vasoconstriction. We observed that exogenous angiotensin II infusion abolished the rise in pulmonary artery pressure, the right ventricular hypertrophy, and the vascular changes induced during chronic hypoxia in control saline-infused rats with or without indomethacin. The protective effect of angiotensin II was lost when indomethacin was given to block prostaglandin synthesis. During acute hypoxia, both angiotensin II and prostacyclin infusions similarly prevented the rise in pulmonary artery pressure observed in saline-infused rats and in rats given indomethacin or saralasin in addition to angiotensin II. Thus exogenous angiotensin II infusion prevents chronic hypoxic pulmonary hypertension, associated right ventricular hypertrophy, and vascular changes and blocks acute hypoxic pulmonary hypertension, and this is likely related to its ability to release vasodilator prostaglandins.

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.

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.

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 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.

Importance of Relative Pulmonary Hypertension in Cardiac Surgery: The Mean Systemic-to-Pulmonary Artery Pressure Ratio

2006 ◽  
Vol 20 (3) ◽  
pp. 331-339 ◽  
Author(s):  
Arnaud Robitaille ◽  
André Y. Denault ◽  
Pierre Couture ◽  
Sylvain Bélisle ◽  
Annik Fortier ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Surgery ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pressure Ratio ◽  
Artery Pressure ◽  
The Mean

scholarly journals Vasoactive Substances in Pulmonary Embolism

1977 ◽  
Author(s):  
M.H. Todd ◽  
J.B. Forrest ◽  
J. Hirsh
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Autologous Blood ◽  
Venous Blood ◽  
Pulmonary Vasculature ◽  
Artery Pressure ◽  
Vasoactive Substances ◽  
Arterial Blood ◽  
The Right

Embolisation of the pulmonary vasculature with microspheres releases prostaglandin-1ike substances, PGLS (Piper and Vane, N.Y. Acad. Sei. 180: 363, 1971) but the capacity of autologous blood clots (ABC) to release pulmonary vasoactive substances is disputed. Ten normal mongrel dogs were anesthetised with pentobarbitone sodium and instrumented. Pulmonary venous blood was continuously superfused over isolated tissues for bioassay and then returned to the animal. Injection of ABC into the right atrium increased pulmonary artery pressure from 21 ± 6.5 mm Hg to 38 ± 15 mm Hg (mean ± S.D.), increased arterial pCO2 and decreased arterial pO2. No significant changes in heart rate, systemic arterial blood pressure or cardiac output occurred. In three animals contractions of the blood superfused assay tissues occurred following embolism. This effect was produced in normal assay tissues and those pretreated with antagonists of ACh, Serotonin, Histamine and Catecholamines and could therefore be attributed to PGLS. No cardiovascular or assay tissue tension changes were observed when equivalent volumes of saline or clot lysate were injected into the right atrium.Therefore, pulmonary embolism with ABC can release PGLS which may contribute to the pulmonary artery pressure rise. Vasoactive substances may normally be inactivated in the lung but in some animals appear in pulmonary venous blood.(Supported by the Ontario Heart Foundation)

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