Expressions of adrenomedullin mRNA and protein in rats with hypobaric hypoxia-induced pulmonary hypertension

2004 ◽  
Vol 286 (6) ◽  
pp. H2159-H2168 ◽  
Author(s):  
Kuniaki Nakanishi ◽  
Hiroshi Osada ◽  
Maki Uenoyama ◽  
Fumiko Kanazawa ◽  
Nobuhiro Ohrui ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Late Phase ◽  
Pulmonary Arteries ◽  
Hypoxic Environment ◽  
Male Wistar Rats ◽  
Pulmonary Arterial ◽  
The Right ◽  
The Brain ◽  
Altitude Level

Experimental pulmonary hypertension induced in a hypobaric hypoxic environment (HHE) is characterized by structural remodeling of the heart and pulmonary arteries. Adrenomedullin (AM) has diuretic, natriuretic, and hypotensive effects. To study the possible effects of HHE on the AM synthesis system, 150 male Wistar rats were housed in a chamber at the equivalent of a 5,500-m altitude level for 21 days. After 14 days of exposure to HHE, pulmonary arterial pressure (PAP) was significantly increased (compared with control rats). The plasma AM protein level was significantly increased on day 21 of exposure to HHE. In the right ventricle (RV), right atrium, and left atrium of the heart, the expressions of AM mRNA and protein were increased in the middle to late phase (5–21 days) of HHE, whereas in the brain and lung they were increased much earlier (0.5–5 days). In situ hybridization and immunohistochemistry showed AM mRNA and protein staining to be more intense in the RV in animals in the middle to late phase of HHE exposure than in the controls. During HHE, these changes in AM synthesis, which occurred strongly in the RV, occurred alongside the increase in PAP. Conceivably, AM may play a role in modulating pulmonary hypertension in HHE.

scholarly journals Hypercapnia attenuates hypoxic pulmonary hypertension by inhibiting lung radical injury

2009 ◽  
pp. S79-S86 ◽  
Author(s):  
M Chovanec ◽  
J Novotná ◽  
J Wilhelm ◽  
V Hampl ◽  
M Vízek ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Male Rats ◽  
Pulmonary Vasculature ◽  
Hypoxic Pulmonary Hypertension ◽  
Hypoxic Injury ◽  
Arterial Blood ◽  
Hypoxic Environment ◽  
Pulmonary Arterial ◽  
The Right

Chronic lung hypoxia results in hypoxic pulmonary hypertension. Concomitant chronic hypercapnia partly inhibits the effect of hypoxia on pulmonary vasculature. Adult male rats exposed to 3 weeks hypoxia (Fi02=0.1) combined with hypercapnia (FiC02=0.04-0.05) had lower pulmonary arterial blood pressure, increased weight of the right heart ventricle, and less pronounced structural remodeling of the peripheral pulmonary arteries compared with rats exposed only to chronic hypoxia (Fi02=0.1). According to our hypothesis, hypoxic pulmonary hypertension is triggered by hypoxic injury to the walls of the peripheral pulmonary arteries. Hypercapnia inhibits release of both oxygen radicals and nitric oxide at the beginning of exposure to the hypoxic environment. The plasma concentration of nitrotyrosine, the marker of peroxynitrite activity, is lower in hypoxic rats exposed to hypercapnia than in those exposed to hypoxia alone. Hypercapnia blunts hypoxia-induced collagenolysis in the walls of prealveolar pulmonary arteries. We conclude that hypercapnia inhibits the development of hypoxic pulmonary hypertension by the inhibition of radical injury to the walls of peripheral pulmonary arteries.

Effect of selective embolization of various sized pulmonary arteries in dogs

1963 ◽  
Vol 204 (4) ◽  
pp. 619-625 ◽  
Author(s):  
John W. Hyland ◽  
George T. Smith ◽  
Lockhart B. McGuire ◽  
Donald C. Harrison ◽  
Florence W. Haynes ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Internal Diameter ◽  
Polystyrene Spheres ◽  
Selective Embolization ◽  
Blood Clots ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary embolism was produced in 30 closed-chest 8-kg dogs with polystyrene spheres, glass beads, or blood clots of precise graded size. The sizes matched selectively the internal diameter of pulmonary arteries from lobar branches (5–6 mm) down to atrial arteries (0.17 mm). Emboli were injected into the right atrium until the pressure in the pulmonary artery rose 5–10 mm Hg. The number of emboli of a given size required to produce this incipient pulmonary hypertension was compared with the number of vessels of that same size as determined from the literature as well as by postmortem injection with Schlesinger mass. The number of emboli bore a constant relation to the number of vessels of that same size. With each size, the majority of vessels had to be occluded before pulmonary hypertension appeared. This was true even in the absence of anesthesia. The results support the thesis that mechanical blockade rather than vasoconstriction is the mechanism by which pulmonary hypertension is produced by emboli occluding pulmonary arterial (as opposed to arteriolar) vessels.

Hypoxia Inducible Factor-1 Alpha Correlates the Expression of Heme Oxygenase 1 Gene in Pulmonary Arteries of Rat with Hypoxia-induced Pulmonary Hypertension

2004 ◽  
Vol 36 (2) ◽  
pp. 133-140 ◽  
Author(s):  
Qi-Fang Li ◽  
Ai-Guo Dai
Keyword(s):  
Pulmonary Hypertension ◽  
Heme Oxygenase ◽  
Hypoxia Inducible Factor ◽  
Pulmonary Arteries ◽  
Heme Oxygenase 1 ◽  
Hypoxia Inducible Factor 1 ◽  
Mean Pulmonary Arterial Pressure ◽  
Male Wistar Rats ◽  
Pulmonary Arterial ◽  
Tunica Intima

Abstract To test the hypothesis that hypoxia inducible factor-1 alpha (HIF-1α) up-regulated the expression of heme oxygenase-1 (HO-1) gene in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension, 8 male Wistar rats in each of 5 groups were exposed to hypoxia for 0, 3, 7, 14 or 21 d, respectively. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricle hypertrophy index were measured. Lungs were inflation fixed for immunohistochemistry, in situ hybridization; frozen for later measurement of HO-1 enzyme activity. mPAP increased significantly after 7 d of hypoxia [(18.4 ± 0.4) mmHg, P<0.05], reaching its peak after 14 d of hypoxia, then remained stable. Pulmonary artery remodeling became to develop significantly after 14 d of hypoxia. HIF-1α protein in control was poorly positive (0.05 ± 0.01), but was up-regulated in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, the levels of HIF-1α protein were markedly up-regulated after 3 d and 7 d of hypoxia (0.20 ± 0.02; 0.22 ± 0.02, P<0.05), then declined after 14 d and 21 d of hypoxia. HIF-1α mRNA staining was poorly positive in control, hypoxia for 3 and 7 d, but enhanced significantly after 14 d of hypoxia (0.20 ± 0.02, P<0.05), then remained stable. HO-1 protein increased after 7 d of hypoxia (0.10 ± 0.01, P<0.05), reaching its peak after 14 d of hypoxia (0.21 ± 0.02, P<0.05), then remained stable. HO-1 mRNA increased after 3 d of hypoxia, reaching its peak after 7 d of hypoxia (0.17 ± 0.01, P<0.05), then declined. Linear correlation analysis showed that HIF-1α mRNA, HO-1 protein and mPAP were associated with pulmonary remodeling. HIF-1α protein (tunica intima) was conversely correlated with HIF-1α mRNA (r=0.921, P<0.01), HO-1 protein was conversely correlated with HIF-1α protein (tunica intima) (r=0.821, P<0.01). HIF-1α and HO-1 were both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rat. Hypoxia inducible factor-1 alpha correlated the expression of heme oxygenase 1 gene in pulmonary arteries of rat with hypoxia-induced pulmonary hypertension.

scholarly journals The isobaric pulmonary arterial compliance in pulmonary hypertension

2021 ◽  
pp. 00941-2020
Author(s):  
Denis Chemla ◽  
Emmanuelle Berthelot ◽  
Jason Weatherald ◽  
Edmund M. T. Lau ◽  
Laurent Savale ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Compliance ◽  
Pulmonary Arteries ◽  
Right Heart ◽  
Right Heart Catheterisation ◽  
Strain Behaviour ◽  
Arterial Load ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
The Right

Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries which increases right ventricular pulsatile loading. High pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further decreases PA compliance (PAC) at a given pulmonary vascular resistance (PVR) compared to precapillary PH, thus responsible for a higher total arterial load. In all other vascular beds, arterial compliance is considered as mainly determined by the distending pressure, due to non-linear stress-strain behaviour of arteries. We tested the applicability, advantages and drawbacks of two comparison methods of PAC depending on the level of mean PA pressure mPAP (isobaric PAC) or PVR.Right heart catheterisation data including PAC (stroke volume/pulse pressure) were obtained in 112Pc-PH (of whom 61 had combined postcapillary and precapillary PH) and 719 idiopathic pulmonary arterial hypertension (iPAH).PAC could be compared over the same mPAP range (25–66 mmHg) in 792/831 patients (95.3%) and over the same PVR range (3–10.7 WU) in only 520/831 patients (62.6%). The main assumption underlying comparisons at a given PVR was not verified as the PVR×PAC product (RC-time) was not constant but on the contrary more variable than mPAP. In the 788/831 (94.8%) patients studied over the same PAC range (0.62–6.5 mL·mmHg−1), PVR and thus total arterial load tended to be higher in iPAH.Our study favours comparing PAC at fixed mPAP level (isobaric PAC) rather than at fixed PVR. A reappraisal of the effects of PAWP on the pulsatile and total arterial load put on the right heart is needed, and this point deserves further studies.

In situ central pulmonary artery thrombosis in primary pulmonary hypertension

2005 ◽  
Vol 46 (7) ◽  
pp. 696-700 ◽  
Author(s):  
P. P. Agarwal ◽  
A. L. Wolfsohn ◽  
F. R. Matzinger ◽  
J. M. Seely ◽  
R. A. Peterson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Bronchial Arteries ◽  
Artery Thrombosis ◽  
Central Pulmonary Artery ◽  
Pulmonary Arterial ◽  
Segmental Arteries

A rare case of extensive in situ central pulmonary artery thrombosis in primary pulmonary hypertension (PPH) is presented. The differentiation from chronic thromboembolic pulmonary arterial hypertension (CTEPH) is of paramount importance because of different therapeutic strategies. In this case, the presence of mural thrombus in the central pulmonary arteries on computed tomography made the distinction difficult. However, the possibility of in situ thrombosis was suggested on the basis of absence of other findings of CTEPH (abrupt narrowing/truncation of segmental arteries, variation in size of segmental vessels, arterial webs, mosaic attenuation, pulmonary infarcts, and dilated bronchial arteries), and this was confirmed on final pathology.

scholarly journals Recovery from Hypoxic Pulmonary Hypertension in Rats

2011 ◽  
Vol 54 (2) ◽  
pp. 73-75
Author(s):  
Hana Maxová ◽  
Alena Baňasová ◽  
Viera Povýšilová ◽  
Jan Herget ◽  
Martin Vízek
Keyword(s):  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Time Frame ◽  
Hypoxic Exposure ◽  
Mean Pulmonary Arterial Pressure ◽  
Male Wistar Rats ◽  
Pulmonary Arterial ◽  
The Right

To characterize the time frame of changes in pulmonary arterial pressure, right ventricular hypertrophy and morphology of small pulmonary arteries male Wistar rats were exposed to isobaric hypoxia (3 weeks, FIO2 0.1) and then let to recover on air for 1 or 5 weeks. Normoxic animals (group N) served as controls. Mean pulmonary arterial pressure (PAP), ratio of the weight of the right heart ventricle to the sum of the weights of the left ventricle and septum (RV/LV+S) and percentage of double laminated pulmonary vessels ( % DL) were measured at the end of hypoxic exposure (group H), after 1 or 5 weeks of recovery (groups 1R and 5R), and in controls kept in air (group N). Three weeks in hypoxia resulted in increase in PAP, RV/LV+S and % DL. After 1 week of recovery RV/LV+S normalized, PAP decreased, while % DL did not change. After 5 weeks in air PAP returned to control values and % DL diminished significantly but did not normalize. Our results suggest that recovery depends on the degree of HPH and that knowledge of the time-frame of recovery is important for future studies in our rat model.

scholarly journals In situ fracture of stents implanted for relief of pulmonary arterial stenosis in patients with congenitally malformed hearts

2008 ◽  
Vol 18 (4) ◽  
pp. 405-414 ◽  
Author(s):  
Doff B. McElhinney ◽  
Lisa Bergersen ◽  
Audrey C. Marshall
Keyword(s):  
Cohort Analysis ◽  
Pulmonary Arteries ◽  
Arterial Stenosis ◽  
Related Factors ◽  
Increased Risk ◽  
Right Pulmonary Artery ◽  
Pulmonary Arterial ◽  
The Right ◽  
Pulmonary Arterial Stenosis

AbstractBackgroundOne of the most common uses of stents in patients with congenitally malformed hearts is treatment of pulmonary arterial stenosis. Although there are reports of fractured pulmonary arterial stents, little is known about the risk factors for, and implications of, such fractures.MethodsWe reviewed angiograms to identify fractures in stents previously inserted to relieve stenoses in pulmonary arteries from 1990 through 2001 in patients who also underwent follow-up catheterization at least 3 years after placement of the stent. We undertook matched cohort analysis, matching a ratio of 2 fractured to 1 unfractured stent.ResultsOverall, 166 stents meeting the criterions of our study had been placed in 120 patients. We identified fractures in 35 stents (21%) in 29 patients. All fractured stents were in the central pulmonary arteries, 24 (69%) in the central part of the right pulmonary artery, and all were complete axial fractures, or complex fractures along at least 2 planes. Stent-related factors associated with increased risk of fracture identified by multivariable logistic regression included placement in close apposition to the ascending aorta (p = 0.001), and a larger expanded diameter (p = 0.002). There was obstruction across 28 of 35 fractured stents, which was severe in 11. We re-stented 21 of the fractured stents, and recurrent fracture was later diagnosed in 3 of these. A fragment of the fractured stent embolized distally in 2 patients, without clinically important effects.ConclusionsIn situ fracture of pulmonary arterial stents is relatively common, and in most cases is related to compression by the aorta. There is usually recurrent obstruction across the fractured stent, but fractured stents rarely embolize, and are not associated with other significant complications.

scholarly journals EXPRESS: Chronic thromboembolic pulmonary hypertension following pulmonary embolism with a right ventricular thrombus: A report of two cases

2021 ◽  
pp. 204589402110136
Author(s):  
Tailong Zhang ◽  
Weitao Liang ◽  
Longrong Bian ◽  
Zhong Wu
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Imaging Features ◽  
Pulmonary Endarterectomy ◽  
Right Heart ◽  
Thromboembolic Pulmonary Hypertension ◽  
The Right ◽  
Cardiac Masses

Right heart thrombus (RHT) accompanied by chronic thromboembolic pulmonary hypertension (CTEPH) is a rare entity. RHT may develop in the peripheral veins or in situ within the right heart chambers. The diagnosis of RHT is challenging, since its symptoms are typically non-specific and its imaging features resemble those of cardiac masses. Here, we report two cases of RHT with CTEPH that presented as right ventricular masses initially. Both patients underwent simultaneous pulmonary endarterectomy (PEA) and resection of the ventricular thrombi. Thus, when mass-like features are confirmed by imaging, RHT should be suspected in patients with CTEPH, and simultaneous RHT resection is required along with PEA.

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.

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