scholarly journals Depletion of Alveolar Macrophages Attenuates Hypoxic Pulmonary Hypertension but not Hypoxia-Induced Increase in Serum Concentration of MCP-1

2016 ◽  
pp. 763-768 ◽  
Author(s):  
M. ŽALOUDÍKOVÁ ◽  
R. VYTÁŠEK ◽  
O. VAJNEROVÁ ◽  
O. HNILIČKOVÁ ◽  
M. VÍZEK ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Alveolar Macrophages ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Hypertension ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Mean Pulmonary Arterial Pressure ◽  
Selective Elimination ◽  
Pulmonary Arterial

Exposure to hypoxia, leading to hypoxic pulmonary hypertension (HPH), is associated with activation of alveolar macrophages (AM). However, it remains unclear how AM participate in this process. There are studies which imply that the AM product monocyte chemoattractant protein-1 (MCP-1) plays an important role. Thus we tested: 1. if the selective elimination of AM attenuates HPH in rats, 2. the correlation of MCP-1 plasmatic concentrations with the presence and absence of AM during exposure to hypoxia, 3. the direct influence of hypoxia on MCP-1 production in isolated AM. We found that experimental depletion of AM attenuated the chronic hypoxia-induced increase in mean pulmonary arterial pressure, but did not affect the serum MCP-1 concentrations. Furthermore, the MCP-1 production by AM in vitro was unaffected by hypoxia. Thus we conclude that AM play a significant role in the mechanism of HPH, but MCP-1 release from these cells is most likely not involved in this process. The increase of MCP-1 accompanying the development of HPH probably originates from other sources than AM.

L-Arginine, a precursor of EDRF in vitro, produces pulmonary vasodilation in lambs

1991 ◽  
Vol 261 (5) ◽  
pp. H1563-H1569 ◽  
Author(s):  
J. R. Fineman ◽  
R. Chang ◽  
S. J. Soifer
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Phosphodiesterase Inhibitor ◽  
Hemodynamic Effects ◽  
Synthesis Inhibitor ◽  
Pulmonary Vasodilation ◽  
Pulmonary Arterial ◽  
Rate Limiting

There is increasing evidence that resting pulmonary vascular tone is mediated in part by the release of endothelium-derived relaxing factors (EDRF). Because L-arginine may be a precursor for EDRF synthesis, we studied the pulmonary vasodilating effects of L-arginine at rest and during pulmonary hypertension in 16 intact newborn lambs. At rest, the intravenous infusions of L-arginine (150 mg/kg) had no hemodynamic effects. However, during pulmonary hypertension induced by hypoxia or the infusion of U-46619 (a thromboxane A2 mimic), L-arginine decreased pulmonary arterial pressure by 22 and 27%, respectively (P less than 0.05). The decrease in pulmonary arterial pressure produced by L-arginine was blocked by methylene blue, a guanylate cyclase inhibitor, and augmented by Zapranast, a guanosine 3',5'-cyclic monophosphate (cGMP) phosphodiesterase inhibitor (-17.9 vs. -31.2%, P less than 0.05). In addition, L-arginine partially reversed the pulmonary hypertension induced by N omega-nitro-L-arginine, a competitive EDRF synthesis inhibitor, but D-arginine had no hemodynamic effects. This study suggests that L-arginine produces pulmonary vasodilation by increasing cGMP concentrations, supporting the in vitro hypothesis that L-arginine is a precursor for EDRF synthesis, whose availability may become rate limiting during pulmonary hypertension.

Living and training in moderate hypoxia does not improveV˙o 2 max more than living and training in normoxia

2001 ◽  
Vol 90 (6) ◽  
pp. 2057-2062 ◽  
Author(s):  
Kyle K. Henderson ◽  
Richard L. Clancy ◽  
Norberto C. Gonzalez
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Maximal Exercise ◽  
Pulmonary Arterial Pressure ◽  
Moderate Hypoxia ◽  
Mean Pulmonary Arterial Pressure ◽  
Maximal Cardiac Output ◽  
Pulmonary Arterial ◽  
And Training ◽  
Hypoxic Exercise

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired Po 2(Pi O2 ) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10° incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (V˙o 2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However,V˙o 2 max and O2 transport variables were not significantly different between NTN and HTH:V˙o 2 max 86.6 ± 1.5 vs. 86.8 ± 1.1 ml · min−1 · kg−1; maximal cardiac output 456 ± 7 vs. 443 ± 12 ml · min−1 · kg−1; tissue blood O2 delivery (cardiac output × arterial O2 content) 95 ± 2 vs. 96 ± 2 ml · min−1 · kg−1; and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 ± 0.01 vs. 0.90 ± 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS ( P < 0.05) at rest (24.5 ± 0.8 vs. 18.1 ± 0.8) and during maximal exercise (32.0 ± 0.9 vs. 23.8 ± 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 ± 0.8) and during maximal exercise (29.2 ± 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.

Correlation of acute with chronic hypoxic pulmonary hypertension in cattle

1975 ◽  
Vol 38 (3) ◽  
pp. 495-498 ◽  
Author(s):  
D. H. Will ◽  
J. L. Hicks ◽  
C. S. Card ◽  
J. T. Reeves ◽  
A. F. Alexander
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Common Mechanism ◽  
Mean Pulmonary Arterial Pressure ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Highly Correlated

We investigated acute and chronic hypoxic pulmonary pressor responses in two groups of calves, one bred to be susceptible, the other resistant to high-altitude pulmonary hypertension. Twelve 5-mo-old susceptible calves residing at 1,524 m increased their mean pulmonary arterial pressure from 26 +/- 2 (SE) to 55 +/- 4 mmHg during 2 h at a simulated altitude of 4,572 m. In 10 resistant calves pressure increased from 22 +/- 1 to 37 +/- 2 mmHg. Five calves were selected from each group for further study. When 9 mo old, the 5 susceptible calves again showed a greater pressor response to acute hypoxia (27 +/- 1 to 55 +/- 4 mmHg) than did 5 resistant calves (23 +/- 1 to 41 +/- 3 mmHg). When 12 mo old, the 5 susceptible calves also developed a greater increase in pulmonary arterial pressure (21 +/- 2 to 9 +/- 4 mmHg) during 18 days at 4,572 m than did the 5 resistant calves (21 +/- 1 to 64 +/- 4 mmHg). Acute and chronic hypoxic pulmonary pressor responses were highly correlated (r = 0.91; P less than 0.001) indicating that they were probably produced through a common mechanism.

scholarly journals Impact of the updated hemodynamic definitions on diagnosis rates of pulmonary hypertension

2020 ◽  
Vol 10 (3) ◽  
pp. 204589402093129
Author(s):  
Seda Tanyeri ◽  
Ozgur Y. Akbal ◽  
Berhan Keskin ◽  
Aykun Hakgor ◽  
Ali Karagoz ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
European Society ◽  
Pulmonary Arterial Pressure ◽  
Heart Catheterization ◽  
Mean Pulmonary Arterial Pressure ◽  
Pressure Threshold ◽  
Normal Mean ◽  
Pulmonary Arterial ◽  
European Society Of Cardiology

We evaluated whether updated pulmonary hypertension definitive criteria proposed in sixth World Symposium on Pulmonary Hypertension had an impact on diagnosis of overall pulmonary hypertension and pre-capillary and combined pre- and post-capillary phenotypes as compared to those in European Society of Cardiology/European Respiratory Society 2015 pulmonary hypertension Guidelines. Study group comprised the retrospectively evaluated 1300 patients (age 53.1 ± 18.8 years, female 807, 62.1%) who underwent right heart catheterization with different indications between 2006 and 2018. Mean pulmonary arterial pressure ≥25 mmHg (European Society of Cardiology) and PAMP (mean pulmonary arterial pressure) >20 mmHg (World Symposium on Pulmonary Hypertension) right heart catheterization definitions criteria were used, respectively. For pre-capillary pulmonary hypertension, pulmonary artery wedge pressure ≤15 mmHg and pulmonary vascular resistance ≥3 Wood units criteria were included in the both definitions. Normal mean pulmonary arterial pressure (<21 mmHg), borderline mean pulmonary arterial pressure elevation (21–24 mmHg), and overt pulmonary hypertension (≥25 mmHg) were documented in 21.1, 9.8, and 69.1% of the patients, respectively. The pre-capillary and combined pre- and post-capillary pulmonary hypertension were noted in 2.9 and 1.1%, 8.7 and 2.5%, and 34.6 and 36.6% of the patients with normal mean pulmonary arterial pressure, borderline, and overt pulmonary hypertension subgroups, respectively. The World Symposium on Pulmonary Hypertension versus European Society of Cardiology/European Respiratory Society definitions resulted in a net 9.8% increase in the diagnosis of overall pulmonary hypertension whereas increases in the pre-capillary pulmonary hypertension and combined pre- and post-capillary pulmonary hypertension diagnosis were only 0.8 and 0.3%, respectively. The re-definition of mean pulmonary arterial pressure threshold seems to increase the frequency of the overall pulmonary hypertension diagnosis. However, this increase was mainly originated from those in post-capillary pulmonary hypertension subgroup whereas its impact on pre-capillary and combined pre- and post-capillary pulmonary hypertension was negligible. Moreover, criteria of pre-capillary pulmonary vascular disease and combined pre- and post-capillary phenotypes were still detectable even in the presence of normal mean pulmonary arterial pressure. The obligatory criteria of pulmonary vascular resistance ≥3 Wood units seems to keep specificity for discrimination between pre-capillary versus post-C pulmonary hypertension after lowering the definitive mean pulmonary arterial pressure threshold to 20 mmHg.

scholarly journals High Tissue Factor Microparticle Level in Major Thalassemic Patients with Pulmonary Hypertension

2019 ◽  
Vol 7 (2) ◽  
pp. 88-95
Author(s):  
Dimmy Prasetya ◽  
Pandji Irani Fianza ◽  
Erwan Martanto ◽  
Teddy Arnold Sihite
Keyword(s):  
Pulmonary Hypertension ◽  
Tissue Factor ◽  
Pulmonary Arterial Pressure ◽  
Secondary Data ◽  
Primary Data ◽  
Mean Pulmonary Arterial Pressure ◽  
Significant Difference ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Clinical Characteristic

Objective: To analyze the correlation between tissue factor microparticles (TF-MP) levels and pulmonary hypertension (PH) in adult thalassemic patients. Methods: This study was conducted from September to October 2018, using secondary and primary data. The secondary data consisted of the PH parameter, which was retrieved from a 2017 previous study entitled ‘Clinical Characteristic and Complication due to Iron Overload in Thalassaemic Patients‘in 2017 while the primary data were the TF-MP, which were obtained from the analysis of frozen serum of the same population using ELISA method. The mean pulmonary arterial pressure (mPAP) values were obtained from echocardiography results and PH was defined as mPAP >25 mmHg. Results: Seven (16.7%) major thalassemic patients experienced PH. The median values of TF-MP levels were higher among major thalassemic patients with PH when compared to the non-PH patients (1569 vs 11.5 pg/dL; p=0.023). No significant difference was observed in the median TF-MP levels between subjects with splenectomy and subjects without splenectomy (11.6 vs 12.3 pg/dL; p=0.44). There was also no difference in mPAP values between subjects with splenectomy and subjects without splenectomy (18.0 vs 17.0 mmHg; p=0.663). When the median TF-MP levels among major thalassemic patients were analyzed in terms of correlation with transfusion level, no statistically significant difference was seen between subjects who received sufficient transfusions (≥180 mL/kgbb/year) and those who received insufficient transfusions (<180 mL/kgbb/year) (r= 0.138; p=0.390). Conclusions: There is a positive correlation between the TF-MP levels and PH in adult major thalassemic subjects.

scholarly journals Hyperuricemia in patients with pulmonary hypertension: A study in a tertiary care center

2021 ◽  
Vol 6 (3) ◽  
pp. 173-177
Author(s):  
C H Raju ◽  
M Ravindranath
Keyword(s):  
Pulmonary Hypertension ◽  
Uric Acid ◽  
Arterial Pressure ◽  
Serum Uric Acid ◽  
Pulmonary Arterial Pressure ◽  
Nyha Class ◽  
High Serum ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary Hypertension is one of a life-threatening disease with high rate of patient mortality. Decreased cardiac output and tissue hypoxia is measured using Uric acid as a marker for assessment of pulmonary hypertension. 75 patients who were diagnosed with a mean pulmonary arterial pressure of &#62;22mmHg were categorized as group A and 75 healthy patients were considered to be Group B. Blood was collected for Uric acid, creatinine and total Bilirubin estimation. Pulmonary arterial systolic pressure as well as the ventricular function of the patients was evaluated using Colour Doppler ECG and a value of ≥50 mmHg, or a mean pulmonary arterial pressure (at rest) of ≥25 mmHg was taken and the right arterial pressure was calculated. Using the Simpson’s formula, the right and left ventricular ejaculation factors (RVEF, LVEF) were calculated. The serum uric acid levels among the patients were 8.3±1.4mg/dL, creatinine levels were 2.1 ± 0.5 mg/dL, and the total bilirubin levels were 1.9 ± 0.8 mg/dL all of which was significantly higher than the controls. The uric acid levels were also positively correlated to the NHYA class. The blood pressure and the pulmonary arterial pressure were also higher than that of the controls. The correlation was done between the elevated uric acid and ejection fractions and the correlation coefficients of MPAP, LVEF, RVEF and the NYHA class were all significantly associated and the values were 0.394, -0.513, -0.467 and 0.38 respectively. High serum uric acid levels is significantly associated with higher blood pressure, pulmonary arterial pressure and NYHA class. High serum uric acid levels can be a reliable prognostic marker for the detection of pulmonary hypertension. Early therapy may help in the reduction of mortality rate.

scholarly journals Korelasi Forced Expiratory Volume in 1 Second % Prediksi dengan Tekanan Rerata Arteri Pulmonalis Menggunakan Ekokardiografi pada Penderita Penyakit Paru Obstruktif Kronik Stabil

2017 ◽  
Vol 3 (4) ◽  
pp. 177
Author(s):  
Munadi Munadi ◽  
M Yamin ◽  
Anna Ujainah ◽  
Cleopas Martin Rumende
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Right Heart ◽  
Obstructive Pulmonary Disease ◽  
Mean Pulmonary Arterial Pressure ◽  
Copd Patients ◽  
Pulmonary Arterial

Pendahuluan. Hipertensi pulmonal merupakan komplikasi tersering pada penyakit paru obstruktif kronis (PPOK). Angka kematian akan meningkat tajam apabila pasien PPOK sudah mengalami komplikasi ini. Selama ini pengukuran tekanan arteri pulmonalis hanya diukur pada saat pasien PPOK eksaserbasi dirawat di ruang intesif dengan cara invasif menggunakan alat right heart catherization (RHC). Data kelompok PPOK stabil yang mengalami hipertensi pulmonal yang diukur dengan cara non invasif masih relatif sedikit yang dipublikasi. Saat ini sudah ada ekokardiografi yang dapat digunakan sebagai pengganti RHC pada kelompok PPOK stabil. Penelitian ini dilakukan untuk mengetahui apakah ada hubungan antara penurunan forced expiratory volume in 1 second (FEV1) % prediksi dengan peningkatan rerata tekanan arteri pulmonalis (mean pulmonary arterial pressure, mPAP) dan mencari titik potong terbaik secara klinis antara FEV1 % prediksi dan mPAP.Metode. Studi potong lintang pada lima puluh delapan subjek PPOK stabil yang dilakukan spirometri dan pengukuran mPAP dengan menggunakan ekokardiografi doppler pada potongan short axis setinggi aorta.Hasil. Nilai rerata FEV1 % prediksi 26,6 (SB 4,7) dan rerata mPAP 37,61 (18,1-59) mmHg. 74 % subjek mengalami hipertensi pulmonal, dengan karakteristik 24 % ringan, 31 % sedang dan 19 % berat. Terdapat korelasi negatif kuat antara penurunan FEV1 % prediksi dengan peningkatan mPAP. Semakin turun FEV1% prediksi semakin meningkat mPAP. Nilai titik potong terbaik secara klinis 55,3 % dengan sensitivitas 93%.Simpulan. FEV1 % prediksi berkorelasi negatif yang sangat kuat dengan tekanan rerata arteri pulmonalis. FEV1 % prediksi 55,3 % memiliki kemampuan yang cukup baik membedakan PPOK stabil yang sudah mengalami hipertensi pulmonal.Kata Kunci: ekokardiografi, FEV1 %, mPAP, PPOK stabil, spirometri  Correlation of Forced Expiratory Volume in 1 Second Prediction with Mean Pulmonary Arterial Pressure Using Echocardiography in Stable Chronic Obstructive Pulmonary Disease Introduction. Pulmonary hypertension is the most common complication of chronic obstructive pulmonary disease (COPD). Mortality rate will increase when COPD complication with pulmonary hypertension. Right heart catheterization (RHC) is the most common tool to measure mean pulmonary arterial pressure (mPAP) either in COPD patients with exacerbations treated in intensive care unit. Data of pulmonary hypertension in stable COPD group is still relatively rare. Alternatively to RHC, nowadays echocardiography is used to measure mean pulmonary arterial pressure in stable COPD group.Methods. A cross-sectional study was conducted on fifty-eight stable male COPD patients (mean age: 67,6) underwent spirometry. Mean pulmonary arterial pressure was measured using transthoracic echocardiography at short axis view in aortic level. Results. Mean value of forced expiratory volume in 1 second (FEV1)% was 26,6 % (SD 4,7) with median value of mean pulmonary arterial pressure was 37,61 mmHg (range 18,3-59). As many as 74% subjects were pulmonary hypertension; 24 % mild, 31 % moderate and 19% severe respectively. The correlation test showed a significant strong-negative correlation (r = -0,948, p <0,001). The best cut-off point of FEV1% prediction, which had a clinical value correlated with mPAP, was 55,3% with the sensitivity 93 %. Conclusions. Forced expiratory volume in one second (FEV1)% prediction has a significant correlation with mean pulmonary arterial pressure in stable COPD patients. The cut-off point FEV1% prediction 55,3% has a good capability to discriminate pulmonary hypertension in stable COPD patient. Keywords: echocardiography, FEV1% prediction, mean pulmonary arterial pressure, stable COPD

Loss of endothelium-dependent vasodilation in the pulmonary vessels of sheep after prolonged endotoxin

1994 ◽  
Vol 76 (1) ◽  
pp. 361-369 ◽  
Author(s):  
J. A. Spath ◽  
P. J. Sloane ◽  
M. H. Gee ◽  
K. H. Albertine
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Prolonged Exposure ◽  
Pulmonary Arterial Pressure ◽  
Necrosis Factor Alpha ◽  
Pulmonary Vessels ◽  
Endotoxin Infusion ◽  
Pulmonary Arterial ◽  
Endothelium Dependent Relaxation

We examined the hemodynamic response of awake sheep to prolonged endotoxin infusion (10 ng.kg-1 x min-1 for 12 h) and the in vitro endothelium-dependent relaxation of pulmonary arterial vessels excised 12 h after the end of endotoxin infusion to determine whether the development of pulmonary hypertension after endotoxin is associated with loss of endothelium-dependent relaxation. In seven of nine sheep, there was a maintained increase (4–68% of baseline) in pulmonary arterial pressure 24 h after the beginning of endotoxin infusion. The greater the increase in pulmonary arterial pressure in vivo, the greater was the in vitro deficit in endothelium-dependent relaxation of the pulmonary vessels. The maximum in vitro vessel dilation was 59% for pulmonary artery rings isolated from sheep without a sustained increase in pulmonary arterial pressure 24 h after endotoxin. Prolonged endotoxin infusion did not alter the in vitro response of pulmonary arterial vessels to KCl or 10(-5) M norepinephrine. Force development, response to 10(-5) M norepinephrine, and vasodilation in response to acetylcholine were also not altered in pulmonary vessels taken from control sheep and exposed in vitro to tumor necrosis factor-alpha (400 U/ml). Our results suggest that loss of endothelium-dependent relaxation in pulmonary vessels supports the sustained pulmonary hypertension that develops after prolonged exposure to endotoxin.

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