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.

Pregnancy-induced pulmonary hypertension in cows susceptible to high mountain disease

1979 ◽  
Vol 46 (1) ◽  
pp. 184-188 ◽  
Author(s):  
L. G. Moore ◽  
J. T. Reeves ◽  
D. H. Will ◽  
R. F. Grover
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
High Mountain ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Observations in several species suggest that pulmonary vascular reactivity may be reduced during pregnancy. We tested this hypothesis in two groups of unanesthetized cows, one “susceptible” and one “resistant” to high mountain or brisket disease. At the altitude of residence (1,524 m), mean pulmonary arterial pressure was elevated during pregnancy by 18% and total pulmonary vascular resistance by 32% in susceptible but not in resistant cows. During acute exposure to simulated altitudes of 2,120--4,550 m, pulmonary arterial pressure was increased by 16% and total pulmonary resistance by 28% during pregnancy in susceptible cows. The pulmonary pressor response to a 5 microgram/kg bolus of prostaglandin FIalpha was not different during pregnancy in either group. Resistant cows hyperventilated while pregnant, raising arterial partial pressure of oxygen (PaO2) by 6 Torr both at 1,524 m and, on the average, by 7 Torr at altitudes of 2,120--4,550 m. Susceptible cows increased their PaO2 less than did the resistant cows during pregnancy. The results indicated that pregnancy was associated with a greater rise in pulmonary arterial pressure and total pulmonary vascular resistance during acute hypoxia and failed to elicit as great a ventilatory response in susceptible than in resistant cows.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

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.

Hypoxic pulmonary vasoconstriction during steady and pulsatile flow in ferrets

1984 ◽  
Vol 57 (1) ◽  
pp. 205-212 ◽  
Author(s):  
T. J. Gregory ◽  
M. L. Ellsworth ◽  
J. C. Newell
Keyword(s):  
Arterial Pressure ◽  
Steady Flow ◽  
Pulsatile Flow ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Flow Curves ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Pulsatile Perfusion

We examined the effects of hypoxia and pulsatile flow on the pressure-flow relationships in the isolated perfused lungs of Fitch ferrets. When perfused by autologous blood from a pump providing a steady flow of 60 ml/min, the mean pulmonary arterial pressure rose from 14.6 to 31.3 Torr when alveolarPO2 was reduced from 122 to 46 Torr. This hypoxic pressor response was characterized by a 10.1-Torr increase in the pressure-axis intercept of the extrapolated pressure-flow curves and an increase in the slope of these curves from 130 to 240 Torr X l–1 X min. With pulsatile perfusion from a piston-typepump, mean pulmonary arterial pressure increased from 17.5 to 36.3 Torr at the same mean flow.Thishypoxic pressor response was also characterized by increases in the intercept pressure and slope of thepressure-flow curves. When airway pressure was raised during hypoxia, the intercept pressure increased further to 25 +/- 1 Torr with a further increase in vascular resistance to 360 Torr X l–1 X min. Thus, in contrast to the dog lung, in the ferret lung pulsatile perfusion does not result in lower perfusion pressures during hypoxia when compared with similar mean levels of steady flow. Since the effects of high airway pressure and hypoxia are additive, they appear to act at or near the same site in elevating perfusion pressure.

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

Thromboxane does not mediate pulmonary hypertension in phorbol ester-induced acute lung injury in dogs

1990 ◽  
Vol 69 (1) ◽  
pp. 345-352 ◽  
Author(s):  
A. H. Stephenson ◽  
R. S. Sprague ◽  
T. E. Dahms ◽  
A. J. Lonigro
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
H2 Receptor Antagonist ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Relationship

Thromboxane (Tx) has been suggested to mediate the pulmonary hypertension of phorbol myristate acetate- (PMA) induced acute lung injury. To test this hypothesis, the relationship between Tx and pulmonary arterial pressure was evaluated in a model of acute lung injury induced with PMA in pentobarbital sodium-anesthetized male mongrel dogs. Sixty minutes after administration of PMA (20 micrograms/kg iv, n = 10), TxB2 increased 10-fold from control in both systemic and pulmonary arterial blood and 8-fold in bronchoalveolar lavage (BAL) fluid. Concomitantly, pulmonary arterial pressure (Ppa) increased from 14.5 +/- 1.0 to 36.2 +/- 3.5 mmHg, and pulmonary vascular resistance (PVR) increased from 5.1 +/- 0.4 to 25.9 +/- 2.9 mmHg.l-1.min. Inhibition of Tx synthase with OKY-046 (10 mg/kg iv, n = 6) prevented the PMA-induced increase in Tx concentrations in blood and BAL fluid but did not prevent or attenuate the increase in Ppa. OKY-046 pretreatment did, however, attenuate but not prevent the increase in PVR 60 min after PMA administration. Pretreatment with the TxA2/prostaglandin H2 receptor antagonist ONO-3708 (10 micrograms.kg-1.min-1 iv, n = 7) prevented the pressor response to bolus injections of 1-10 micrograms U-46619, a Tx receptor agonist, but did not prevent or attenuate the PMA-induced increase in Ppa. ONO-3708 also attenuated but did not prevent the increase in PVR. These results suggest that Tx does not mediate the PMA-induced pulmonary hypertension but may augment the increases in PVR in this model of acute lung injury.

scholarly journals Acute Deterioration of Pulmonary Arterial Hypertension (PAH) in a Patient with Neurofibromatosis Type 1 (NF1)

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Seiya Tanaka ◽  
Fuko Kawahara ◽  
Taro Miyamoto ◽  
Satoshi Tsurusaki ◽  
Yoshihito Sanuki ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Pressure ◽  
Arterial Hypertension ◽  
Neurofibromatosis Type 1 ◽  
Pulmonary Arterial Pressure ◽  
Neurofibromatosis Type ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

A 56-year-old woman was diagnosed as having chronic obstructive pulmonary disease with heavy smoking. Mild pulmonary hypertension (mean pulmonary arterial pressure: 31 mmHg) was detected at the first visit. She was diagnosed with pulmonary hypertension due to pulmonary disease and medicated only with bronchodilators. Simultaneous, multiple freckling in the trunk of her body and café au lait macules in her back with some cutaneous neurofibromas were also detected. A plastic surgeon removed one of the neurofibromas and pathologically diagnosed it as neurofibromatosis type 1 (NF1). We finally rediagnosed her with pulmonary hypertension with unclear and/or multifactorial factors when she deteriorated 1 year after being treated only with bronchodilators. We then administrated upfront combination therapy with macitentan and tadalafil. Mean pulmonary arterial pressure rapidly improved. Learning Objective. Pulmonary arterial hypertension (PAH) in neurofibromatosis type 1 (NF1) can occur due to lung disease or due to certain involvement of pulmonary arteries, or a combination of both. Increased awareness of PAH in NF1 is very important for patients survival. The current therapeutic strategy is almost identical to that of idiopathic PAH; however, there is no clinical evidence. Insights gained from clinical experiences should help identify promising novel therapeutic approaches in NF1-PAH.

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