Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

1989 ◽  
Vol 66 (1) ◽  
pp. 151-160 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Thornton ◽  
R. M. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Systemic Hemodynamic ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Air Control

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

Repeated inhalation of adrenomedullin ameliorates pulmonary hypertension and survival in monocrotaline rats

2003 ◽  
Vol 285 (5) ◽  
pp. H2125-H2131 ◽  
Author(s):  
Noritoshi Nagaya ◽  
Hiroyuki Okumura ◽  
Masaaki Uematsu ◽  
Wataru Shimizu ◽  
Fumiaki Ono ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Systemic Arterial Pressure ◽  
Inhalation Therapy ◽  
Rank Test ◽  
Pulmonary Resistance ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Adrenomedullin (AM) is a potent vasodilator peptide. We investigated whether inhalation of aerosolized AM ameliorates monocrotaline (MCT)-induced pulmonary hypertension in rats. Male Wistar rats given MCT (MCT rats) were assigned to receive repeated inhalation of AM ( n = 8) or 0.9% saline ( n = 8). AM (5 μg/kg) or saline was inhaled as an aerosol using an ultrasonic nebulizer for 30 min four times a day. After 3 wk of inhalation therapy, mean pulmonary arterial pressure and total pulmonary resistance were markedly lower in rats treated with AM than in those given saline [mean pulmonary arterial pressure: 22 ± 2 vs. 35 ± 1 mmHg (–37%); total pulmonary resistance: 0.048 ± 0.004 vs. 0.104 ± 0.006 mmHg · ml–1 · min–1 · kg–1 (–54%), both P < 0.01]. Neither systemic arterial pressure nor heart rate was altered. Inhalation of AM significantly attenuated the increase in medial wall thickness of peripheral pulmonary arteries in MCT rats. Kaplan-Meier survival curves demonstrated that MCT rats treated with aerosolized AM had a significantly higher survival rate than those given saline (70% vs. 10% 6-wk survival, log-rank test, P < 0.01). In conclusion, repeated inhalation of AM inhibited MCT-induced pulmonary hypertension without systemic hypotension and thereby improved survival in MCT rats.

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.

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.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

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 Exposure of Stored Packed Erythrocytes to Nitric Oxide Prevents Transfusion-associated Pulmonary Hypertension

2016 ◽  
Vol 125 (5) ◽  
pp. 952-963 ◽  
Author(s):  
Stefan Muenster ◽  
Arkadi Beloiartsev ◽  
Binglan Yu ◽  
E Du ◽  
Sabia Abidi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Erythrocyte Deformability ◽  
Pulmonary Vasculature ◽  
Prolonged Storage ◽  
Systemic Hemodynamic ◽  
Promising Therapeutic Approach ◽  
Erythrocyte Survival ◽  
Pulmonary Arterial

Abstract Background Transfusion of packed erythrocytes stored for a long duration is associated with increased pulmonary arterial pressure and vascular resistance. Prolonged storage decreases erythrocyte deformability, and older erythrocytes are rapidly removed from the circulation after transfusion. The authors studied whether treating stored packed ovine erythrocytes with NO before transfusion could prevent pulmonary vasoconstriction, enhance erythrocyte deformability, and prolong erythrocyte survival after transfusion. Methods Ovine leukoreduced packed erythrocytes were treated before transfusion with either NO gas or a short-lived NO donor. Sheep were transfused with autologous packed erythrocytes, which were stored at 4°C for either 2 (“fresh blood”) or 40 days (“stored blood”). Pulmonary and systemic hemodynamic parameters were monitored before, during, and after transfusion. Transfused erythrocytes were labeled with biotin to measure their circulating lifespan. Erythrocyte deformability was assessed before and after NO treatment using a microfluidic device. Results NO treatment improved the deformability of stored erythrocytes and increased the number of stored erythrocytes circulating at 1 and 24 h after transfusion. NO treatment prevented transfusion-associated pulmonary hypertension (mean pulmonary arterial pressure at 30 min of 21 ± 1 vs. 15 ± 1 mmHg in control and NO–treated packed erythrocytes, P &lt; 0.0001). Washing stored packed erythrocytes before transfusion did not prevent pulmonary hypertension. Conclusions NO treatment of stored packed erythrocytes before transfusion oxidizes cell-free oxyhemoglobin to methemoglobin, prevents subsequent NO scavenging in the pulmonary vasculature, and limits pulmonary hypertension. NO treatment increases erythrocyte deformability and erythrocyte survival after transfusion. NO treatment might provide a promising therapeutic approach to prevent pulmonary hypertension and extend erythrocyte survival.

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.

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