scholarly journals THE TRANSPULMONARY GRADIENT BUT NOT THE SYSTOLIC OR MEAN PULMONARY ARTERIAL PRESSURE CORRELATES WITH THE WALL THICKNESS OF PERIPHERAL PULMONARY ARTERIES AND VEINS IN PATIENTS WITH CHRONIC HEART FAILURE

2014 ◽  
Vol 63 (12) ◽  
pp. A1491
Author(s):  
Vera D. Aiello ◽  
Pompeu R. Campos ◽  
Victor Issa ◽  
Ronaldo Honorato ◽  
Alfredo I. Fiorelli ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Arterial Pressure ◽  
Wall Thickness ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Arteries And Veins

Chronic lung lymph fistula that only drains the left lung

1995 ◽  
Vol 269 (4) ◽  
pp. R943-R947
Author(s):  
Y. Kikuchi ◽  
H. Nakazawa ◽  
D. L. Traber
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Mediastinal Lymph Node ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Left Lung ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
The Right ◽  
Arteries And Veins

We developed a chronic lung fistula that drains only the left lung, allowing for evaluation of injury in a single lung. To remove lymph drainage from the right lung into the caudal mediastinal lymph node, the right lower pulmonary ligament was severed. Pneumatic occluders were placed on the left pulmonary arteries and veins. To ensure that lymph drained from only the left lung, we increased the right pulmonary arterial pressure (RPAP) from 21.2 +/- 0.5 to 36.5 +/- 0.6 mmHg. The left pulmonary arterial pressure (LPAP) was kept at wedge pressure level for 1 h by inflating pneumatic occluders. Lymph flow from the left lung fistula was stable during this occlusion. Six hours after recovery was increased the LPAP from a baseline level of 19.1 +/- 1.0 to 36.4 +/- 0.9 mmHg and the RPAP from 21.2 +/- 0.5 to 38.0 +/- 0.8 mmHg for 2 h by inflating the pneumatic occluders on the left and right pulmonary veins. Lymph flow increased from 5.3 +/- 1.0 to 28.0 +/- 2.9 ml/h. Reflection coefficient was calculated at 0.80 +/- 0.02.

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.

scholarly journals Determinants and prognostic value of pulmonary arterial pressure in patients with chronic heart failure

2010 ◽  
Vol 31 (18) ◽  
pp. 2280-2290 ◽  
Author(s):  
Thibaud Damy ◽  
Kevin M. Goode ◽  
Anna Kallvikbacka-Bennett ◽  
Christian Lewinter ◽  
James Hobkirk ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Arterial Pressure ◽  
Prognostic Value ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

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.

Treatment of Severe Hypertension with Minoxidil and its Effects on Systemic and Pulmonary Haemodynamics

1976 ◽  
Vol 51 (s3) ◽  
pp. 587s-589s ◽  
Author(s):  
D. Hall ◽  
K. L. Froer ◽  
C. Loracher
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Severe Hypertension ◽  
Chronic Administration ◽  
Direct Result ◽  
Small Decrease ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Haemodynamics ◽  
Pulmonary Arterial

1. The chronic administration of minoxidil, 0024–0·212 mmol (5–40 mg) daily, to fifty-two severely hypertensive patients resulted in an average reduction of mean arterial pressure from 170 to 111 mmHg. 2. Haemodynamic studies in twelve of these patients indicated that the rise in pulmonary arterial pressure in patients without heart failure appears to be a direct result of a disproportionately large increase in cardiac output with respect to a relatively small decrease in pulmonary vascular resistance. Anti-hypertensive treatment of patients with congestive heart failure resulted in a decrease in mean pulmonary arterial pressure.

BMPR-II heterozygous mice have mild pulmonary hypertension and an impaired pulmonary vascular remodeling response to prolonged hypoxia

2004 ◽  
Vol 287 (6) ◽  
pp. L1241-L1247 ◽  
Author(s):  
Hideyuki Beppu ◽  
Fumito Ichinose ◽  
Noriko Kawai ◽  
Rosemary C. Jones ◽  
Paul B. Yu ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Wild Type ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Alveolar Capillary

Heterozygous mutations of the bone morphogenetic protein type II receptor ( BMPR-II) gene have been identified in patients with primary pulmonary hypertension. The mechanisms by which these mutations contribute to the pathogenesis of primary pulmonary hypertension are not fully elucidated. To assess the impact of a heterozygous mutation of the BMPR-II gene on the pulmonary vasculature, we studied mice carrying a mutant BMPR-II allele lacking exons 4 and 5 ( BMPR-II+/− mice). BMPR-II+/− mice had increased mean pulmonary arterial pressure and pulmonary vascular resistance compared with their wild-type littermates. Histological analyses revealed that the wall thickness of muscularized pulmonary arteries (<100 μm in diameter) and the number of alveolar-capillary units were greater in BMPR-II+/− than in wild-type mice. Breathing 11% oxygen for 3 wk increased mean pulmonary arterial pressure, pulmonary vascular resistance, and hemoglobin concentration to similar levels in BMPR-II+/− and wild-type mice, but the degree of muscularization of small pulmonary arteries and formation of alveolar-capillary units were reduced in BMPR-II+/− mice. Our results suggest that, in mice, mutation of one copy of the BMPR-II gene causes pulmonary hypertension but impairs the ability of the pulmonary vasculature to remodel in response to prolonged hypoxic breathing.

A computed method for noninvasive MRI assessment of pulmonary arterial hypertension

2004 ◽  
Vol 96 (2) ◽  
pp. 463-468 ◽  
Author(s):  
Eric Laffon ◽  
Christophe Vallet ◽  
Virginie Bernard ◽  
Michel Montaudon ◽  
Dominique Ducassou ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Cross Sectional Area ◽  
Physical Parameters ◽  
Sectional Area ◽  
Biophysical Parameters ◽  
Cross Sectional ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Mean

The present method enables the noninvasive assessment of mean pulmonary arterial pressure from magnetic resonance phase mapping by computing both physical and biophysical parameters. The physical parameters include the mean blood flow velocity over the cross-sectional area of the main pulmonary artery (MPA) at the systolic peak and the maximal systolic MPA cross-sectional area value, whereas the biophysical parameters are related to each patient, such as height, weight, and heart rate. These parameters have been measured in a series of 31 patients undergoing right-side heart catheterization, and the computed mean pulmonary arterial pressure value (PpaComp) has been compared with the mean pressure value obtained from catheterization (PpaCat) in each patient. A significant correlation was found that did not differ from the identity line PpaComp = PpaCat ( r = 0.92). The mean and maximal absolute differences between PpaComp and PpaCat were 5.4 and 11.9 mmHg, respectively. The method was also applied to compute the MPA systolic and diastolic pressures in the same patient series. We conclude that this computed method, which combines physical (whoever the patient) and biophysical parameters (related to each patient), improves the accuracy of MRI to noninvasively estimate pulmonary arterial pressures.

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