Adrenomedullin activity in chronically hypoxic rat lungs

1996 ◽  
Vol 271 (2) ◽  
pp. H622-H629 ◽  
Author(s):  
L. Zhao ◽  
L. A. Brown ◽  
A. A. Owji ◽  
D. J. Nunez ◽  
D. M. Smith ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Mrna Levels ◽  
Rat Lung ◽  
Artery Pressure ◽  
Isolated Perfused Lung ◽  
Calcitonin Gene ◽  
Perfused Lung ◽  
Hypotensive Response

Adrenomedullin (AM) is a novel vasodilator with structural similarities to calcitonin gene-related peptide (CGRP). This study investigated AM activity in the rat lung during hypoxia-induced pulmonary hypertension. Both rat AM (0.2-10 nmol) and alpha-CGRP (0.2-2 nmol) produced dose-related reductions in pulmonary artery pressure in the isolated perfused lung ventilated with 2% O2. Pretreatment with alpha-CGRP, which demonstrated tachyphylaxis, or its antagonist, CGRP-(8–37), reduced the hypotensive response to AM, suggesting that part of the response to AM is mediated by CGRP receptors. 125I-labeled AM and 125I-labeled CGRP binding was significantly increased in lung membranes from 7-day hypoxic animals (AM from 1.94 +/- 0.3 to 3.36 +/- 0.4 and CGRP from 0.06 +/- 0.01 to 0.12 +/- 0.02 pmol/mg protein), with no change in dissociation constant. Moreover, the hypotensive response to both peptides was increased in the lungs of 7-day hypoxic rats. There was no significant change in lung immunoreactive AM concentrations (hypoxic 5.04 +/- 0.48 vs. control 6.28 +/- 0.76 pmol/g wet wt of tissue) or steady-state AM mRNA levels in 7-day hypoxic rats. Nonetheless, AM may be useful for the acute pharmacological manipulation of pulmonary artery pressure in hypoxia-induced pulmonary hypertension.

Endothelin-A receptor antagonist prevents acute hypoxia-induced pulmonary hypertension in the rat

1995 ◽  
Vol 268 (1) ◽  
pp. L95-L100 ◽  
Author(s):  
S. Oparil ◽  
S. J. Chen ◽  
Q. C. Meng ◽  
T. S. Elton ◽  
M. Yano ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Receptor Antagonist ◽  
Pulmonary Artery Pressure ◽  
Saline Control ◽  
Mrna Levels ◽  
Artery Pressure ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Endothelin A

Exposure to hypoxia is associated with increased pulmonary artery pressure and plasma endothelin-1(ET-1) levels and with selective enhancement in ET-1 peptide and mRNA and endothelin-A (ETA) receptor mRNA levels in rat lung. The current study tested the hypothesis that endogenous ET-1 can account for hypoxia-induced pulmonary hypertension via a paracrine effect on ETA receptors in lung. Intravenous infusion of the ETA receptor antagonist BQ-123 (D-Trp-D-Asp-Pro-D-Val-Leu) (0.4 mg/microliters at 1 microliter/h) into Sprague-Dawley rats beginning 4 h before and for 90 min during normobaric hypoxia (10% O2) markedly attenuated the hypoxic response: mean pulmonary artery pressure increased from 17.2 +/- 0.7 to 29.0 +/- 1.2 mmHg in saline control rats but did not increase from baseline in BQ-123-treated rats. BQ-123 did not alter systemic arterial pressure, heart rate, or plasma endothelin-1 levels. These findings suggest that ET-1 synthesized in lung in response to hypoxia acts locally on ETA receptors to cause pulmonary hypertension.

scholarly journals Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1212
Author(s):  
Fabian Mueller-Graf ◽  
Jonas Merz ◽  
Tim Bandorf ◽  
Chiara Albus ◽  
Maike Henkel ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Transit Time ◽  
Pulse Wave ◽  
Correlation Coefficients ◽  
Physiological Basis ◽  
Artery Pressure ◽  
Hypoxic Vasoconstriction ◽  
Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

scholarly journals The Relationship between Vitamin D Deficiency and Pulmonary Hypertension

2013 ◽  
Vol 114 (3) ◽  
pp. 154-161 ◽  
Author(s):  
Mehmet Demir ◽  
U. Uyan ◽  
S. Keçeoçlu ◽  
C. Demir
Keyword(s):  
Vitamin D ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vitamin D Deficiency ◽  
Pulmonary Artery Pressure ◽  
Control Group ◽  
Systolic Pulmonary Artery Pressure ◽  
Control Groups ◽  
Artery Pressure ◽  
Vitamin D Levels

Vitamin D deficiency actives renin-angiotensin-aldosterone system (RAAS) which affects cardiovascular system. Activation of RAAS is associated with pulmonary hypertension (PHT). Relation between vitamin D deficiency and PHT could be therefore suggested. In  our study we compared pulmonary artery pressure between vitamin D deficiency and control groups. 115 consecutive patients (average age: 61.86 ± 5.86) who have detected very low vitamin D (vitamin D levels < 10 ng/ml) were enrolled. 117 age matched persons (average age: 61.74 ± 5.99) were selected as the control group. All groups underwent transthoracic echocardiography. Routine biochemical measurement of 25-OH vitamin D and parathormon (PTH) levels were performed. Baseline characteristics of the study groups were comparable. Systolic pulmonary artery pressure (SPAP) of patients in  the low vitamin D group was higher than the control groups. As a  result our study, a  relation between vitamin D deficiency and pulmonary artery hypertension was revealed.

Importance of Relative Pulmonary Hypertension in Cardiac Surgery: The Mean Systemic-to-Pulmonary Artery Pressure Ratio

2006 ◽  
Vol 20 (3) ◽  
pp. 331-339 ◽  
Author(s):  
Arnaud Robitaille ◽  
André Y. Denault ◽  
Pierre Couture ◽  
Sylvain Bélisle ◽  
Annik Fortier ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Surgery ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pressure Ratio ◽  
Artery Pressure ◽  
The Mean

scholarly journals Bacillus anthracis lethal toxin, but not edema toxin, increases pulmonary artery pressure and permeability in isolated perfused rat lungs

2019 ◽  
Vol 316 (5) ◽  
pp. H1076-H1090 ◽  
Author(s):  
Xizhong Cui ◽  
Wanying Xu ◽  
Pranita Neupane ◽  
Andie Weiser-Schlesinger ◽  
Ray Weng ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Bacillus Anthracis ◽  
Vascular Permeability ◽  
Pulmonary Artery Pressure ◽  
Lethal Toxin ◽  
Rat Lung ◽  
Fluid Accumulation ◽  
Pulmonary Vascular Permeability ◽  
Artery Pressure ◽  
Edema Toxin

Although lethal toxin (LT) and edema toxin (ET) contribute to lethality during Bacillus anthracis infection, whether they increase vascular permeability and the extravascular fluid accumulation characterizing this infection is unclear. We employed an isolated perfused Sprague-Dawley rat lung model to investigate LT and ET effects on pulmonary vascular permeability. Lungs ( n ≥ 6 per experimental group) were isolated, ventilated, suspended from a force transducer, and perfused. Lung weight and pulmonary artery (Ppa) and left atrial pressures were measured over 4 h, after which pulmonary capillary filtration coefficients (Kf.c) and lung wet-to-dry weight ratios (W/D) were determined. When compared with controls, LT increased Ppa over 4 h and Kf.c and W/D at 4 h ( P < 0.0001). ET decreased Ppa in a significant trend ( P = 0.09) but did not significantly alter Kf.c or W/D ( P ≥ 0.29). Edema toxin actually blocked LT increases in Ppa but not LT increases in Kf.c and W/D. When Ppa was maintained at control levels, LT still increased Kf.c and W/D ( P ≤ 0.004). Increasing the dose of each toxin five times significantly increased and a toxin-directed monoclonal antibody decreased the effects of each toxin ( P ≤ 0.05). Two rho-kinase inhibitors (GSK269962 and Y27632) decreased LT increases in Ppa ( P ≤ 0.02) but actually increased Kf.c and W/D in LT and control lungs ( P ≤ 0.05). A vascular endothelial growth factor receptor inhibitor (ZM323881) had no significant effect ( P ≥ 0.63) with LT. Thus, LT but not ET can increase pulmonary vascular permeability independent of increased Ppa and could contribute to pulmonary fluid accumulation during anthrax infection. However, pulmonary vascular dilation with ET could disrupt protective hypoxic vasoconstriction. NEW & NOTEWORTHY The most important findings from the present study are that Bacillus anthracis lethal toxin increases pulmonary artery pressure and pulmonary permeability independently in the isolated rat lung, whereas edema toxin decreases the former and does not increase permeability. Each effect could be a basis for organ dysfunction in patients with this lethal infection. These findings further support the need for adjunctive therapies that limit the effects of both toxins during infection.

Pulmonary Hypertension

2013 ◽  
Author(s):  
George K Istaphanous ◽  
Andreas W Loepke
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Pulmonary Artery Pressure ◽  
Disease Process ◽  
Underlying Disease ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Made In

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.

Sarcoidosis-Associated Pulmonary Hypertension

2020 ◽  
Vol 41 (05) ◽  
pp. 659-672
Author(s):  
Marloes P. Huitema ◽  
Harold Mathijssen ◽  
Johannes J. Mager ◽  
Repke J. Snijder ◽  
Jan C. Grutters ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Lung Transplant ◽  
Pulmonary Function Tests ◽  
High Morbidity ◽  
Artery Pressure ◽  
Extrinsic Compression ◽  
Tertiary Center ◽  
Parenchymal Disease

AbstractPulmonary hypertension (PH) is a well-known complication of sarcoidosis, defined by a mean pulmonary artery pressure of ≥25 mm Hg. Since both PH and sarcoidosis are rare diseases, data on sarcoidosis-associated PH (SAPH) is retrieved mostly from small retrospective studies. Estimated prevalence of SAPH ranges from 3% in patients referred to a tertiary center up to 79% in patients awaiting lung transplant. Most patients with SAPH show advanced parenchymal disease as the underlying mechanism. However, some patients have disproportional elevated pulmonary artery pressure, and PH can occur in sarcoidosis patients without parenchymal disease. Other mechanisms such as vascular disease, pulmonary embolisms, postcapillary PH, extrinsic compression, and other sarcoidosis-related comorbidities might contribute to SAPH. The diagnosis of PH in sarcoidosis is challenging since symptoms and signs overlap. Suspicion can be raised based on symptoms or tests, such as pulmonary function tests, laboratory findings, electrocardiography, or chest CT. PH screening mainly relies on transthoracic echocardiography. Right heart catheterization should be considered on a case-by-case basis in patients with clinical suspicion of PH, taking into account clinical consequences. Treatment options are considered on patient level in a PH expert center, and might include oxygen therapy, immunosuppressive, or PH-specific therapy. However, qualitative evidence is scarce. Furthermore, in a subset of patients, interventional therapy or eventually lung transplant can be considered. SAPH is associated with high morbidity. Mortality is higher in sarcoidosis patients with PH compared with those without PH, and increases in patients with more advanced stages of sarcoidosis and/or PH.

Impact of mild pulmonary hypertension on mortality and pulmonary artery pressure profile after heart transplantation

2001 ◽  
Vol 20 (9) ◽  
pp. 942-948 ◽  
Author(s):  
Juan F Delgado ◽  
Miguel A Gómez-Sánchez ◽  
Carlos Sáenz de la Calzada ◽  
Violeta Sánchez ◽  
Pilar Escribano ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Heart Transplantation ◽  
Pulmonary Artery Pressure ◽  
Pressure Profile ◽  
Artery Pressure
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