Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation

1992 ◽  
Vol 73 (1) ◽  
pp. 117-122 ◽  
Author(s):  
S. A. Lang ◽  
M. B. Maron ◽  
K. C. Maender ◽  
C. F. Pilati
Keyword(s):  
Pulmonary Hypertension ◽  
Neuropeptide Y ◽  
Sympathetic Activation ◽  
Pulmonary Hemodynamics ◽  
Vasoactive Agent ◽  
Lung Lobe ◽  
Lower Lung ◽  
Capillary Pressures ◽  
Additional Lobes

We tested the possibility that neuropeptide Y (NPY) may contribute to the pulmonary hypertension that occurs after massive sympathetic activation produced by intracisternal veratrine administration in the chloralose-anesthetized dog. In six dogs, veratrine caused arterial NPY-like immunoreactivity (NPY-LI) to rise from 873 +/- 150 (SE) pg/ml to peak values of 3,780 +/- 666 pg/ml by 60–120 min. (In 3 animals, adrenalectomy significantly reduced the increases in NPY-LI.) In five additional dogs, we infused porcine NPY for 30 min in doses that increased arterial NPY-LI to 8,354 +/- 1,514 pg/ml and observed only minor changes in pulmonary hemodynamics. In three isolated perfused canine left lower lung lobe (LLL) preparations, increasing doses of NPY were administered, producing levels of plasma NPY-LI, at the highest dose, that exceeded those observed after veratrine administration by three orders of magnitude. No changes in LLL arterial or double-occlusion capillary pressures were observed at any dose. Similarly, no changes in LLL hemodynamics were observed in three additional lobes when NPY was administered while norepinephrine was being infused. We conclude that it is unlikely that NPY plays a role as a circulating vasoactive agent in producing the pulmonary hypertension and edema that occur in this model.

Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema

1990 ◽  
Vol 68 (3) ◽  
pp. 912-918 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Pulmonary Edema ◽  
Canine Model ◽  
Neurogenic Pulmonary Edema ◽  
Plasma Catecholamine ◽  
Pulmonary Hemodynamics ◽  
Lung Lobe ◽  
Pulmonary Vasoconstriction ◽  
Lower Lung ◽  
Severe Degree ◽  
Plasma Catecholamine Concentrations

The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL) perfusion of seven splenectomized (to keep hematocrit and blood viscosity constant) dogs was isolated so the LLL could be perfused at constant flow and outflow pressure with blood pumped from the pulmonary artery. The LLL was denervated by removing it from the dog. Veratrine (40-160 micrograms/kg) increased LLL arterial pressure by 39.2% and produced large increases in plasma catecholamine concentrations. The double-occlusion technique indicated that 74% of the increase in the LLL arteriovenous pressure gradient was due to an increase in venous tone. This pattern of vasoconstriction was similar to that previously observed during the infusion of exogenous catecholamines and suggested that catecholamines mediated the LLL response. The more severe degree of PH observed in the intact animal in NPE, however, suggests that passive rather than active changes in pulmonary hemodynamics are predominantly responsible for the development of PH in this disorder.

Effect of high doses of aspirin on pulmonary hemodynamics and lung water

1985 ◽  
Vol 248 (2) ◽  
pp. H225-H231
Author(s):  
M. B. Maron
Keyword(s):  
Cyclooxygenase Inhibitors ◽  
Lung Water ◽  
Venous Tone ◽  
Pulmonary Hemodynamics ◽  
Lung Lobe ◽  
Pulmonary Vasoconstriction ◽  
Lower Lung ◽  
Occlusion Technique ◽  
High Doses ◽  
Pressure Changes

The purpose of this study was to determine if aspirin, in doses that elevate plasma salicylate concentrations to values reported in patients with salicylate-induced pulmonary edema, produce pulmonary vasoconstriction in a canine, isolated perfused left lower lung lobe (LLL) preparation. In 10 LLL's, aspirin (avg 97.8 mg/dl plasma) caused LLL arterial pressure to rise from 9.1 +/- 0.3 to 23.0 +/- 1.8 (SE) Torr. In contrast, no vascular pressure changes were observed in placebo-treated control LLL's. Sodium meclofenamate and indomethacin, structurally dissimilar cyclooxygenase inhibitors, elicited similar responses to aspirin, suggesting that a mechanism involving products of prostaglandin cyclooxygenase was involved in producing the vasoconstriction. The double-occlusion technique was used to localize the sites of the vasoconstriction. The results suggested that all three drugs caused both lobar arterial and venous tone to increase. Although high doses of aspirin produced pulmonary vasoconstriction in the isolated, perfused LLL, the aspirin-treated LLL's gained less weight and extravascular water than the control lobes.

Adrenal component to pulmonary hypertension caused by nicotine administration in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 66-72 ◽  
Author(s):  
M. B. Maron ◽  
D. A. Rickaby ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Lung Lobe ◽  
Nicotine Administration ◽  
Lower Lung

In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.

Adrenal component to pulmonary hypertension induced by elevated cerebrospinal fluid pressure

1979 ◽  
Vol 47 (1) ◽  
pp. 153-160 ◽  
Author(s):  
M. B. Maron ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Cerebrospinal Fluid ◽  
Intact Animal ◽  
Venous Pressure ◽  
Venous Blood ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Mixed Venous Blood ◽  
Vasoactive Agent ◽  
Lung Lobe

In this study we investigated the possibility that a circulating vasoactive agent contributes to the pulmonary hypertension elicited by elevated cerebrospinal fluid pressure (PCSF) using a denervated canine left lower lung lobe (LLL) preparation that was pump perfused with mixed venous blood at constant flow and venous pressure. Raising the PCSF to an average 190 Torr resulted in a 34.3% increase in LLL inflow pressure. This response was eliminated by adrenal venous occlusion and also by alpha-blockade of the LLL. The results indicated that adrenal catecholamines were responsible for the LLL response. The passively induced elevation of left atrial pressure (Pla) that occurs in the intact animal during elevated PCSF was stimulated in the LLL by raising the outflow pressure. This maneuver attenuated the increase in LLL vascular resistance and suggested that the elevation in Pla seen in the intact animal could mask humorally mediated responses of the magnitude we observed.

Region-Specific Neuropeptide Y Overflows at Rest and During Sympathetic Activation in Humans

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 137-143 ◽  
Author(s):  
Margaret J. Morris ◽  
Helen S. Cox ◽  
Gavin W. Lambert ◽  
David M. Kaye ◽  
Garry L. Jennings ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Sympathetic Activation

scholarly journals Serotonin contributes to high pulmonary vascular tone in a sheep model of persistent pulmonary hypertension of the newborn

2013 ◽  
Vol 304 (12) ◽  
pp. L894-L901 ◽  
Author(s):  
Cassidy Delaney ◽  
Jason Gien ◽  
Gates Roe ◽  
Nicole Isenberg ◽  
Jenai Kailey ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Tryptophan Hydroxylase ◽  
Late Gestation ◽  
Persistent Pulmonary Hypertension ◽  
Sheep Model ◽  
Pulmonary Hemodynamics ◽  
Fetal Sheep ◽  
Pulmonary Arterial

Although past studies demonstrate that altered serotonin (5-HT) signaling is present in adults with idiopathic pulmonary arterial hypertension, whether serotonin contributes to the pathogenesis of persistent pulmonary hypertension of the newborn (PPHN) is unknown. We hypothesized that 5-HT contributes to increased pulmonary vascular resistance (PVR) in a sheep model of PPHN and that selective 5-HT reuptake inhibitor (SSRI) treatment increases PVR in this model. We studied the hemodynamic effects of 5-HT, ketanserin (5-HT2A receptor antagonist), and sertraline, an SSRI, on pulmonary hemodynamics of the late gestation fetal sheep with PPHN caused by prolonged constriction of the ductus arteriosis. Brief intrapulmonary infusions of 5-HT increased PVR from 1.0 ± 0.07 (baseline) to 1.4 ± 0.22 mmHg/ml per minute of treatment ( P < 0.05). Ketanserin decreased PVR from 1.1 ± 0.15 (baseline) to 0.82 ± 0.09 mmHg/ml per minute of treatment ( P < 0.05). Sertraline increased PVR from 1.1 ± 0.17 (baseline) to 1.4 ± 0.17 mmHg/ml per minute of treatment ( P = 0.01). In addition, we studied 5-HT production and activity in vitro in experimental PPHN. Compared with controls, pulmonary artery endothelial cells from fetal sheep with PPHN exhibited increased expression of tryptophan hydroxylase 1 and 5-HT production by twofold and 56%, respectively. Compared with controls, 5-HT2A R expression was increased in lung homogenates and pulmonary artery smooth muscle cell lysates by 35% and 32%, respectively. We concluded that increased 5-HT contributes to high PVR in experimental PPHN through activation of the 5-HT2A receptor and that SSRI infusion further increases PVR in this model.

Effect of Pulmonary Blood Flow on Lung Water and Pulmonary Hemodynamics in the Canine Lung Lobe

1990 ◽  
Vol 22 (3) ◽  
pp. 136-142 ◽  
Author(s):  
K. Nakahara ◽  
S. Nanjo ◽  
A. Matsumura ◽  
Y. Kawashima
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Lung Water ◽  
Pulmonary Hemodynamics ◽  
Lung Lobe

scholarly journals The incremental shuttle walk test predicts mortality in non-group 1 pulmonary hypertension: results from the ASPIRE Registry

2019 ◽  
Vol 9 (2) ◽  
pp. 204589401984864 ◽  
Author(s):  
Catherine G. Billings ◽  
Robert Lewis ◽  
Judith A. Hurdman ◽  
Robin Condliffe ◽  
Charlie A. Elliot ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Ceiling Effect ◽  
Walk Test ◽  
Limited Information ◽  
Pulmonary Hemodynamics ◽  
Disease Etiology ◽  
Invasive Test ◽  
Group 2 ◽  
Test Distance ◽  
Group 1

Pulmonary hypertension (PH) is classified into five groups based on disease etiology but there is only limited information on the prognostic value of exercise testing in non-group 1 PH. In group 1 PH, the incremental shuttle walking test (ISWT) distance has been shown to correlate with pulmonary hemodynamics and predict survival without a ceiling effect. This study assessed the ISWT in non-group 1 PH. Data were retrieved from the ASPIRE Registry (Assessing the Spectrum of Pulmonary hypertension Identified at a REferral centre) for consecutive patients diagnosed with PH. Patients were required to have been systematically assessed as group 2–5 PH and to have a baseline ISWT within three months of cardiac catheterization. Patients were stratified according to incremental shuttle walk test distance (ISWD) and ISWT distance percent predicted (ISWD%pred). A total of 479 patients with non-group 1 PH were identified. ISWD and ISWD%pred correlated significantly with symptoms and hemodynamic severity. ISWD and ISWD%pred predicted survival with no ceiling effect. The test was prognostic in groups 2, 3, and 4. ISWD and ISWD%pred and change in ISWD and ISWD%pred at one year were all significant predictors of outcome. In patients with non-group 1 PH the ISWT is a simple non-invasive test that is easy to perform, is predictive of survival at baseline and follow-up, reflects change, and can be used in the assessment of PH of any etiology.

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