Norepinephrine induces lung vascular prostacyclin synthesis via alpha 1-adrenergic receptors

1989 ◽  
Vol 67 (1) ◽  
pp. 330-338 ◽  
Author(s):  
H. L. Wang ◽  
N. F. Voelkel
Keyword(s):  
Pulmonary Artery ◽  
Contractile Response ◽  
Main Pulmonary Artery ◽  
Feedback Mechanism ◽  
Physiological Solution ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Tightly Coupled ◽  
Passive Stretch ◽  
Systemic Arteries

Sympathetic nerve stimulation can cause pulmonary vasoconstriction related to norepinephrine (NE) release. Because of recent reports that NE caused prostacyclin (PGI2) release from systemic arteries, we wondered whether NE caused pulmonary vascular PGI2 release and whether a feedback mechanism existed whereby PGI2 modulated NE-induced vasoconstriction. NE-induced PGI2 synthesis in rat main pulmonary artery rings was larger than that induced by KCl, passive stretch, or a thromboxane analogue, was alpha-adrenergic receptor dependent, and was enhanced by endothelium removal. The NE-induced PGI2 synthesis was not tightly coupled to the magnitude of the pulmonary artery ring contractile response, and inhibition of NE-induced PGI2 production by cyclooxygenase blockade in either the pulmonary artery ring preparation or in isolated rat lungs perfused with a physiological solution did not augment the magnitude of the contractile response. We concluded that NE is a potent stimulus for PGI2 synthesis in the rat main pulmonary artery ring and in the rat lung, yet PGI2 is not important as a modulator of NE-induced vasoconstriction in the rat lung.

In vivo treatment with endotoxin induces nitric oxide synthase in rat main pulmonary artery

1995 ◽  
Vol 268 (3) ◽  
pp. L509-L518 ◽  
Author(s):  
M. J. Griffiths ◽  
S. Liu ◽  
N. P. Curzen ◽  
M. Messent ◽  
T. W. Evans
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Contractile Response ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
No Synthase ◽  
Oxide Synthase ◽  
Lps Treatment

Our aim was to demonstrate increased NO activity from inducible NO synthase (iNOS) in pulmonary arteries (PA) from rats treated with endotoxin [lipopolysaccharide (LPS), 20 mg/kg ip]. LPS treatment diminished the contractile response of PA to potassium chloride (KCl) and phenylephrine (PE) and increased levels of guanosine 3',5'-cyclic monophosphate (cGMP) in endothelium-denuded vessels. Both the NO synthase (NOS) antagonists NG-monomethyl-L-arginine (L-NMMA; nonselective) and aminoguanidine (selective for iNOS) enhanced PE-induced contraction in endothelium-denuded vessels from LPS-treated rats. Furthermore, L-NMMA-induced contraction of endothelium-denuded vessels from LPS-treated rats was stereospecifically antagonized by L-arginine and associated with decreased cGMP levels. These data suggest that NO is produced in increased amounts from PA smooth muscle after LPS treatment. LPS treatment caused increased expression of mRNA for iNOS in PA. This effect of LPS was attenuated by pretreatment with dexamethasone, suggesting that induction of NOS in PA smooth muscle underlies the increased NO activity associated with LPS administration.

scholarly journals Cellular disposition of transported polyamines in hypoxic rat lung and pulmonary arteries

2000 ◽  
Vol 278 (3) ◽  
pp. L610-L617 ◽  
Author(s):  
Pavel Babal ◽  
S. Machelle Manuel ◽  
Jack W. Olson ◽  
Mark N. Gillespie
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Lung Tissue ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Rat Lung ◽  
Polyamine Transport ◽  
Pulmonary Arterial ◽  
Polyamine Uptake

The polyamines putrescine, spermidine (SPD), and spermine are a family of low-molecular-weight organic cations essential for cell growth and differentiation and other aspects of signal transduction. Hypoxic pulmonary vascular remodeling is accompanied by depressed lung polyamine synthesis and markedly augmented polyamine uptake. Cell types in which hypoxia induces polyamine transport in intact lung have not been delineated. Accordingly, rat lung and rat main pulmonary arterial explants were incubated with [14C]SPD in either normoxic (21% O2) or hypoxic (2% O2) environments for 24 h. Autoradiographic evaluation confirmed previous studies showing that, in normoxia, alveolar epithelial cells are dominant sites of polyamine uptake. In contrast, hypoxia was accompanied by prominent localization of [14C]SPD in conduit, muscularized, and partially muscularized pulmonary arteries, which was not evident in normoxic lung tissue. Hypoxic main pulmonary arterial explants also exhibited substantial increases in [14C]SPD uptake relative to control explants, and autoradiography revealed that enhanced uptake was most evident in the medial layer. Main pulmonary arterial explants denuded of endothelium failed to increase polyamine transport in hypoxia. Conversely, medium conditioned by endothelial cells cultured in hypoxic, but not in normoxic, environments enabled hypoxic transport induction in denuded arterial explants. These findings in arterial explants were recapitulated in rat cultured main pulmonary artery cells, including the enhancing effect of a soluble endothelium-derived factor(s) on hypoxic induction of [14C]SPD uptake in smooth muscle cells. Viewed collectively, these results show in intact lung tissue that hypoxia enhances polyamine transport in pulmonary artery smooth muscle by a mechanism requiring elaboration of an unknown factor(s) from endothelial cells.

Simultaneous pulmonary trunk and pulmonary arterial wave intensity analysis in fetal lambs: evidence for cyclical, midsystolic pulmonary vasoconstriction

2008 ◽  
Vol 294 (5) ◽  
pp. R1554-R1562 ◽  
Author(s):  
Joseph J. Smolich ◽  
Jonathan P. Mynard ◽  
Daniel J. Penny
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Compression Wave ◽  
Main Pulmonary Artery ◽  
Pulmonary Trunk ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

The physiological basis of a characteristically low blood flow to the fetal lungs is incompletely understood. To determine the potential role of pulmonary vascular interaction in this phenomenon, simultaneous wave intensity analysis (WIA) was performed in the pulmonary trunk (PT) and left pulmonary artery (LPA) of 10 anesthetized late-gestation fetal sheep instrumented with PT and LPA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity ( U). Studies were performed at rest and during brief complete occlusion of the ductus arteriosus to augment pulmonary vasoconstriction ( n = 4) or main pulmonary artery to abolish wave transmission from the lungs ( n = 3). Wave intensity (d IW) was calculated as the product of the P and U rates of change. Forward and backward components of d IW were determined after calculation of wave speed. PT and LPA WIA displayed an early systolic forward compression wave (FCWis) increasing P and U, and a late systolic forward expansion wave decreasing P and U. However, a marked midsystolic fall in LPA U to near-zero was related to an extremely prominent midsystolic backward compression wave (BCWms) that arose ∼5 cm distal to the LPA, was threefold larger than the PT BCWms ( P < 0.001), of similar size to FCWis at rest ( P > 0.6), larger than FCWis following ductal occlusion ( P < 0.05) and abolished after main pulmonary artery occlusion. These findings suggest that the absence of pulmonary arterial midsystolic forward flow which accompanies a low fetal lung blood flow is due to a BCWms generated in part by cyclical vasoconstriction within the pulmonary microcirculation.

Pulmonary arterial distension does not cause pulmonary vasoconstriction

1986 ◽  
Vol 61 (2) ◽  
pp. 741-745 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Artery ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Main Pulmonary Artery ◽  
Pulmonary Vasoconstriction ◽  
Balloon Distension ◽  
Pressor Responses ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Arterial Branch

Distension of the main pulmonary artery or its major branches with an intraluminal balloon has been reported to cause pulmonary vasoconstriction by an unknown mechanism. This study was an attempt to confirm the pressor response and explore its cause. Several balloon distension methods were tried and discarded because they caused unintentional obstruction. Ultimately, I inflated a balloon placed retrogradely and confined to the left main pulmonary artery of six anesthetized open-chest dogs after ligating left lobar arterial branches. Blood flow and systemic gas composition were controlled by interposing an external pump oxygenator between the left ventricle and aorta. Pressures in the aorta, main pulmonary artery, and left atrium were recorded. Alveolar hypoxia was used as an independent test of pulmonary vasoreactivity. Although hypoxic pressor responses occurred, challenges with arterial distension did not change lung perfusion pressure. Silicone rubber casts were made of the arteries of six dogs used in pilot experiments. These revealed the limited lengths in which distenders can be placed without unintentional encroachment on flow. I could not support the conclusion that arterial distension causes vasoconstriction and am suspicious that the perfusion pressure increases reported by others may have been caused by undetected obstruction of a major arterial branch.

Effect of endotoxemia on hypoxic pulmonary vasoconstriction in unanesthetized sheep

1985 ◽  
Vol 58 (5) ◽  
pp. 1463-1468 ◽  
Author(s):  
A. A. Hutchison ◽  
M. L. Ogletree ◽  
J. R. Snapper ◽  
K. L. Brigham
Keyword(s):  
Escherichia Coli ◽  
Carotid Artery ◽  
Pulmonary Artery ◽  
Jugular Vein ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Main Pulmonary Artery ◽  
Base Line ◽  
Pulmonary Vasoconstriction ◽  
The Mean ◽  
Lung Lymph

This study examined the effect of acute endotoxemia on hypoxic pulmonary vasoconstriction (HPV) in awake sheep. Thirteen sheep were chronically instrumented with Silastic catheters in the pulmonary artery, left atrium, jugular vein, and carotid artery; with a Swan-Ganz catheter in the main pulmonary artery; with a chronic lung lymph fistula; and with a tracheostomy. Base-line HPV was determined by measuring the change in pulmonary vascular resistance (PVR) while sheep breathed 12% O2 for 7 min. Concentrations of immunoreactive 6-keto-PGF1 alpha and thromboxane B2 (TXB2) were measured in lung lymph during the hypoxic challenge. Escherichia coli endotoxin (0.2–0.5 micrograms/kg) was infused intravenously. Four hours after endotoxemia, HPV was measured. In five sheep, meclofenamate was infused at 4.5 h after endotoxemia and HPV measured again. During the base-line hypoxic challenge, PVR increased by 36 +/- 9% (mean +/- SE). There was no significant change in lung lymph 6-keto-PGF1 alpha or TXB2 levels with hypoxia. Twelve of the 13 sheep showed a decrease in HPV 4 h after endotoxemia; the mean change in PVR with hypoxia was -8 +/- 5%, which was significantly (P less than 0.05) reduced compared with base-line HPV. The infusion of meclofenamate at 4.5 h after endotoxin did not restore HPV.

scholarly journals Influence of group B streptococci on piglet pulmonary artery response to bradykinin

1999 ◽  
Vol 86 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Richard M. Whitehurst ◽  
Rachel Laskey ◽  
Ronald N. Goldberg ◽  
Donald Herbert ◽  
Cornelius Van Breemen
Keyword(s):  
Pulmonary Artery ◽  
Contractile Response ◽  
Isometric Force ◽  
Control Group ◽  
Relaxed Controls ◽  
Vascular Response ◽  
Group B Streptococci ◽  
Resting Tension ◽  
Neonatal Group ◽  
Group B

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with N G-nitro-l-arginine methyl ester (l-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group ( P = 0.034) at a concentration of 10−5 M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls ( P < 0.001). BK (10−6 M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls ( P < 0.001), and preincubation withl-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.

scholarly journals Pulmonary atresia with a ventricular septal defect and left pulmonary artery discontinuity: a case report 

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Hyun-Hwa Cha ◽  
Hae Min Kim ◽  
Won Joon Seong
Keyword(s):  
Pulmonary Artery ◽  
Subclavian Artery ◽  
Septal Defect ◽  
Left Subclavian Artery ◽  
Ductus Arteriosus ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Pulmonary Atresia ◽  
Left Pulmonary Artery ◽  
Right Pulmonary Artery

Abstract Background Unilateral pulmonary artery discontinuity is a rare malformation that is associated with other intracardiac abnormalities. Cases accompanied by other cardiac abnormalities are often missed on prenatal echocardiography. The prenatal diagnosis of isolated unilateral pulmonary artery discontinuity can also be delayed. However, undiagnosed this malformation would have an effect on further prognosis. We report our case of a prenatal diagnosis of pulmonary atresia with ventricular septal defect and left pulmonary artery discontinuity. Case presentation A 33-year-old Asian woman visited our institution at 24 weeks of gestation because of suspected fetal congenital heart disease. Fetal echocardiography revealed a small atretic main pulmonary artery giving rise to the right pulmonary artery without bifurcation and the left pulmonary artery arising from the ductus arteriosus originating from the left subclavian artery. The neonate was delivered by cesarean section at 376/7 weeks of gestation. Postnatal echocardiography and multidetector computed tomography showed a right aortic arch, with the small right pulmonary artery originating from the atretic main pulmonary artery and the left pulmonary artery originating from the left subclavian artery. Patency of the ductus arteriosus from the left subclavian artery was maintained with prostaglandin E1. Right ventricular outflow tract reconstruction and pulmonary angioplasty with Gore-Tex graft patch was performed 25th day after birth. Unfortunately, the neonate died because of right heart failure 8 days postoperation. Conclusion There is a possibility that both pulmonary arteries do not arise from the same great artery (main pulmonary artery or common arterial trunk). Therefore, clinicians should check the origin of both pulmonary arteries.

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