Direct Effects of Ouabain on the Pulmonary Vasculature and its Enhancement of the Vasoconstrictor Response to Hypoxia1

2015 ◽  
pp. 273-284 ◽  
Author(s):  
F. Haas ◽  
W. M. Foster ◽  
E. H. Bergofsky
Keyword(s):  
Pulmonary Vasculature ◽  
Direct Effects ◽  
Vasoconstrictor Response

Characterization of endothelin receptors in newborn piglet lung

1995 ◽  
Vol 268 (4) ◽  
pp. L607-L614 ◽  
Author(s):  
T. Perreault ◽  
J. Baribeau
Keyword(s):  
Perfusion Pressure ◽  
Late Onset ◽  
Pulmonary Vasculature ◽  
Binding Studies ◽  
Vasoconstrictor Response ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Constrictor Response ◽  
Arteries And Veins

Endothelins (ET-1, ET-2, and ET-3) cause dilation and constriction as a result of binding to different ET receptors. ETA receptor is responsible for the vasoconstrictor response, while ETB receptors lead to vasodilation (ETB1) or vasoconstriction (ETB2). Although the effects of ETs have been described in the neonatal pulmonary vasculature, ET receptors have not been characterized extensively. Therefore, in newborn piglets we aimed to characterize ET receptors by studying 1) in isolated perfused lungs the effects of ET-1, ET-3, and the ETB receptor agonists sarafotoxin S6c (S6c) and BQ-3020 on perfusion pressure with or without an ETA antagonist, BQ-123, or an ETB1 antagonist, RES-701-1, and 2) the concentration-dependence of ET-1 and ET-3 on their binding to microsomes from arteries and veins of piglet lungs. ET-1, ET-3, S6c, and BQ-3020 cause an early-onset dilation followed by a late-onset constriction. The dilator response to ET-3 is blunted by RES-701-1 (P < 0.005), while the inhibition of the dilator response of ET-1 almost reaches significance (P = 0.06). BQ-123 inhibits incompletely (P < 0.05) the constrictor response to ET-1, while it does not alter the response to ET-3. This suggests that constriction may follow binding to ETA as well as ETB2 receptors. Binding studies reveal that ET receptors are abundant in pulmonary vessels. ETA receptors are predominant, but ETB1 and likely ETB2 receptors are also present. Also, receptor affinities are higher in veins than in arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral chemoreceptor modulation of the pulmonary vasculature in the cat

1992 ◽  
Vol 73 (1) ◽  
pp. 20-29 ◽  
Author(s):  
R. S. Fitzgerald ◽  
G. A. Dehghani ◽  
J. S. Sham ◽  
M. Shirahata ◽  
W. A. Mitzner
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Significant Rise ◽  
Aortic Flow ◽  
Pulmonary Vasculature ◽  
Peripheral Chemoreceptor ◽  
Pulmonary Vasodilation ◽  
Vasoconstrictor Response ◽  
Pulmonary Arterial ◽  
Stimulation Of

The present study was undertaken to determine whether stimulation of the carotid and aortic bodies (cb and ab) could affect the pulmonary vasculature. Our hypothesis was that each promoted vasodilation and thus could modulate the pulmonary vasoconstrictor response to hypoxia. The experimental design of the first set of experiments took advantage of the facts that 1) the ab, but not the cb, increases its neural output in response to CO, whereas both respond to a decreased arterial PO2 (hypoxic hypoxia, HH) and 2) the aortic nerves in cats are easily transected. Hence, both cb and ab sent neural activity to the brain stem when the intact cat was exposed to 10% O2 in N2. Only the ab sent information during CO hypoxia (COH intact). Only the cb did so during HH in the cat in which the aortic nerves had been transected, removing the aortic body (HH abr); neither ab nor cb did so during COH abr. Fifteen anesthetized paralyzed artificially ventilated cats were fit with catheters in the femoral artery and vein, right and left atria, left ventricle, and pulmonary artery and with an aortic flow probe. In the HH intact and HH abr conditions, there was a significant rise in cardiac output, whereas pulmonary arterial pressure (Ppa) rose initially but then leveled off while cardiac output continued to rise. During the 15-min exposure to HH, pulmonary vascular resistance [PVR = (Ppa - Pla)/cardiac output, where Pla is left atrial pressure] rose initially and then decreased significantly at 2–3 min. In response to COH, PVR showed only a significant decrease. In the second set of experiments, seven cats were instrumented as above and had loops placed in the common carotid arteries for selectively perfusing the cbs. In response to a brief infusion of venous blood mixed with 0.3–0.5 micrograms NaCN, which selectively stimulated only the cb, aortic flow remained relatively constant while heart rate and Ppa - alveolar pressure difference decreased significantly; so also did PVR. These data are consistent with the hypothesis that stimulation of the ab and cb singly or together can provoke a significant pulmonary vasodilation in the anesthetized paralyzed artificially ventilated cat.

Effect of protein kinase C inhibition on hypoxic pulmonary vasoconstriction

2001 ◽  
Vol 280 (5) ◽  
pp. L888-L895 ◽  
Author(s):  
Scott A. Barman
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasculature ◽  
Kinase C ◽  
Vasoconstrictor Response ◽  
Voltage Dependent

The current study was done to test the hypothesis that protein kinase C (PKC) inhibitors prevent the increase in pulmonary vascular resistance and compliance that occurs in isolated, blood-perfused dog lungs during hypoxia. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. Hypoxia significantly increased pulmonary arterial resistance, pulmonary venous resistance, and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. The nonspecific PKC inhibitor staurosporine (10−7 M), the specific PKC blocker calphostin C (10−7 M), and the specific PKC isozyme blocker Gö-6976 (10−7 M) inhibited the effect of hypoxia on pulmonary vascular resistance and compliance. In addition, the PKC activator thymeleatoxin (THX; 10−7 M) increased pulmonary vascular resistance and compliance in a manner similar to that in hypoxia, and the L-type voltage-dependent Ca2+channel blocker nifedipine (10−6 M) inhibited the response to both THX and hypoxia. These results suggest that PKC inhibition blocks the hypoxic pressor response and that the pharmacological activation of PKC by THX mimics the hypoxic pulmonary vasoconstrictor response. In addition, L-type voltage-dependent Ca2+channel blockade may prevent the onset of the hypoxia- and PKC-induced vasoconstrictor response in the canine pulmonary vasculature.

Effects of static and fluctuating airway pressure on intact pulmonary circulation

1986 ◽  
Vol 60 (1) ◽  
pp. 114-122 ◽  
Author(s):  
B. P. Fuhrman ◽  
D. L. Smith-Wright ◽  
T. J. Kulik ◽  
J. E. Lock
Keyword(s):  
Pulmonary Circulation ◽  
Airway Pressure ◽  
Intact Animal ◽  
Left Lung ◽  
Pulmonary Vasculature ◽  
Direct Effects ◽  
Independent Measurement ◽  
Lung Blood Flow ◽  
Alpha Chloralose ◽  
Pressure Changes

The direct effects on the pulmonary circulation of static and fluctuation airway pressure were compared in intact close-chest infant lambs with reactive pulmonary vasculature under alpha-chloralose anesthesia. A preparation developed to permit independent ventilation of right and left lungs and independent measurement of right and left lung blood flow was employed to separate direct from indirect effects of unilateral airway pressure changes on pulmonary vascular resistance (PVR). Both static and fluctuating unilateral airway pressure interventions directly elevated ipsilateral PVR. For purposes of comparison mean alveolar pressure (PA) was estimated for both static and fluctuating trials. Fluctuating interventions increased PVR more than did static trials at comparable levels of PA. Substantially less PA was needed to double ipsilateral PVR by fluctuating than by static interventions (16 vs. 26 mmHg, respectively). These data indicate that, in the intact animal with reactive pulmonary vasculature, both PA and the waveform of airway pressure applied can influence PVR.

Potentiation of pulmonary vasoconstrictor response with repeated intermittent hypoxia

1977 ◽  
Vol 43 (4) ◽  
pp. 662-667 ◽  
Author(s):  
M. Unger ◽  
M. Atkins ◽  
W. A. Briscoe ◽  
T. K. King
Keyword(s):  
Pulmonary Artery ◽  
Blood Gases ◽  
Systemic Blood Pressure ◽  
Repeated Exposure ◽  
Pulmonary Vasculature ◽  
Hypoxic Exposure ◽  
Base Line ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Vasoconstrictor Response

To determine the consistency of the pulmonary vasoconstrictor response to hypoxia, dogs were anesthetized, intubated, and ventilated alternately with air and 10% oxygen. Catheters were placed in the pulmonary artery for measurement of pulmonary artery pressure (PAP), pulmonary capillary wedge pressure, and cardiac output and in the femoral artery for monitoring systemic blood pressure and arterial blood gases. Arterial PCO2 and pH were kept at steady levels throughout by ventilating the dogs with a respirator so that only the isolated effect of hypoxia on the pulmonary vasculature was studied. It was found that there was a progressive rise in the PAP with repeated exposure to the same hypoxic stimulus. In 12 dogs, the mean increase in the PAP was 28% above the base line on the 1st hypoxic exposure, rising to 99% by the 10th exposure over the course of 5 h. It was concluded that interpretation of action of agents blocking or enhancing the hypoxic response must take into account this inherent potentiation of the response on repeated exposure to hypoxia.

scholarly journals Direct Effects of Cigarette Smoke in Pulmonary Arterial Cells alter Vascular Tone through Arterial Remodeling and Kv7.4 Channel Dysregulation

2019 ◽  
Author(s):  
J Sevilla-Montero ◽  
D Labrousse-Arias ◽  
C Fernández-Pérez ◽  
B Barreira ◽  
G Mondejar-Parreño ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Molecular Mechanisms ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Chronic Obstructive ◽  
Proliferative Potential ◽  
Direct Effects ◽  
Obstructive Pulmonary Disease ◽  
Cell Contractility ◽  
Pulmonary Arterial

AbstractChronic obstructive pulmonary disease (COPD) is a widespread disease, with no curative therapies nowadays. Exposure to cigarette smoking is considered the chief leading cause of COPD. Current drugs therapies improve patient quality of life, however they do not revert the progression of the disease. Therefore, a deeper study of the cellular and molecular mechanisms that underlie this pathology is required to be able to carry out targeted and effective treatments. Although the effects of cigarette smoke in the progressive deterioration of the airway have been extensively studied in COPD patients, its effects on pulmonary vasculature have been unexplored, due to the classic conception that vascular damage is a consequence of alveolar hypoxia and loss of capillary bed. In this paper, we aimed to study the effects of cigarette smoke extract (CSE) in regulating pulmonary arterial cells phenotypic modulation, in particular the effects in fibroblasts (hPAFib) and smooth muscle cells (hPASMC), and in murine pulmonary arteries. Our results demonstrated that CSE exposure had direct effects on hPAFib and hPASMC, promoting a senescent phenotype that in turn contributed, through the secretion of inflammatory molecules, to increase the proliferative potential of non-exposed cells. CSE also increased total ROS levels in hPAFib and hPASMC, and upregulated NADPH oxidase subunits NOX1 and p22phox. Most importantly, CSE affected cell contractility and dysregulated the expression and activity of voltage-gated K+ channel Kv7.4. This contributed to limit vascular responses impairing vasoconstriction and endothelium-dependent and independent relaxation.

Cardiopulmonary effects of unilateral airway pressure changes in intact infant lambs

1984 ◽  
Vol 56 (5) ◽  
pp. 1439-1448 ◽  
Author(s):  
B. P. Fuhrman ◽  
J. Everitt ◽  
J. E. Lock
Keyword(s):  
Blood Flow ◽  
Airway Pressure ◽  
Left Lung ◽  
Right Atrial ◽  
Pulmonary Vasculature ◽  
Direct Effects ◽  
Vascular Effects ◽  
Lung Blood Flow ◽  
End Tidal ◽  
Pressure Changes

Direct effects of airway pressure changes on the pulmonary vascular bed of the intact infant lamb were studied under chloralose anesthesia using a preparation developed to permit independent ventilation of right and left lungs and independent measurement of right and left lung blood flow. A specially designed endobronchial tube eliminated the need for thoracotomy the day of study. Unilateral changes in positive end-expiratory pressure (PEEP) during volume-regulated ventilation increased ipsilateral but not contralateral airway pressure, confirming adequate separation of right and left lungs and suggesting rigidity of the mediastinum. Such interventions ( UPEEP ) at levels of 5, 10, and 15 cmH2O reduced ipsilateral but not contralateral pulmonary blood flow (by 10, 25, and 46%, respectively) but did not alter end-tidal PCO2 of either lung. UPEEP had less effect on cardiac output, stroke volume, right atrial, left atrial, esophageal, and pulmonary arterial pressures than did PEEP applied to both lungs. Because this preparation separates the predominantly direct effects of UPEEP on the ipsilateral lung from its indirect effects on the contralateral lung, it is well suited to studies of direct pulmonary vascular effects of airway pressure changes in an intact closed-chest preparation with reactive pulmonary vasculature.

Direct effects of hCG on the human endometrium

1998 ◽  
Vol 5 (1) ◽  
pp. 109A-109A ◽  
Author(s):  
R FANCHIN ◽  
E PELTIER ◽  
C RIGHINI ◽  
F OLIVENNES ◽  
R FRYDMAN ◽  
...  
Keyword(s):  
Human Endometrium ◽  
Direct Effects

Childhood Intelligence Predicts Adult Trait Openness

2016 ◽  
Vol 37 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Adrian Furnham ◽  
Helen Cheng
Keyword(s):  
Structural Equation Modeling ◽  
Structural Equation ◽  
Social Background ◽  
Study Data ◽  
Equation Modeling ◽  
Direct Effects ◽  
Data Set ◽  
National Child Development Study ◽  
Nationally Representative ◽  
The Uk

Abstract. This study used a longitudinal data set of 5,672 adults followed for 50 years to determine the factors that influence adult trait Openness-to-Experience. In a large, nationally representative sample in the UK (the National Child Development Study), data were collected at birth, in childhood (age 11), adolescence (age 16), and adulthood (ages 33, 42, and 50) to examine the effects of family social background, childhood intelligence, school motivation during adolescence, education, and occupation on the personality trait Openness assessed at age 50 years. Structural equation modeling showed that parental social status, childhood intelligence, school motivation, education, and occupation all had modest, but direct, effects on trait Openness, among which childhood intelligence was the strongest predictor. Gender was not significantly associated with trait Openness. Limitations and implications of the study are discussed.

A Moment to Come Together: Personal Reflections on Trayvon Martin

2013 ◽  
Vol 5 (1) ◽  
pp. 131-137
Author(s):  
Roxanne Christensen ◽  
LaSonia Barlow ◽  
Demetrius E. Ford
Keyword(s):  
Civil Rights ◽  
Doctoral Students ◽  
Professional Psychology ◽  
Direct Effects ◽  
The Social ◽  
To Come ◽  
Professional Responses ◽  
The Individual ◽  
Personal Reflections ◽  
Unique Individual

Three personal reflections provided by doctoral students of the Michigan School of Professional Psychology (Farmington Hills, Michigan) address identification of individual perspectives on the tragic events surrounding Trayvon Martin’s death. The historical ramifications of a culture-in-context and the way civil rights, racism, and community traumatization play a role in the social construction of criminals are explored. A justice orientation is applied to both the community and the individual via internal reflection about the unique individual and collective roles social justice plays in the outcome of these events. Finally, the personal and professional responses of a practitioner who is also a mother of minority young men brings to light the need to educate against stereotypes, assist a community to heal, and simultaneously manage the direct effects of such events on youth in society. In all three essays, common themes of community and growth are addressed from varying viewpoints. As worlds collided, a historical division has given rise to a present unity geared toward breaking the cycle of violence and trauma. The authors plead that if there is no other service in the name of this tragedy, let it at least contribute to the actualization of a society toward growth and healing.

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