Action of carbon dioxide on hypoxic pulmonary vasoconstriction in the rat lung

1993 ◽  
Vol 21 (5) ◽  
pp. 740-746 ◽  
Author(s):  
SIMON V. BAUDOUIN ◽  
TIMOTHY W. EVANS
Keyword(s):  
Carbon Dioxide ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction

Metabolic and respiratory hydrogen ion effects on hypoxic pulmonary vasoconstriction

1984 ◽  
Vol 57 (2) ◽  
pp. 545-550 ◽  
Author(s):  
C. Marshall ◽  
L. Lindgren ◽  
B. E. Marshall
Keyword(s):  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Regression Equations ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Ion Effects

Hypoxic pulmonary vasoconstriction (HPV) was studied in the ventilated-perfused rat lung in vitro. Respiratory acidosis and alkalosis were obtained by ventilating with 2, 7, or 10% CO2 (21% O2-balance N2). Metabolic acidosis and alkalosis were produced by the addition of 0.9 N NaHCO3 or 1 N lactic acid to the perfusate at constant PCO2. At each pH the pressor responses to 2 and 4% O2 were compared with the maximum pressor response (R%max) obtained with zero O2 and 5% CO2 at a normal pH (approximately 7.35). HPV was maximal when the [H+] was between 38 and 50 nM and was attenuated by changes of pH in either direction. Both respiratory and metabolic pH changes had similar effects. The combined linear regression equations were as follows: with 2% O2 the response to acidosis was R%max = 101.37 – 0.52 [H+] and to alkalosis was R%max = 2.03 [H+] - 3.85; with 4% O2 the response to acidosis was R%max = 56.88 – 0.3 [H+] and to alkalosis was R%max = 1.16 [H+] - 4.95. These effects were not due to changes of ionized calcium.

Effect of tumor necrosis factor on hypoxic pulmonary vasoconstriction

1992 ◽  
Vol 72 (3) ◽  
pp. 1044-1049 ◽  
Author(s):  
S. F. Liu ◽  
A. Dewar ◽  
D. E. Crawley ◽  
P. J. Barnes ◽  
T. W. Evans
Keyword(s):  
Endothelial Dysfunction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Detectable Effect ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Endothelium Dependent Relaxation ◽  
Necrosis Factor ◽  
Lung Preparation

The effects of tumor necrosis factor (TNF) on hypoxic pulmonary vasoconstriction (HPV) and endothelium-dependent relaxation were examined in a blood-perfused rat lung preparation. Lungs from TNF-treated rats (0.26 mg/kg iv 12 h before experimentation) had a significantly greater HPV and a reduced vasorelaxant response to the endothelium-dependent vasodilator acetylcholine (ACh) but a similar vasorelaxant response to the endothelium-independent vasodilator nitroprusside compared with lungs from control rats (pretreated with 0.1 ml saline iv). Pentoxifylline (20 mg/kg iv and ip 20 min before administration of TNF) had no detectable effect on either HPV or ACh-induced relaxation but completely negated the augmentation on HPV and the inhibiting action on ACh-induced relaxation caused by TNF. The TNF effect on ACh relaxation was unaffected by pretreatment with L-arginine. These results indicate that TNF induces endothelial dysfunction and enhances HPV, effects that are inhibited by pentoxifylline.

The Respiratory System

2019 ◽  
Author(s):  
Zerlina Wong ◽  
Michael Nurok
Keyword(s):  
Carbon Dioxide ◽  
Respiratory System ◽  
Airway Resistance ◽  
Respiratory Mechanics ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lung Compliance ◽  
The Body ◽  
Elastic Recoil ◽  
Carbon Dioxide Transport ◽  
Pulmonary Vasoconstriction

The pulmonary system is crucial for survival. Managing respiratory mechanics and airway requires a sophisticated understanding of pulmonary physiology. This chapter discusses the ways in which oxygen is brought into the body and carbon dioxide is expelled and reviews the principles of respiratory mechanics, including lung compliance, airway resistance, chemoreceptor and mechanoreceptor control of ventilation, hypoxic pulmonary vasoconstriction, distribution of perfusion, and other properties that affect oxygen and carbon dioxide transport. The respiratory system exists in a state of equilibrium, where the inward elastic recoil of the lungs is balanced with the outward elastic recoil of the chest wall. Airway resistance and compliance are important factors that affect ventilation and air movement. This chapter reviews the role that chemoreceptors and mechanoreceptors have on controlling ventilation, as well as the effects that hypercarbia and hypoxemia have on pulmonary and cerebral circulation, and the Bohr and Haldane effects that elucidate understanding of the hemoglobin dissociation curve. These principles all inform the care of patients who require mechanical ventilation, as we endeavor to support them through their surgery or intensive care stay. This review contains 7 figures and 38 references. Key Words: apneic oxygenation, Bohr effect, chemoreceptors, compliance, Haldane effect, hypoxic pulmonary vasoconstriction, resistance, respiratory mechanics, ventilation-perfusion

Precursors and inhibitors of hydrogen sulfide synthesis affect acute hypoxic pulmonary vasoconstriction in the intact lung

2012 ◽  
Vol 112 (3) ◽  
pp. 411-418 ◽  
Author(s):  
Jane A. Madden ◽  
Susan B. Ahlf ◽  
Mark W. Dantuma ◽  
Kenneth R. Olson ◽  
David L. Roerig
Keyword(s):  
Hydrogen Sulfide ◽  
Arterial Pressure ◽  
Lung Tissue ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Tissue Homogenate ◽  
Rat Lung ◽  
Western Blots ◽  
Pulmonary Vasoconstriction

The effects of hydrogen sulfide (H2S) and acute hypoxia are similar in isolated pulmonary arteries from various species. However, the involvement of H2S in hypoxic pulmonary vasoconstriction (HPV) has not been studied in the intact lung. The present study used an intact, isolated, perfused rat lung preparation to examine whether adding compounds essential to H2S synthesis or to its inhibition would result in a corresponding increase or decrease in the magnitude of HPV. Western blots performed in lung tissue identified the presence of the H2S-synthesizing enzymes, cystathionine γ-lyase (CSE) and 3-mercaptopyruvate sulfur transferase (3-MST), but not cystathionine β-synthase (CBS). Adding three H2S synthesis precursors, cysteine and oxidized or reduced glutathione, to the perfusate significantly increased peak arterial pressure during hypoxia compared with control ( P < 0.05). Adding α-ketoglutarate to enhance the 3-MST enzyme pathway also resulted in an increase ( P < 0.05). Both aspartate, which inhibits the 3-MST synthesis pathway, and propargylglycine (PPG), which inhibits the CSE pathway, significantly reduced the increases in arterial pressure during hypoxia. Diethylmaleate (DEM), which conjugates sulfhydryls, also reduced the peak hypoxic arterial pressure at concentrations >2 mM. Finally, H2S concentrations as measured with a specially designed polarographic electrode decreased markedly in lung tissue homogenate and in small pulmonary arteries when air was added to the hypoxic environment of the measurement chamber. The results of this study provide evidence that the rate of H2S synthesis plays a role in the magnitude of acute HPV in the isolated perfused rat lung.

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