scholarly journals The relationship between hypoxic pulmonary vasoconstriction and arterial oxygen tension in the intact dog.

1983 ◽  
Vol 338 (1) ◽  
pp. 61-74 ◽  
Author(s):  
C H Orchard ◽  
R Sanchez de Leon ◽  
M K Sykes
Keyword(s):  
Oxygen Tension ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Pulmonary Vasoconstriction ◽  
The Relationship

PERIODIC BREATHING AND APNEA IN PRETERM INFANTS. II. HYPOXIA AS A PRIMARY EVENT

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 219-228
Author(s):  
Henrique Rigatto ◽  
June P. Brady
Keyword(s):  
Preterm Infants ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Blood Gases ◽  
Periodic Breathing ◽  
Capillary Blood ◽  
Arterial Oxygen ◽  
Primary Event ◽  
The Relationship

We studied nine healthy preterm infants during the first 35 days of life to define the relationship between periodic breathing, apnea, and hypoxia. For this purpose we compared ventilation/apnea (V/A), minute ventilation, and alveolar and capillary blood gases during periodic breathing induced by hypoxia and during spontancous periodic breathing in room air. We induced periodic breathing by giving the baby in sequence 21, 19, 17, and 15% O2 to breathe for 5 minutes each, and also by giving 21, 15, and 21% O2. We measured ventilation with a nosepiece and a screen flowmeter. With a decrease in arterial oxygen tension, preterm infants (1) hypoventilated, (2) breathed periodically more frequently, and (3) showed a decrease in V/A due to an increase in the apneic interval. In one baby this led to apnea lasting 30 seconds. These findings support our hypothesis that preterm infants breathing periodically hypoventilate and suggest that hypoxia may be a primary event leading to periodic breathing and apnea.

Congenital NOS2 deficiency prevents impairment of hypoxic pulmonary vasoconstriction in murine ventilator-induced lung injury

2007 ◽  
Vol 293 (5) ◽  
pp. L1300-L1305 ◽  
Author(s):  
Rong Liu ◽  
Yukako Hotta ◽  
Amanda R. Graveline ◽  
Oleg V. Evgenov ◽  
Emmanuel S. Buys ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Left Lung ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Lung Edema ◽  
Wild Type ◽  
Ventilator Induced Lung Injury ◽  
Pulmonary Vasoconstriction

Hypoxic pulmonary vasoconstriction (HPV) preserves systemic arterial oxygenation during lung injury by diverting blood flow away from poorly ventilated lung regions. Ventilator-induced lung injury (VILI) is characterized by pulmonary inflammation, lung edema, and impaired HPV leading to systemic hypoxemia. Studying mice congenitally deficient in inducible nitric oxide synthase (NOS2) and wild-type mice treated with a selective NOS2 inhibitor, l- N6-(1-iminoethyl)lysine (l-NIL), we investigated the contribution of NOS2 to the impairment of HPV in anesthetized mice subjected to 6 h of either high tidal volume (HVT) or low tidal volume (LVT) ventilation. HPV was estimated by measuring the changes of left lung pulmonary vascular resistance (LPVR) in response to left mainstem bronchus occlusion (LMBO). LMBO increased the LPVR similarly in wild-type, NOS2−/−, and wild-type mice treated with l-NIL 30 min before commencing 6 h of LVT ventilation (96% ± 30%, 103% ± 33%, and 80% ± 16%, respectively, means ± SD). HPV was impaired in wild-type mice subjected to 6 h of HVT ventilation (23% ± 16%). In contrast, HPV was preserved after 6 h of HVT ventilation in NOS2−/− and wild-type mice treated with l-NIL either 30 min before or 6 h after commencing HVT ventilation (66% ± 22%, 82% ± 29%, and 85% ± 16%, respectively). After 6 h of HVT ventilation and LMBO, systemic arterial oxygen tension was higher in NOS2−/− than in wild-type mice (192 ± 11 vs. 171 ± 17 mmHg; P < 0.05). We conclude that either congenital NOS2 deficiency or selective inhibition of NOS2 protects mice from the impairment of HPV occurring after 6 h of HVT ventilation.

Hypoxic Pulmonary Vasoconstriction in Nonventilated Lung Areas Contributes to Differences in Hemodynamic and Gas Exchange Responses to Inhalation of Nitric Oxide 

1997 ◽  
Vol 86 (6) ◽  
pp. 1254-1261 ◽  
Author(s):  
Albert Benzing ◽  
Georg Mols ◽  
Thomas Brieschal ◽  
Klaus Geiger
Keyword(s):  
Nitric Oxide ◽  
Gas Exchange ◽  
Oxygen Tension ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Arterial Oxygen ◽  
Mixed Venous Blood ◽  
Respiratory Response ◽  
Pulmonary Vasoconstriction ◽  
Wide Range ◽  
Mixed Venous

Background Enhancement of hypoxic pulmonary vasoconstriction (HPV) in nonventilated lung areas by almitrine increases the respiratory response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS). Therefore the authors hypothesized that inhibition of HPV in nonventilated lung areas decreases the respiratory effects of NO. Methods Eleven patients with severe ARDS treated by venovenous extracorporeal lung assist were studied. Patients' lungs were ventilated at a fraction of inspired oxygen (F[I(O2)]) of 1.0. By varying extracorporeal blood flow, mixed venous oxygen tension (P[O2]; partial oxygen pressure in mixed venous blood [PV(O2)]) was adjusted randomly to four levels (means, 47, 54, 64 and 84 mmHg). Extracorporeal gas flow was adjusted to prevent changes in mixed venous carbon dioxide tension [PV(CO2)]). Hemodynamic and gas exchange variables were measured at each level before, during, and after 15 ppm NO. Results Increasing PV(O2) from 47 to 84 mmHg resulted in a progressive decrease in lung perfusion pressure (PAP-PAWP; P &lt; 0.05) and pulmnonary vascular resistance index (PVRI; P &lt; 0.05) and in an increase in intrapulmonary shunt (Q[S]/Q[T]; P &lt; 0.05). PV(CO2) and cardiac index did not change. Whereas the NO-induced reduction in PAP-PAWP was smaller at high PV(O2), NO-induced decrease in Q(S)/Q(T) was independent of baseline PV(O2). In response to NO, arterial P(O2) increased more and arterial oxygen saturation increased less at high compared with low PV(O2). Conclusion In patients with ARDS, HPV in nonventilated lung areas modifies the hemodynamic and respiratory response to NO. The stronger the HPV in nonventilated lung areas the more pronounced is the NO-induced decrease in PAP-PAWP. In contrast, the NO-induced decrease in Q(S)/Q(T) is independent of PV(O2) over a wide range of PV(O2) levels. The effect of NO on the arterial oxygen tension varies with the level of PV(O2) by virtue of its location on the oxygen dissociation curve.

Intra-arterial Oxygen Tension Monitoring

1987 ◽  
Vol 25 (3) ◽  
pp. 199-208 ◽  
Author(s):  
STEVEN J. BARKER ◽  
KEVIN K. TREMPER
Keyword(s):  
Oxygen Tension ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen

Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses

1996 ◽  
Vol 23 (2) ◽  
pp. 75-77
Author(s):  
P. Dobromylskyj ◽  
P.M. Taylor ◽  
J.C. Brearley ◽  
C.B. Johnson ◽  
S.P.L. Luna
Keyword(s):  
Oxygen Tension ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen

scholarly journals Impaired hypoxic pulmonary vasoconstriction in a mouse model of Leigh syndrome

2019 ◽  
Vol 316 (2) ◽  
pp. L391-L399 ◽  
Author(s):  
Grigorij Schleifer ◽  
Eizo Marutani ◽  
Michele Ferrari ◽  
Rohit Sharma ◽  
Owen Skinner ◽  
...  
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Inflammation ◽  
Leigh Syndrome ◽  
Arterial Oxygen ◽  
Inborn Errors ◽  
Pulmonary Vasoconstriction ◽  
Progressive Encephalopathy ◽  
Alveolar Hypoxia ◽  
The Impact ◽  
Deficient Mice

Hypoxic pulmonary vasoconstriction (HPV) is a physiological vasomotor response that maintains systemic oxygenation by matching perfusion to ventilation during alveolar hypoxia. Although mitochondria appear to play an essential role in HPV, the impact of mitochondrial dysfunction on HPV remains incompletely defined. Mice lacking the mitochondrial complex I (CI) subunit Ndufs4 ( Ndufs4−/−) develop a fatal progressive encephalopathy and serve as a model for Leigh syndrome, the most common mitochondrial disease in children. Breathing normobaric 11% O2 prevents neurological disease and improves survival in Ndufs4−/− mice. In this study, we found that either genetic Ndufs4 deficiency or pharmacological inhibition of CI using piericidin A impaired the ability of left mainstem bronchus occlusion (LMBO) to induce HPV. In mice breathing air, the partial pressure of arterial oxygen during LMBO was lower in Ndufs4−/− and in piericidin A-treated Ndufs4+/+ mice than in respective controls. Impairment of HPV in Ndufs4−/− mice was not a result of nonspecific dysfunction of the pulmonary vascular contractile apparatus or pulmonary inflammation. In Ndufs4-deficient mice, 3 wk of breathing 11% O2 restored HPV in response to LMBO. When compared with Ndufs4−/− mice breathing air, chronic hypoxia improved systemic oxygenation during LMBO. The results of this study show that, when breathing air, mice with a congenital Ndufs4 deficiency or chemically inhibited CI function have impaired HPV. Our study raises the possibility that patients with inborn errors of mitochondrial function may also have defects in HPV.

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