scholarly journals Tissue hypoxia inhibits prostaglandin and nitric oxide production and prevents ductus arteriosus reopening

2000 ◽  
Vol 279 (1) ◽  
pp. R278-R286 ◽  
Author(s):  
Hiroki Kajino ◽  
Yao-Qi Chen ◽  
Sylvain Chemtob ◽  
Nahid Waleh ◽  
Cameron J. Koch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Concentration ◽  
Ductus Arteriosus ◽  
Tissue Hypoxia ◽  
No Production ◽  
Active Tension ◽  
Tissue Oxygen ◽  
Ambient Oxygen ◽  
Inner Vessel ◽  
Oxygen Concentrations

Regulation of ductus arteriosus (DA) tension depends on a balance between oxygen-induced constriction and PG and nitric oxide (NO)-mediated relaxation. After birth, increasing PaO2 produces DA constriction. However, as the full-term ductus constricts, it develops severe tissue hypoxia in its inner vessel wall (oxygen concentration <0.2%). We used isolated rings of fetal lamb DA to determine why the constricted ductus does not relax and reopen as it becomes hypoxic. We used a modification of the 2-(2-nitro-1 H-imidazol-1-yl)- N-(2,2,3,3,3-pentafluoropropyl) acetamide (EF5) technique (Clyman RI, Chan CY, Mauray F, Chen YQ, Cox W, Seidner SR, Lord EM, Weiss H, Wale N, Evan SM, and Koch CJ. Pediatr Res 45: 19–29, 1999) to determine mean tissue oxygen concentration. A decrease in the ductus' mean tissue oxygen concentration from 1.4 to 0.1% lowers the isometric tone of the ductus by 15 ± 10% of its maximal active tension (the maximal tension that can be produced by the ductus). Although decreases in oxygen concentration diminish ductus tension, most of the vasoconstrictor tone in the ductus is independent of ambient oxygen concentration. This oxygen-independent tone is equivalent to 64 ± 10% of the maximal active tension. At mean tissue oxygen concentrations >0.2%, endogenous PGs and NO inhibit more than 40% of the active tension developed by the ductus. However, when tissue oxygen concentrations drop below 0.2%, the constitutive relaxation of the ductus by endogenous PGs and NO is lost. In the absence of PG and NO production, tension increases to a level normally observed only after treatment of the ductus with indomethacin and nitro-l-arginine methyl ester (inhibitors of PG and NO production). Therefore, under conditions of severe hypoxia (tissue oxygen concentration <0.2% oxygen), the loss of PG- and NO-mediated relaxation more than compensates for the loss of oxygen-induced tension. We hypothesize that this increased ductus tone enables the vessel to remain closed as it undergoes tissue remodeling.

Influence of some factors on oxygen uptake of canine cardiac Purkinje fibers

1963 ◽  
Vol 204 (1) ◽  
pp. 5-8 ◽  
Author(s):  
Kalman Greenspan ◽  
Paul F. Cranefield
Keyword(s):  
Oxygen Uptake ◽  
Oxygen Concentration ◽  
Diffusion Limitation ◽  
Purkinje Fibers ◽  
Ambient Oxygen ◽  
Cardiac Purkinje Fibers ◽  
Lower Oxygen ◽  
Wet Weight ◽  
Oxygen Tensions ◽  
Oxygen Concentrations

The rate of oxygen uptake of quiescent Purkinje fibers of the dog's heart was determined using a flow respirometer and oxygen polarography. At ambient oxygen concentrations of 60% or higher the rate of uptake was 0.739 mm3/mg wet weight per hr at 35 C. The temperature coefficient over the range 25–35° was 2.3. The uptake was independent of the ambient oxygen concentration at oxygen concentrations equal to or greater than 60% of an atmosphere. In lower oxygen concentrations the rate of uptake was found to be depressed. The depression of uptake in the lower oxygen tensions is probably the result of diffusion limitation; it may, however, reflect dependence of resting uptake on oxygen concentration.

Comparative Study on Spray Auto-Ignition of Di-n-Butyl Ether and Diesel Blends at Engine-Like Conditions

2020 ◽  
Vol 143 (4) ◽  
Author(s):  
Yuanhang Guan ◽  
Wang Liu ◽  
Dong Han
Keyword(s):  
Heat Release ◽  
Oxygen Concentration ◽  
Pressure Rise ◽  
Fuel Spray ◽  
Release Rates ◽  
Butyl Ether ◽  
Auto Ignition ◽  
Ambient Oxygen ◽  
Ignition And Combustion ◽  
Oxygen Concentrations

Abstract Di-n-butyl ether (DBE), a promising lignocellulosic biofuel, has been suggested as a potential alternative fuel for compression ignition engines. In this study, the spray auto-ignition characteristics of diesel/DBE blends were experimentally measured on a constant volume combustion chamber. Time-resolved pressure traces and heat release rates in fuel spray combustion were measured at changed fuel blending fractions, ambient temperatures, and oxygen concentrations. Further, ignition delay and combustion delay that evaluates fuel spray ignition tendency were derived and compared for different test blends. Experimental results indicated that fuel spray ignition tendency is promoted with DBE addition, evidenced by the advanced pressure rise and heat release processes, and the shortened ignition and combustion delays. Peak heat release rates are fuel-dependent at high ambient oxygen concentrations since the relative fractions of the premixed and diffusive burns alter with changed DBE addition. However, as the oxygen concentration drops to 11%, fuel effects on the peak heat release rates become less noticeable. Reduced ambient oxygen concentration effectively extends fuel ignition and combustion delays, and typical two-stage pressure rises and heat releases are observed for all test blends, as the oxygen concentration drops to 11%.

Abstract 238: Oxygen Regulates the Flux of Nitric Oxide Diffusion across the Vascular Wall

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Xiaoping Liu ◽  
Parthasarathy Srinivasan ◽  
Eric Collard ◽  
Paula Grajdeanu ◽  
Jay L Zweier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Concentration ◽  
Rate Constant ◽  
Aortic Wall ◽  
Vascular Wall ◽  
Surrounding Tissue ◽  
Diffusion Distance ◽  
First Order ◽  
No Consumption ◽  
Oxygen Concentrations

Endothelium-derived nitric oxide (NO) plays an important role in maintaining vascular tone. It is known that NO may be consumed by heme proteins, superoxide and oxygen during diffusion from the endothelium to smooth muscle cells in the vascular wall. Due to the limitation of available techniques, it is unclear to what extent these consumptions can affect the diffusion distance of NO, and if the vascular NO consumption could serve as a “sensor” of oxygen concentrations in the blood vessels. In this study, rat aortas were used as an experimental model for studying NO diffusion process in the vascular system. A Clark-type NO electrode was used to directly measure the flux of NO diffusion across the vascular wall at 37 °C. A segment of aorta was isolated from a 12-week old WKY rat. After the aorta was cleaned and surrounding tissue was removed, it was longitudinally opened. A specifically-designed aorta holder was attached on the tip of the Clark-type NO electrode. The aorta holder surface and the electrode tip surface were aligned in the same plane so that the opened aorta segment could be placed flat on the electrode tip surface and pinned to the aorta holder. Using this technique, we measured the flux of NO diffusion across the aortic wall at different oxygen concentration. It was observed that the NO flux increased 6 to 10 fold when oxygen concentrations dropped from 200 μM to zero. A mathematical model describing the steady-state diffusion-reaction was used in analyzing the experimental data. It was found that the rate of NO decay is first order with respect to [O 2 ] and first order with respect to [NO], and hence of the form k[O 2 ][NO]. The rate constant k was determined as (3.8±0.4)x10 −3 μM −1 s −1 (n=6). With this rate constant, the half-life of NO in the aortic wall in the presence of 200 μM O 2 (equilibrium with room air) will be 0.9 seconds. Our results show that the flux and diffusion distance of NO in the aortic wall is largely regulated by oxygen concentration. When oxygen concentrations drop, NO diffusion distance will significantly increase. As a result, the blood vessel will dilate to a larger extent to allow more blood to be delivered to the hypoxic tissues. Therefore this vascular NO consumption appears to play the role of an oxygen sensor in the regulation of blood flow in the body.

Evidence for an effector role of endothelin in closure of the ductus arteriosus at birth

1992 ◽  
Vol 70 (7) ◽  
pp. 1061-1064 ◽  
Author(s):  
Flavio Coceani ◽  
Lois Kelsey ◽  
Eric Seidlitz
Keyword(s):  
Oxygen Concentration ◽  
Oxygen Tension ◽  
Ductus Arteriosus ◽  
Critical Role ◽  
Blood Oxygen ◽  
Endothelin 1 ◽  
A Value ◽  
Near Term ◽  
Oxygen Concentrations

The ductus arteriosus is a special muscular shunt that in the fetus allows blood to bypass the unexpanded lungs. It closes rapidly after birth and this event is initiated by the physiologic rise in blood oxygen tension. Endothelin-1 has been proposed by us as a local mediator for oxygen after demonstrating that it is formed within the ductus and is a potent ductus constrictor. To confirm this possibility, we have now measured the release of endothelin-1 from the isolated ductus of near-term fetal lambs at different oxygen concentrations of the medium. In addition, using the same preparation, we have examined the effect on contractile tone of compounds interfering with the synthesis (phosphoramidon, 50 μM) and action (BQ123, 1 μM) of endothelin-1. We report that release of endothelin-1 from the ductus tends to increase with the oxygen concentration up to a value mimicking the neonatal condition. Phosphoramidon and, to a greater degree, BQ123 inhibit the contraction of the vessel to oxygen. These results implicate endothelin-1 as the effector agent for oxygen in the ductus and, by extension, assign to this peptide a critical role in the closure of the vessel at birth.Key words: ductus arteriosus closure, oxygen, endothelin.

Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

2003 ◽  
Vol 94 (5) ◽  
pp. 2058-2067 ◽  
Author(s):  
Gregory M. T. Hare ◽  
C. David Mazer ◽  
William Mak ◽  
Reginald M. Gorczynski ◽  
Kathryn M. Hum ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxygen Delivery ◽  
Tissue Hypoxia ◽  
Tissue Oxygen ◽  
Cerebral Tissue ◽  
Acute Anemia ◽  
Oxide Synthase ◽  
Nos Gene

Severe hemodilutional anemia may reduce cerebral oxygen delivery, resulting in cerebral tissue hypoxia. Increased nitric oxide synthase (NOS) expression has been identified following cerebral hypoxia and may contribute to the compensatory increase in cerebral blood flow (CBF) observed after hypoxia and anemia. However, changes in cerebral NOS gene expression have not been reported after acute anemia. This study tests the hypothesis that acute hemodilutional anemia causes cerebral tissue hypoxia, triggering changes in cerebral NOS gene expression. Anesthetized rats underwent hemodilution when 30 ml/kg of blood were exchanged with pentastarch, resulting in a final hemoglobin concentration of 51.0 ± 1.2 g/l ( n = 7 rats). Caudate tissue oxygen tension (PbrO2 ) decreased transiently from 17.3 ± 4.1 to 14.4 ± 4.1 Torr ( P < 0.05), before returning to baseline after ∼20 min. An increase in CBF may have contributed to restoring PbrO2 by improving cerebral tissue oxygen delivery. An increase in neuronal NOS (nNOS) mRNA was detected by RT-PCR in the cerebral cortex of anemic rats after 3 h ( P < 0.05, n = 5). A similar response was observed after exposure to hypoxia. By contrast, no increases in mRNA for endothelial NOS or interleukin-1β were observed after anemia or hypoxia. Hemodilutional anemia caused an acute reduction in PbrO2 and an increase in cerebral cortical nNOS mRNA, supporting a role for nNOS in the physiological response to acute anemia.

Chronic hypertension impairs flow-induced vasodilation and augments the myogenic response in fetal lung

2002 ◽  
Vol 282 (1) ◽  
pp. L56-L66 ◽  
Author(s):  
Laurent Storme ◽  
Thomas A. Parker ◽  
John P. Kinsella ◽  
Robyn L. Rairigh ◽  
Steven H. Abman
Keyword(s):  
Nitric Oxide ◽  
Ductus Arteriosus ◽  
Fetal Lung ◽  
No Synthase ◽  
Chronic Hypertension ◽  
No Production ◽  
Myogenic Response ◽  
Hemodynamic Effects ◽  
No Signaling ◽  
Synthase Inhibitor

We hypothesized that altered vasoreactivity in perinatal pulmonary hypertension (PH) is characterized by abnormal responses to hemodynamic stress, including the loss of flow-induced vasodilation and an augmented myogenic response. Therefore, we studied the acute hemodynamic effects of brief compression of the ductus arteriosus (DA) in control fetal lambs and in lambs during exposure to chronic PH. In both groups, acute DA compression decreased pulmonary vascular resistance (PVR) by 20% at baseline ( day 0). After 2 days of hypertension, acute DA compression paradoxically increased PVR by 50% in PH lambs, whereas PVR decreased by 25% in controls. During the 8-day study period, PVR increased during acute DA compression in PH lambs, whereas acute DA compression continued to cause vasodilation in controls. Brief treatment with the nitric oxide (NO) synthase inhibitor nitro-l-arginine (l-NA) increased basal PVR in control but not PH lambs, suggesting decreased NO production in PH lambs. Chronic hypertension increased the myogenic response afterl-NA in PH lambs, whereas the myogenic response remained unchanged in controls. The myogenic response was inhibited by nifedipine in PH lambs, suggesting that the myogenic response is dependent upon the influx of extracellular calcium. We conclude that chronic PH impairs flow-induced vasodilation and increases the myogenic response in fetal lung. We speculate that decreased NO signaling and an augmented myogenic response contributes to abnormal vasoreactivity in PH.

Ambient oxygen regulates epithelial metabolism and nitric oxide production in the human nose

2002 ◽  
Vol 93 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Hitoshi Nakano ◽  
Hiroshi Ide ◽  
Toshiyuki Ogasa ◽  
Shinobu Osanai ◽  
Masanobu Imada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Cell Metabolism ◽  
Ambient Air ◽  
No Production ◽  
Gradual Decline ◽  
Nasal Epithelial Cells ◽  
Hypoxia Exposure ◽  
Ambient Oxygen ◽  
Human Nose

The effects of ambient O2tension on epithelial metabolism and nitric oxide (NO) production (V˙no) in the nasal airway were examined in nine healthy volunteers. Nasal V˙no, O2consumption (V˙o2), and CO2production (V˙co2) were measured during normoxia followed by gradual hypoxia from 21 to 0% O2concentration. Nasal V˙o2,V˙co2, and respiratory quotient during normoxia were determined to be 1.19 ± 0.04 ml/min, 1.60 ± 0.04 ml/min, and 1.35 ± 0.04, respectively. Hypoxia exposure to the nasal cavity significantly decreased bothV˙co2and V˙no[V˙co2: 1.60 ± 0.04 to 0.96 ± 0.03 ml/min ( P < 0.01), V˙no: 530 ± 15 to 336 ± 9 nl/min ( P < 0.01)].V˙no was reduced commensurately with gradual decline in O2tension, and the apparent Kmvalue for O2was determined to be 23.0 μM. These results indicate that the nasal epithelial cells exchange O2and CO2with ambient air in the course of their metabolism and that nasal epithelial cells can synthesize NO by using ambient O2as a substrate. We conclude that air-borne O2diffuses into the epithelium where it may be utilized for either cell metabolism or NO synthesis.

Role of neuronal nitric oxide synthase in regulation of vascular and ductus arteriosus tone in the ovine fetus

2000 ◽  
Vol 278 (1) ◽  
pp. L105-L110 ◽  
Author(s):  
Robyn L. Rairigh ◽  
Laurent Storme ◽  
Thomas A. Parker ◽  
Timothy D. le Cras ◽  
Neil Markham ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Ductus Arteriosus ◽  
Fetal Lung ◽  
Late Gestation ◽  
No Production ◽  
Potential Contribution ◽  
Type I ◽  
Maximum Increase ◽  
Great Vessels

Nitric oxide (NO) is produced by NO synthase (NOS) and contributes to the regulation of vascular tone in the perinatal lung. Although the neuronal or type I NOS (NOS I) isoform has been identified in the fetal lung, it is not known whether NO produced by the NOS I isoform plays a role in fetal pulmonary vasoregulation. To study the potential contribution of NOS I in the regulation of basal fetal pulmonary vascular resistance (PVR), we studied the hemodynamic effects of a selective NOS I antagonist, 7-nitroindazole (7-NINA), and a nonselective NOS antagonist, N-nitro-l-arginine (l-NNA), in chronically prepared fetal lambs (mean age 128 ± 3 days, term 147 days). Brief intrapulmonary infusions of 7-NINA (1 mg) increased basal PVR by 37% ( P < 0.05). The maximum increase in PVR occurred within 20 min after infusion, and PVR remained elevated for up to 60 min. Treatment with 7-NINA also increased the pressure gradient between the pulmonary artery and aorta, suggesting constriction of the ductus arteriosus (DA). To test whether 7-NINA treatment selectively inhibits the NOS I isoform, we studied the effects of 7-NINA andl-NNA on acetylcholine-induced pulmonary vasodilation. The vasodilator response to acetylcholine remained intact after treatment with 7-NINA but was completely inhibited after l-NNA, suggesting minimal effects on endothelial or type III NOS after 7-NINA infusion. Western blot analysis detected NOS I protein in the fetal lung and great vessels including the DA. NOS I protein was detected in intact and endothelium-denuded vessels, suggesting that NOS I is present in the medial or adventitial layer. We conclude that 7-NINA, a selective NOS I antagonist, increases basal PVR, systemic arterial pressure, and DA tone in the late-gestation fetus and that NOS I protein is present in the fetal lung and great vessels. We speculate that NOS I may contribute to NO production in the regulation of basal vascular tone in the pulmonary and systemic circulations and the DA.

The relationships between ambient oxygen concentration, temperature, body weight, and oxygen consumption for Mysis relicta (Malacostraca: Mysidacea)

1980 ◽  
Vol 58 (6) ◽  
pp. 1032-1036 ◽  
Author(s):  
I. M. Sandeman ◽  
D. C. Lasenby
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Oxygen Concentration ◽  
Oxygen Consumption Rate ◽  
Consumption Rate ◽  
Mysis Relicta ◽  
Ambient Oxygen ◽  
Kootenay Lake ◽  
Oxygen Concentrations

The relationships between ambient oxygen concentration, temperature, body weight, and oxygen consumption for Mysis relicta in Kootenay Lake, B.C. are examined. Mysis oxygen consumption rate declined with both decreasing temperatures and ambient oxygen concentrations.

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