Effects of ambient pressure on pulmonary nitric oxide

2012 ◽  
Vol 112 (4) ◽  
pp. 580-586 ◽  
Author(s):  
Tryggve E. Hemmingsson ◽  
Dag Linnarsson ◽  
Claes Frostell ◽  
Alain Van Muylem ◽  
Yannick Kerckx ◽  
...  

Airway nitric oxide (NO) has been proposed to play a role in the development of high-altitude pulmonary edema. We undertook a study of the effects of acute changes of ambient pressure on exhaled and alveolar NO in the range 0.5–4 atmospheres absolute (ATA, 379–3,040 mmHg) in eight healthy subjects breathing normoxic nitrogen-oxygen mixtures. On the basis of previous work with inhalation of low-density helium-oxygen gas, we expected facilitated backdiffusion and lowered exhaled NO at 0.5 ATA and the opposite at 4 ATA. Instead, the exhaled NO partial pressure (PeNO) did not differ between pressures and averaged 1.21 ± 0.16 (SE) mPa across pressures. As a consequence, exhaled NO fractions varied inversely with pressure. Alveolar estimates of the NO partial pressure differed between pressures and averaged 88 ( P = 0.04) and 176 ( P = 0.009) percent of control (1 ATA) at 0.5 and 4 ATA, respectively. The airway contribution to exhaled NO was reduced to 79% of control ( P = 0.009) at 4 ATA. Our finding of the same PeNO at 0.5 and 1 ATA is at variance with previous findings of a reduced PeNO with inhalation of low-density gas at normal pressure, and this discrepancy may be due to the much longer durations of low-density gas breathing in the present study compared with previous studies with helium-oxygen breathing. The present data are compatible with the notion of an enhanced convective backtransport of NO, compensating for attenuated backdiffusion of NO with increasing pressure. An alternative interpretation is a pressure-induced suppression of NO formation in the airways.

2009 ◽  
Vol 55 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Tomas Javier ACOSTA ◽  
Mamadou Bousa BAH ◽  
Anna KORZEKWA ◽  
Izabela WOCLAWEK-POTOCKA ◽  
Wlodzimierz MARKIEWICZ ◽  
...  

2002 ◽  
Vol 282 (2) ◽  
pp. F238-F244 ◽  
Author(s):  
Akira Nishiyama ◽  
Shoji Kimura ◽  
Toshiki Fukui ◽  
Matlubur Rahman ◽  
Hirohito Yoneyama ◽  
...  

We examined responses of renal interstitial guanosine 3′,5′-cyclic monophosphate (cGMP) to changes in renal perfusion pressure (RPP) within and below the range of renal blood flow (RBF) autoregulation. A microdialysis method was used to monitor renal cortical and medullary interstitial cGMP levels in anesthetized rabbits. RPP was reduced in two steps: from ambient pressure (89 ± 3 mmHg) to 70 ± 2 mmHg ( step 1) and then to 48 ± 3 mmHg ( step 2). RBF was maintained in step 1 but was significantly decreased in step 2 from 2.94 ± 0.23 to 1.47 ± 0.08 ml · min−1 · g−1. Basal interstitial concentrations of cGMP were significantly lower in the cortex than in the medulla (12.1 ± 1.4 and 19.9 ± 0.4 nmol/l, respectively). Cortical and medullary cGMP did not change in step 1 but were significantly decreased in step 2, with significantly less reduction in cGMP concentrations in the medulla than in the cortex (−25 ± 3 and −44 ± 3%, respectively). Over this pressure range, changes in cortical and medullary cGMP were highly correlated with changes in RBF ( r= 0.94, P < 0.005 for cortex; r = 0.82, P < 0.01 for medulla). Renal interstitial nitrate/nitrite was not changed in step 1 but was significantly decreased in step 2 (−38 ± 2% in cortex and −20 ± 2% in medulla). Nitric oxide synthase inhibition with N G-nitro-l-arginine methyl ester (l-NAME, 30 mg/kg bolus, 50 mg · kg−1 · h−1 iv infusion) significantly decreased RBF (by −46 ± 4%) and interstitial concentrations of cGMP (−27 ± 4% in cortex and −22 ± 4% in medulla, respectively). During l-NAME treatment, renal interstitial concentrations of cGMP in the cortex and medulla were similarly not altered in step 1. However, l-NAME significantly attenuated cGMP responses to a reduction in RPP in step 2. These results indicate that acute changes in RBF result in alterations in nitric oxide-dependent renal interstitial cGMP levels, with differential effects in the medulla compared with the cortex.


1995 ◽  
Author(s):  
Chan-Hong Chung ◽  
Kenneth D ◽  
Robert Stubbs
Keyword(s):  

1996 ◽  
Vol 126 (suppl_4) ◽  
pp. 1072S-1075S ◽  
Author(s):  
Xiaochun Yang ◽  
Narmer F. Galeano ◽  
Matthias Szabolcs ◽  
Robert R. Sciacca ◽  
Paul J. Cannon

2009 ◽  
Vol 106 (38) ◽  
pp. 16221-16226 ◽  
Author(s):  
T. Agapie ◽  
S. Suseno ◽  
J. J. Woodward ◽  
S. Stoll ◽  
R. D. Britt ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e36672 ◽  
Author(s):  
Emmanuelle Bouzigon ◽  
Florent Monier ◽  
Mekki Boussaha ◽  
Nicole Le Moual ◽  
Hélène Huyvaert ◽  
...  

1999 ◽  
Vol 97 (6) ◽  
pp. 697-706 ◽  
Author(s):  
A. BARDEN ◽  
L. J. BEILIN ◽  
K. BOTH ◽  
J. RITCHIE ◽  
P. LEEDMAN ◽  
...  

In order to evaluate whether lipid abnormalities may contribute to endothelial dysfunction in pre-eclampsia, the present study examined the in vitro effects of very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL), isolated from women with pre-eclampsia and matched controls, on the endothelial synthesis of 6-oxo-prostaglandin F1α (6-oxo-PGF1α; a metabolite of prostacyclin) and endothelin 1, and on the expression of nitric oxide synthase 3 (NOS3) mRNA. VLDL, LDL and HDL cholesterol were isolated from 20 pre-eclamptic and 20 age- and gestation-matched normal pregnant women. The lipoproteins (50 μg/ml) and lipoprotein-free control plasma were incubated for 1, 3 and 6 h at 37 °C with a human umbilical endothelial cell line. The synthesis of 6-oxo-PGF1α and endothelin 1, and NOS3 mRNA expression, were measured at each time point. VLDL from pre-eclamptic women stimulated endothelial cell 6-oxo-PGF1α synthesis to a lesser extent than that from normal pregnant women (P< 0.05). LDL from women with pre-eclampsia also stimulated 6-oxo-PGF1α synthesis to a lesser extent than LDL from normal pregnant women, but the effect was less sustained. The effect of HDL from women with pre-eclampsia on 6-oxo-PGF1α synthesis was similar to that of HDL from normal pregnant women. The pre-incubation levels of lipid peroxides in VLDL and LDL were not different between the normal pregnant and pre-eclamptic women, and cannot account for the decrease in 6-oxo-PGF1α synthesis. VLDL, LDL and HDL from women with pre-eclampsia did not affect endothelial cell synthesis of endothelin 1 or expression of NOS3 mRNA differently from lipoproteins from normal pregnant women. This study suggests that VLDL, and to a lesser extent LDL, from women with pre-eclampsia could potentially contribute to the reduced systemic 6-oxo-PGF1α synthesis observed in the pre-eclamptic syndrome.


Sign in / Sign up

Export Citation Format

Share Document