The Arterial Site of Action of Nitric Oxide in the Neonatal Pig Lung Determined by Microfocal Angiography

Lung ◽  
2001 ◽  
Vol 179 (1) ◽  
pp. 43-55 ◽  
Author(s):  
M. Guarín ◽  
C. A. Dawson ◽  
L. D. Nelin
Keyword(s):  
Nitric Oxide ◽  
Arterial Site ◽  
Site Of Action ◽  
Neonatal Pig

scholarly journals Cimetidine Decreases Nitric Oxide Production In Isolated Neonatal Pig Lungs. 1599

1997 ◽  
Vol 41 ◽  
pp. 269-269
Author(s):  
Kari L. Steffen ◽  
John B. Gordon ◽  
David L. Roerig ◽  
Leif D. Nelin
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Neonatal Pig

scholarly journals Nitric Oxide Production in Neonatal Pig Lungs is Decreased by Cytochrome P450 Inhibitors † 1749

1998 ◽  
Vol 43 ◽  
pp. 298-298
Author(s):  
Kari L Steffen ◽  
John B Gordon ◽  
David L Roerig ◽  
Leif D Nelin
Keyword(s):  
Nitric Oxide ◽  
Cytochrome P450 ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Neonatal Pig ◽  
P450 Inhibitors

Nitric Oxide and Hydrogen Sulfide: A Nice Pair in the Respiratory System

2020 ◽  
Vol 27 (42) ◽  
pp. 7136-7148 ◽  
Author(s):  
Salvatore Fuschillo ◽  
Letizia Palomba ◽  
Rosanna Capparelli ◽  
Andrea Motta ◽  
Mauro Maniscalco
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Respiratory Tract ◽  
Respiratory System ◽  
Experimental Conditions ◽  
Signal Molecule ◽  
Diverse Range ◽  
Site Of Action ◽  
Range Of Functions

: Nitric Oxide (NO) is internationally regarded as a signal molecule involved in several functions in the respiratory tract under physiological and pathogenic conditions. Hydrogen Sulfide (H2S) has also recently been recognized as a new gasotransmitter with a diverse range of functions similar to those of NO. : Depending on their respective concentrations, both these molecules act synergistically or antagonistically as signals or damage promoters. Nevertheless, available evidence shows that the complex biological connections between NO and H2S involve multiple pathways and depend on the site of action in the respiratory tract, as well as on experimental conditions. This review will provide an update on these two gasotransmitters in physiological and pathological processes.

scholarly journals The Vascular Site of Action of Hypoxia in the Neonatal Pig Lung

1994 ◽  
Vol 35 (1) ◽  
pp. 25-29 ◽  
Author(s):  
Leif D Nelin ◽  
David A Rickaby ◽  
John H Linehan ◽  
Christopher A Dawson
Keyword(s):  
Site Of Action ◽  
Neonatal Pig

Effect of hypoxia on nitric oxide production in neonatal pig lung

1996 ◽  
Vol 271 (1) ◽  
pp. H8-H14 ◽  
Author(s):  
L. D. Nelin ◽  
C. J. Thomas ◽  
C. A. Dawson
Keyword(s):  
Nitric Oxide ◽  
Average Rate ◽  
Continuous Production ◽  
Venous Pressure ◽  
Gas Mixture ◽  
No Production ◽  
Exhaled No ◽  
Neonatal Pig ◽  
Nitrite Nitrate ◽  
Hypoxic Gas Mixture

Nitric oxide (NO) synthase inhibitors potentiate hypoxic vasoconstriction (HV), suggesting that NO production during hypoxia normally acts to attenuate HV. To begin to examine the effect of hypoxia on lung NO production, we studied four groups of isolated neonatal pig lungs. In three groups of lungs, the accumulation of nitrite/nitrate (NOx-) was measured in the recirculating perfusate during ventilation with a control gas mixture (Cont), a hypoxic gas mixture (Hyp), or the control gas mixture with N omega-nitro-L-arginine methyl ester (L-NAME) added to the perfusate. Both hypoxia and L-NAME significantly increased perfusion pressure [pulmonary arterial pressure (Pa)-pulmonary venous pressure (Pv)] compared with control. NOx- accumulated in the perfusate at an average rate of 9.1 +/- 2.3 (SE) nmol/min in Cont, 3.7 +/- 0.8 nmol/min (P < 0.05 vs. control) in Hyp, and 3.7 +/- 0.6 nmol/min (P < 0.05 vs. control) in L-NAME. In the fourth group of lungs, exhaled NO output was measured during ventilation with the control gas mixture, the hypoxic gas mixture, and the control gas mixture with L-NAME added to the perfusate. Pa-Pv increased significantly with both hypoxia and L-NAME in these lungs. The exhaled NO output also decreased significantly with both hypoxia and L-NAME. These results suggest that in this preparation there was continuous production of NO that was decreased by hypoxia or L-NAME. It is not clear how the potentiation of HV by NO inhibitors and inhibition of NO production by hypoxia are linked.

Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs

1997 ◽  
Vol 82 (1) ◽  
pp. 23-31 ◽  
Author(s):  
George Cremona ◽  
Tim Higenbottam ◽  
Motoshi Takao ◽  
Edward A. Bower ◽  
Leslie W. Hall
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Steady Flow ◽  
Pulmonary Vascular Resistance ◽  
Venous Occlusion ◽  
Dynamic Resistance ◽  
Arterial Segment ◽  
Site Of Action ◽  
Endogenous Nitric Oxide ◽  
Exogenous Nitric Oxide

Cremona, George, Tim Higenbottam, Motoshi Takao, Edward A. Bower, and Leslie W. Hall. Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs. J. Appl. Physiol. 82(1): 23–31, 1997.—The site of action of endogenous and exogenous nitric oxide (NO) in isolated pig lungs was investigated by using arterial, double, and venous occlusion, which allowed precapillary, postcapillary, and venous segments to be partitioned into arterial, precapillary, postcapillary, and venous segments. N G-nitro-l-arginine (l-NNA; 10−5 M) increased resistance in the arterial (35 ± 6.6%, P = 0.003), precapillary (39.3 ± 5.1%, P = 0.001), and venous (18.3 ± 4.8%, P = 0.01) segments, respectively. Sodium nitroprusside (10−5 M) and NO (80 parts/million) reversed the effects ofl-NNA. Total pulmonary vascular resistance fell with increasing flow, due to a fall in precapillary resistance and dynamic resistance, and was significantly lower than mean total resistance.l-NNA increased the resistances but did not alter the pattern of the pressure-flow relationships. It is concluded that, in isolated pig lungs, the effect of endogenous NO seems to be dependent on flow in the arterial segment and independent of flow in the precapillary segment, but variation of its release does not appear to be fundamental to accommodation to changes in steady flow.

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