No apparent effect of nitric oxide on the local matching of pulmonary perfusion and ventilation in awake sheep.
The respiratory tissue in the lung receives nitric oxide (NO) from two sources; NO produced in upper airways, and NO produced in lung parenchyma. It has been hypothesized that optimal local matching of ventilation and perfusion (which is necessary for effective gas exchange) is ensured because well-ventilated lung tissue has a higher concentration of NO and thereby higher blood flow owing to the vasodilatory effect of NO. To test this hypothesis, we simultaneously measured the distributions of local (regions of approximately 1.5 cm3) blood flow (radioactive microspheres) and local ventilation (fluorescent aerosol) in five tracheostomized, awake and standing sheep. Tracers for perfusion and ventilation were administered (1) at baseline, (2) during endogenous NO production blockage (L-NAME 25 mg kg-1) and administration of NO free air, and (3) when the sheep received exogenous NO ( approximately 30 p.p.m.), but having its endogenous NO production blocked. The intrapulmonary distribution of ventilation was similar in all three situations. Within horizontal levels of the lung, distribution of perfusion was not affected by variable access to NO, but along the gravitational axis perfusion was more evenly distributed when the sheep had no access to NO. Exogenous NO tended to restore the baseline vertical profile. These changes in vertical distribution of perfusion can be explained by the effect of variable NO concentrations on pulmonary arterial pressure and cardiac output. Variable access to NO had no effect on arterial blood gases. We conclude that NO is important for the vertical distribution of pulmonary perfusion, but has no apparent effect on the local matching of ventilation and perfusion within horizontal layers of the lung.
Melsom
M N
MN
Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Norway.
Flatebø
T
T
Nicolaysen
G
G
D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000494:pharmacology* / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D011652:Pulmonary Circulation / Q000187:drug effects* / Q000502:physiology*; D012756:Sheep / Q000502:physiology*; D014692:Ventilation-Perfusion Ratio / Q000187:drug effects* / Q000502:physiology*
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester