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  • Title: Pulmonary blood flow distribution in lobar hypoxia--influence of cardiac output and nitric oxide inhalation.
    Author: Fredén F, Berglund JE, Hedenstierna G.
    Journal: Scand Cardiovasc J; 1999; 33(4):215-21. PubMed ID: 10517208.
    Abstract:
    Inhaled NO is reported to be less effective in patients with ARDS if cardiac output is high (> 10 L/min). It has also been demonstrated that increased blood flow and increased shear stress cause an enhancement of endogenous NO production. In one-lung ventilation and regional hypoxia, nitric oxide (NO) delivered to the ventilated lung may decrease blood flow to the nonventilated lung and improve arterial oxygenation. So far, however, results have been divergent. The present study was performed with the hypothesis that inhaled NO would be less effective if cardiac output was increased. In the anaesthetized pig, hypoxia (5% O2) was induced in the left lower lobe. NO was delivered consecutively to the hypoxic lobe and to the other, oxygenated parts, of the lungs during continuous measurement of lobar blood flow and total lung blood flow. Bleeding and infusion of dextran caused variation in cardiac output. It was found that lobar hypoxia per se reduced lobar blood flow from 22.9+/-3.1% to 4.7+/-0.9% of cardiac output. An increase (3.2+/-0.3 L x min(-1)) and a decrease (2.2+/-0.2 L x min(-1)) in cardiac output did not alter the relative perfusion of the hypoxic lobe from baseline cardiac output (2.6+/-0.2 L x min(-1)) values. When NO was delivered to the hypoxic lobe, there was a marked increase in relative lobar perfusion to 19.0+/-2.9% during low cardiac output and 16.5+/-2.7% during high cardiac output without any significant difference between the two NO-induced increases of lobar perfusion. The increase in lobar perfusion tended to depend inversely on total pulmonary blood flow when cardiac output had been reduced by bleeding but without reaching statistical significance (r = -0.42, p > 0.05). The decrease in mean pulmonary artery pressure and PaO2 seen during NO inhalation to the hypoxic lobe did not correlate with the level of cardiac output. When NO was delivered to the oxygenated parts of the lungs, no significant effect on relative lobar perfusion or arterial oxygenation was observed, either at raised or at lowered cardiac output. The findings give no further evidence to show that variations in cardiac output alter the effect of NO inhalation.
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