M Bruyneel et al.

No abstract

The effect of almitrine bismesylate on hypoxic pulmonary vasoconstriction (HPV) remains controversial. We therefore investigated in a double-blind, placebo-controlled, randomized design the effects of low dose of almitrine bismesylate (4 micrograms/kg/min given intravenously) on blood gases, pulmonary hemodynamics, and ventilation-perfusion (VA/Q) distributions in normal subjects breathing a hypoxic mixture (FIO2, 0.125), room air (FIO2, 0.21), and oxygen (FIO2, 1.0) in a random sequence. In the placebo group (7 subjects), no change was recorded. In the almitrine group (10 subjects), arterial PO2 improved during hypoxia (from 42 +/- 2 to 47 +/- 1 mm Hg, p less than 0.05, mean +/- SEM) and normoxia (from 99 +/- 3 to 104 +/- 2, p less than 0.05). Pulmonary arterial mean pressure and pulmonary vascular resistance index increased with almitrine during hypoxia, respectively, from 20 +/- 1 to 23 +/- 1 mm Hg (p less than 0.01) and from 207 +/- 22 to 283 +/- 35 dyne.s.cm-5.m2 (p less than 0.01), and during normoxia, respectively, from 12 +/- 1 to 14 +/- 1 mm Hg (p less than 0.05) and from 90 +/- 11 to 137 +/- 13 dyne.s.cm-5.m2 (p less than 0.05). The VA/Q distribution improved during hypoxia, with a shift of the blood flow distribution to better oxygenated lung units with higher VA/Q ratios. We conclude that in normal humans low dose of almitrine improves gas exchange by an enhancement of HPV.

To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven patients had an arterial hypoxemia (PaO2 = 69 +/- 6 mm Hg, mean +/- SD), and three patients were normoxemic (PaO2 = 89 +/- 6 mm Hg). In each hypoxemic patient, the VA/Q distributions were characterized by the presence of low VA/Q units. A negative logarithmic correlation was found between the dispersion of the blood flow distribution and the arterial PO2. An acute inspiratory hypoxia (FIO2, 0.125) elicited an increase in pulmonary vascular resistance by 58.5% in the hypoxemic group and by 81.6% in the normoxemic one (p = NS between the two groups). The percent change in pulmonary vascular resistance induced by hypoxia was not correlated with the percent change in the dispersion of the blood flow distribution. A theoretical analysis showed that the mean arterial PO2 of 69 mm Hg of the hypoxemic group differed from a normal reference value of 96 mm Hg as a result of the combined effects of reduced hemoglobin (-4 mm Hg), increased P50 (+4 mm Hg), increased ventilation (+10 mm Hg), low VA/Q (-35 mm Hg), and true shunt (-2 mm Hg). These results show that the "hypoxemia of liver cirrhosis" is essentially caused by VA/Q mismatching, which is not explained by an abnormal hypoxic pulmonary vasoconstriction.