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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.

Hemodynamics, blood gases, lung mechanics, and the distributions of ventilation-perfusion ratios (VA/Q) were studied before and after iv diltiazem, 0.5 mg/kg over 30 min, in 6 patients with pulmonary hypertension secondary to the adult respiratory distress syndrome (ARDS) ventilated with 7 to 20 cm H2O positive end-expiratory pressure (PEEP). Diltiazem decreased systemic and pulmonary arterial pressures without changes in cardiac output and in filling pressures of the heart, and with a slowing of heart rate. Pulmonary vascular resistances decreased from 401 +/- 59 to 329 +/- 58 dyne.s.cm-5.m2 (mean +/- SEM), p less than 0.01. Arterial Po2 decreased from 87 +/- 10 to 80 +/- 11 mm Hg (p less than 0.02) without changes in arterial PCO2, mixed venous PO2, and O2 consumption. Lung compliance and airway resistances did not change. Diltiazem increased true shunt from 23 +/- 5 to 30 +/- 7% of total blood flow (p less than 0.02) without other modification in the pattern of VA/Q distribution as measured by the multiple inert gas elimination technique. These results suggest that pulmonary vascular tone contributes to the maintenance of VA/Q matching in patients with ARDS.

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.

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Pulmonary gas exchange was investigated before and after an increase in pulmonary vascular tone induced by administration of acetylsalicylic acid (ASA), indomethacin, or almitrine in 32 pentobarbital-anesthetized and ventilated (fraction of inspired O2 0.4) dogs with oleic acid lung injury. Pulmonary vascular tone was evaluated by five-point pulmonary arterial pressure (PAP)/cardiac index (Q) plots and intrapulmonary shunt was measured using a SF6 infusion. PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), oleic acid (0.09 ml/kg iv) increased PAP over the range of Q studied (1-5 l.min-1.m-2). At the same Q, arterial PO2 fell from 186 +/- 11 to 65 +/- 8 (SE) Torr and intrapulmonary shunt rose from 5 +/- 1 to 50 +/- 6% 90 min after oleic acid injection. These changes remained stable during the generation of two consecutive PAP/Q plots. ASA (1 g iv, n = 8), indomethacin (2 mg/kg iv, n = 8), and almitrine (8 micrograms.kg-1.min-1 iv, n = 8) produced a further increase in PAP at each level of Q. ASA and indomethacin, respectively, increased arterial PO2 from 61 +/- 4 to 70 +/- 3 Torr (P less than 0.05) and from 70 +/- 6 to 86 +/- 6 Torr (P less than 0.05) and decreased intrapulmonary shunt from 61 +/- 5 to 44 +/- 4% (P less than 0.05) and from 44 +/- 5 to 29 +/- 4% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)