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PubMed1998

Inhaled nitric oxide, almitrine infusion, or their coadministration as a treatment of severe hypoxemic focal lung lesions.

BACKGROUND: The partition of pulmonary blood flow between normal and shunting zones is an important determinant of oxygen tension in arterial blood (PaO2). The authors hypothesized that the combination of inhaled nitric oxide (iNO) and almitrine infusion might have additional effects related to their pharmacologic properties to improve PaO2. Such a combination was tested in patients with hypoxia caused by focal lung lesions, distinct from the acute respiratory distress syndrome. METHODS: Fifteen patients with hypoxic focal lung lesions despite optimal therapy were included and successively treated with (1) 5 ppm iNO, (2) low-dose almitrine infusion (5.5 +/- 1.7 microg x kg(-1) min(-1)) during iNO, and (3) almitrine infusion alone (with NO turned off). Then iNO was reintroduced and we studied the effect of the coadministration in reducing the fractional concentration of oxygen in inspired gas (FI(O2)) and positive end-expiratory pressure (PEEP) levels. Changes in blood gases and pulmonary and systemic hemodynamics were measured. RESULTS: Systemic hemodynamic variables remained stable in all protocol conditions. Use of iNO improved arterial oxygenation and decreased intrapulmonary shunt. Almitrine similarly improved PaO2 but increased pulmonary artery pressure and right atrial pressure. Coadministration of iNO and almitrine improved PaO2 compared with each drug alone and with control. All patients responded (that is, they had at least a +30% increase in PaO2) to this coadministration. When the drug combination was continued, FI(O2) and PEEP could be reduced over 8 h. The hospital mortality rate was 33% and unrelated to hypoxia. CONCLUSIONS: In hypoxemic focal lung lesions, iNO or low-dose almitrine markedly improved PaO2 to a similar extent. Furthermore, the coadministration amplified the PaO2 increase at a level that allowed reductions in FI(O2) and PEEP levels.

Administration, Inhalation↗
PubMed1990

Almitrine-raubasine and cognitive impairment in the elderly: results of a 6-month controlled multicenter study.

Two-hundred four patients between 70 and 85 years of age were included in a double-blind randomized controlled multicenter study (almitrine-raubasine/placebo). Inclusion criteria were a complaint of cognitive disorders and an objective cognitive impairment evaluated by Folstein et al. "Mini-Mental State" (MMS) and by Sandoz Clinical Assessment for Geriatrics (SCAG). Patients were treated for 6 months and evaluations were performed at the beginning of the trial (T0), then 3 (T3) and 6 (T6) months later. Evaluations included a visual analogic self-rating scale and the following psychometric tests: Trail Making A (TMA), Shopping List Task, Word Fluency, Crossing Out Letters, Logical Memory, Digit Span, and Visual Retention. Anxiety and Depression Scales were also used to assess the effects of almitrine-raubasine on affective status. Statistical analysis involving the whole sample did not show any significant difference between the almitrine-raubasine and placebo groups concerning changes in assessment criteria from T0 to T6. However, these results may have been due to the wide heterogeneity of baseline performances in psychometric tests. To prevent this possible bias, further statistical analysis was performed for each psychometric test after patients had been divided into three classes according to baseline score levels. Considering scores on TMA and Digit Span for patients with scores in the intermediate class on TMA, almitrine-raubasine induced a significantly higher improvement in performance from T0 to T6 than that induced by placebo. On the other hand, no side effects were noted with almitrine-raubasine when compared with placebo. These data suggest that almitrine-raubasine enhances concentrated attention in patients with mild to moderate impairment of this function.

Aged↗
PubMed1990

Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease.

The effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.

Almitrine↗
PubMed1996

Action potentials in right and left ventricles from chronic hypoxic rats: effect of almitrine.

Rats were exposed to a 3-wk regimen of chronic normobaric hypoxia, with or without almitrine treatment. Chronic hypoxia led to a significant rise in the right ventricular mass and lengthened the action potential duration (APD) in right ventricle and in nonhypertrophied left ventricle. Hypertrophy and APD lengthening were significantly enhanced by almitrine. The classical acute hypoxia-induced shortening in APD was much larger in hypoxia-adapted hearts. In these hearts, almitrine treatment almost completely prevented such shortening, while the acute hypoxia-induced decrease in cardiac contraction was similar with or without almitrine. It is concluded that APD lengthening during chronic hypoxia can occur independently of ventricular hypertrophy. The similar directional effects of almitrine and chronic hypoxia on APD support the hypothesis of an energy-linked phenomenon. The dissociation of the almitrine effect on APD and contractility is in accordance with the view of a cellular energy compartmentation.

Action Potentials↗
PubMed1989

Stimulus interaction between CO2 and almitrine in the cat carotid chemoreceptors.

The hypothesis that augmentation of the carotid chemoreceptor response to hypoxia by almitrine is due in part to an increased response to CO2 was tested by using single or few fiber preparation of carotid body chemosensory fibers in 12 cats anesthetized with alpha-chloralose. To differentiate between the plausible mechanisms of effects, we also tested the responsiveness of the afferents to cyanide and nicotine before and after almitrine. After a saturation dose of almitrine (1 mg.kg-1 followed by 0.5 mg.kg-1.h-1) the chemosensory responses to CO2 strikingly increased even during hyperoxia: the afferents showing an increased transient peak activity at the onset of hypercapnia, an augmented steady-state response to CO2 stimulus, and a decreased arterial PCO2 stimulus threshold. Thus, the effect of almitrine on carotid chemoreceptor response to hypoxia could be explained, at least in part, by its multiplicative stimulus interaction with CO2. After almitrine, the chemoreceptor response to cyanide, which is dependent on arterial PO2, was not particularly augmented relative to those of nicotine. Accordingly, the O2-sensing mechanism does not appear to be the primary site of almitrine effect. The results also indicate that the site of CO2 chemoreception resides downstream from those of hypoxia.

Almitrine↗
PubMed1990

Almitrine mimics hypoxia in fetal sheep with lateral pontine lesions.

Almitrine bimesylate is a potent and long-lasting respiratory stimulant in adult species. It acts by stimulating the peripheral chemoreceptors, where it has been shown to accumulate specifically, although its exact mechanism of action is uncertain. In the fetal lamb, however, it produces a profound inhibition of breathing even after denervation of the peripheral chemoreceptors. In this respect its action is similar to hypoxia. To investigate whether almitrine is hypoxia mimetic, we examined the effect of almitrine in nine fetal lambs of 120-130 days gestation. Five had lesions in the lateral pons that changed the fetal depressive response to hypoxia to one of stimulation. In the remaining four fetuses, the lesions did not bilaterally encompass the appropriate area of the pons; thus they still showed the normal fetal depressive response to hypoxia and so acted as controls. Almitrine (10 mg iv) caused a pronounced stimulation of breathing that lasted 406 +/- 26 min in all five fetuses with lesions that caused a stimulatory response to hypoxia. However, in the remaining four fetuses, in which the response to hypoxia was inhibitory, almitrine caused an inhibition of breathing that lasted 184 +/- 28 min. We conclude that the action of almitrine is like that of hypoxia and that, because it acts specifically on the chemoreceptors, it may prove to be a useful tool in the study of possible central chemoreceptor mechanisms.

Almitrine↗
PubMed1997

Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm.

The effects of almitrine bimesylate and doxapram HCl on isometric force produced by in vitro rat diaphragm were studied during direct muscle activation at 37 degrees C. Doxapram and almitrine ameliorate respiratory failure clinically by indirectly increasing phrenic nerve activity. This study was carried out to investigate possible direct actions of these agents on the diaphragm before and after fatigue of the fibers. Two age groups of animals were chosen [6-14 wk (group 1) and 50-55 wk (group 2)] because it is known that increasing age decreases a muscle fiber's resistance to fatigue. Muscle strips were isolated from both group 1 and group 2 and directly stimulated (2-ms pulse duration, 5-15 V) to produce twitch tensions of 1.3 and 2.1 N/cm2, respectively. At low concentrations, doxapram (</=20 microg/ml) and almitrine (</=12 microg/ml) had no effect on twitch contraction or 100-Hz tetanic tension. However, 40 microg/ml doxapram and 30 microg/ml almitrine increased twitch tension by 9.0 +/- 1.4 and 11.6 +/- 1.9%, respectively, in animals of group 2 (n = 5). A fatigue protocol consisting of low-frequency stimulation (30-Hz trains, 250-ms duration every 2 s for 5 min) caused a reduction of twitch tension in animals of group 1 (48 +/- 4% of control) and group 2 (28 +/- 4% of control). At 90 min postfatigue, the twitch tension recovered to 72 +/- 3 and 42 +/- 2% of control values in group 1 and group 2, respectively. In the presence of doxapram (20 microg/ml), there was a significant increase in the recovery of twitch tension at 90 min in group 1 and group 2 (84.5 +/- 3.2 and 80.1 +/- 2.8%, respectively) compared with controls at 90 min postfatigue. In the presence of almitrine (12 microg/ml), there was a full recovery from fatigue in group 1 animals (100% of control) and a recovery to 95.6 +/- 2.1% of control in group 2 animals at 90 min. These results demonstrate a significant improvement in the rapidity and magnitude of recovery from fatigue in the rat diaphragm muscle in the presence of both doxapram and, especially, almitrine. These effects may be due to changes in intracellular calcium, ADP/ATP ratios, or oxygen free radical scavenging.

Almitrine↗
PubMed2002

Effects of almitrine on diaphragm contractile properties in young and old rats.

BACKGROUND: Diaphragm muscle force and fatigue are key factors in the development of respiratory failure. Almitrine is used to improve ventilatory drive and ventilation-perfusion matching in respiratory failure. Recently, it has also been shown to improve diaphragm muscle force and endurance in young rats, but it is not known if this effect persists with ageing. OBJECTIVES: To determine the effects of almitrine on diaphragm contractile properties in young and old rats. METHODS: In young and old rats, isometric contractile properties were measured in strips of isolated diaphragm muscle in physiological saline solution at 30 degrees C with or without almitrine. RESULTS: In young animals, almitrine increased twitch tension, reduced half-relaxation time and increased endurance, but had no effect on tetanic tension, contraction time or tension-frequency relationship. Ageing had no effect on endurance, but did reduce twitch and tetanic tension and contraction and half-relaxation time. Almitrine had no effect on contractile tension and kinetics, tension-frequency relationship or on endurance in the old animals. CONCLUSIONS: Ageing negates the beneficial effects of almitrine on diaphragm muscle force and endurance.

Aging↗
PubMed1985

[Almitrine bismesylate in chronic obstructive lung disease and persistent hypoxemia. Controlled double-blind study with oral administration].

Almitrine bismesylate has been shown to be a respiratory stimulating substance which acts primarily via the peripheral chemoreceptors. The effect of the oral administration of Almitrine (200 mg/day for 9 days) was investigated in a controlled double-blind study with 18 patients suffering from chronic obstructive lung disease and hypoxemia (PaO2 less than 60 mm Hg). During the therapy with Almitrine an early and lasting improvement in the PaO2 and PaCO2 could be obtained. This improvement was significant compared with the placebo group. On the last day of treatment with Almitrine the PaO2 increased by 16.2 mm Hg (p less than 0.001) and the PaCO2 decreased by 7.3 mm Hg (p less than 0.01). Simultaneously, an increase in minute ventilation (5.24 liters on day 9) could be observed. This increase was not significant compared with the placebo group. There was a correlation of -0.61 between the changes in minute ventilation and in PaCO2. The lung functional parameters vital capacity (VC), forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) increased on several days in both groups; a change in Rtot was observed in the treatment group only. A reduction of dyspnea also was observed in both groups. In addition to the ventilatory stimulant action on the peripheral chemoreceptors, the changes in blood gases induced by Almitrine also should be discussed as an improvement of the ventilation/perfusion ratio. In this therapeutical trial no side effects during the therapy with Almitrine have been observed.

Administration, Oral↗
PubMed1987

Study of the pharmacokinetics and pharmacodynamic activity of almitrine bismesylate in infants during the recovery phase following bronchopulmonary dysplasia.

The efficacy and pharmacokinetics of almitrine bismesylate were studied in 6 infants (age 2.5-9.5/months) during the recovery phase following bronchopulmonary dysplasia. The infants did not require assisted ventilation, but needed oxygen therapy with an FiO2 of 25-30% in stable condition. One to three hours after a single oral dose of almitrine (1.5 mg/kg), there was a marked increase in transcutaneous PO2 (TcPO2) (mean 2kPa) followed by a regular decrease to the baseline level. Nine to fourteen days after repeated administration of almitrine (1.5 mg/kg/12 h) in 4 children, the mean gain in TcPO2 was only 0.85 kPa. There was a very early flagging in efficacy of almitrine, since none of the children could be weaned from oxygen therapy. The absorption peak occurred 1-3 h after the administration of the compound. The maximum almitrine concentration was 173 +/- 44 ng/ml; plasma clearance was 21.9 +/- 6.6 ml/min and the volume of distribution was 18.7 +/- 2.1 liters/kg. The drug was eliminated biphasically. In the 4 studies with repeated drug administration, the pharmacokinetic results suggested that a steady state was still not achieved after 9-14 days of treatment. These results and the absence of any sustained effect of repeated doses of the drug raise the problem of a particular type of almitrine metabolization in the infant.

Administration, Oral↗
PubMed1988

Effect of almitrine on ventilation-perfusion distribution in adult respiratory distress syndrome.

Almitrine improves ventilation/perfusion relationships (VA/Q) in COPD, but its effects in ARDS, in which VA/Q mismatching is the cause of severe hypoxemia, are not known. The effects of almitrine on pulmonary gas exchange and circulation were assessed in 9 patients with ARDS who were sedated, paralyzed, and mechanically ventilated at constant FlO2 (range, 0.48 to 0.74). Systemic and pulmonary hemodynamics, conventional gas exchange, and the VA/Q distribution by the multiple inert gas elimination technique (MIGT) were measured before (baseline), during (ALM 15), at the end of (ALM 30), and at 30-min intervals after (POSTALM 30, 60, and 90) the intravenous infusion of 0.5 mg/kg body weight of almitrine over 30 min. Almitrine significantly increased PaO2 from 78 +/- 15 mm Hg to 140 +/- 49 at ALM 15 and 138 +/- 52 at ALM 30. AaPO2 and QS/QT decreased during the administration of the drug. The MIGT showed that almitrine redistributed pulmonary blood flow from shunt areas (reduction from 29 +/- 11 to 17 +/- 11% of QT) to lung units with normal VA/Q ratios (increase from 63 +/- 9 to 73 +/- 6% of QT). The Ppa increased from 26 +/- 5 to 30 +/- 5 mm Hg without changes in QT. Changes were transient, returning toward baseline 30 min after stopping the infusion of the drug. Almitrine significantly reduced the VA/Q inequalities present in ARDS and may be useful in the management of those patients.

Adult↗
PubMed1985

Almitrine improves oxygenation when both awake and asleep in patients with hypoxia and carbon dioxide retention caused by chronic bronchitis and emphysema.

Patients with chronic bronchitis and emphysema who are hypoxic when awake become more hypoxic during sleep, with a further rise in their preexisting pulmonary hypertension. Almitrine, a respiratory stimulant, improves arterial blood gas tensions in such patients when they are awake. We have used a double-blind, placebo-controlled, cross-over study to compare the effects of 50 mg almitrine given orally twice a day for 14 days on oxygen saturation (SaO2), respiratory movements, and sleep quality in 9 patients with hypoxic chronic bronchitis and emphysema (FEV1, 0.4 to 1.0 L; PaO2, 51 +/- (SEM) 2 mmHg; PaCO2, 49 +/- 1 mmHg). Almitrine improved arterial blood gas tensions when awake, mean PaO2 rising by 8 mmHg (p less than 0.001) and PaCO2 falling by 4 mmHg (p less than 0.01). Almitrine improved nocturnal oxygenation, mean SaO2 when awake rising from 83 +/- 4% to 89 +/- 3% (p less than 0.01), and the lowest SaO2 during sleep rising on average from 65 +/- 6% to 77 +/- 3% (p less than 0.02). The number of hypoxemic episodes (SaO2 falling by greater than or equal to 10% from the preceding stable baseline during sleep) and the time when SaO2 was below 80% (135 +/- 53 versus 46 +/- 35 min; p less than 0.01) also improved. Almitrine did not improve sleep quality. We conclude that almitrine improves arterial gas tensions when awake and reduces the frequency and severity of nocturnal hypoxemia without impairing sleep quality in patients with chronic bronchitis and emphysema who are both hypoxemic and hypercapnic when awake.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Evolution of peripheral nerve function in hypoxaemic COPD patients taking almitrine bismesylate: a prospective long-term study.

Almitrine bismesylate has been thought to provoke peripheral neuropathies in patients with chronic obstructive pulmonary disease (COPD). However, there seems to exist alterations of peripheral nerve function in patients with COPD, who have not taken almitrine. We have therefore examined 22 patients with COPD and no other cause of peripheral neuropathy (PN), before and after 6 and 12 months of treatment with almitrine (50 mg bd). Seventy-eight similar patients, who did not take almitrine, were also studied (controls). Sixty-four per cent of controls, and 55% of almitrine patients initially had at least one neurophysiological abnormality. There was no change in the studied parameters after 6 months and one year's treatment with almitrine.

Aged↗
PubMed1988

Release of thromboxane A2 by low-dose almitrine in the hypoxic dog.

Potentiation of hypoxic pulmonary vasoconstriction by a low dose of almitrine bismesylate (1 microgram.kg-1.min-1) was evaluated in terms of blood chemical mediator concentrations. Time course changes in the blood concentrations of adrenaline, noradrenaline, serotonin, histamine, thromboxane TXB2 and 6-keto-PGF1 alpha were monitored after administration of almitrine bismesylate for 15 min at 1 microgram.kg-1.min-1) in hypoxic and normoxic beagles. The low almitrine dose significantly increased TXB2 levels in hypoxic beagles, but the levels remained virtually unchanged in the normoxic animals with almitrine bismesylate and in the hypoxic animals with solvent. TXB2 levels did not increase when the almitrine infusion was increased to 5 micrograms.kg-1.min-1 for 15 min in hypoxic conditions. These findings suggest that almitrine is involved in arachidonic acid metabolism at a low rate of infusion and that thromboxane release from hypoxic areas of the lung may cause local vasoconstriction.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

The role of almitrine bismesylate in acute respiratory failure.

Sixteen (16) C.O.L.D. patients with acute respiratory failure entered this preliminary study to evaluate the effects of almitrine bismesylate against placebo. Eight (8) patients received almitrine bismesylate and eight (8) patients received placebo. During the study, (11) patients were intubated and one (1) patient died because of bleeding peptic ulceration. A significant improvement in PaO2 values was noted in the patients given almitrine bismesylate as opposed to those given placebo. This improvement (p = 0.032) became evident on the 2nd day of treatment. The changes in PaO2 levels were not modified by intubation. A surprising evolution of PaCO2 was observed in those patients given almitrine bismesylate whether or not they had been intubated. No side effects were noted in the patients taking almitrine bismesylate during the first 4 days of the trial or during the following 6 days when patients continued to receive almitrine bismesylate.

Acute Disease↗
PubMed1987

Almitrine bismesylate modulates the susceptibility of guinea pig pulmonary artery to catecholamines, PGF2 alpha and adenosine.

The action of almitrine bismesylate, a potent ventilatory stimulant drug, was studied on the contractile responses to some putative transmitters of carotid body (dopamine, noradrenaline, PGF2 alpha, adenosine) in segments of guinea pig pulmonary arteries. Almitrine (10 mumol/l) was capable of mitigating the contractions evoked by dopamine (0.3 mmol/l), noradrenaline (1 mumol/l) and PGF2 alpha (10 mumol/l) as well. In vessels precontracted with noradrenaline, almitrine (added to the nutrient solution of vessels before applying noradrenaline) potentiated the adenosine-induced initial contractile response without influencing the methylxanthine-sensitive relaxing effect of this purine nucleoside. In contrast, almitrine antagonized the adenosine-induced contraction when applied under precontracted state of arteries. It is supposed that the results presented here could provide some explanation for the variable action of almitrine on pulmonary circulation. On the other hand, these results could serve as a pharmacological basis for further studies of the almitrine action on isolated carotid bodies.

Adenosine↗
PubMed1986

Haemodynamic and respiratory effects of post-operative doxapram and almitrine in patients following pneumonectomy.

Respiratory analeptics have been shown to give important increases in pulmonary vascular resistance and pulmonary arterial pressure in hypoxaemic respiratory failure patients, but no studies have been carried out in the post-operative recovery period. The aim of this study was to compare the haemodynamic and respiratory effects of doxapram and almitrine infusion given over 1 h in patients who had just undergone pneumonectomy. Two hours after the end of anaesthesia, three groups of randomly selected patients were therefore given 3 mg kg-1 doxapram (n = 10), 1 mg kg-1 almitrine (n = 10) or placebo (n = 10). Measurements were made before and 15, 30, 60, 90, 120 and 180 min after the beginning of the infusion. There was an immediate 15-20% fall (P less than 0.01) in PaCO2 and a 20% rise in PaO2 (P less than 0.005), identical for both drugs; the variations in the placebo group became significant only after 60 min. Heart rate and cardiac index did not change. Mean arterial pressure did not change with doxapram, but decreased by 20% during the infusion of almitrine (P less than 0.01), remaining low until the 90th min (P less than 0.05). This hypotension was due to a decrease in peripheral arterial resistance (P less than 0.05) and a small decrease in right atrial pressure (P less than 0.05). The mean pulmonary arterial and wedge pressures were increased before starting the infusion, and did not vary significantly. Pulmonary arterial resistance increased with both analeptics but only significantly with the doxapram (P less than 0.05) at 5, 60 and 90 min; however, there was no significant difference between doxapram and almitrine. The post-operative respiratory efficiency of these drugs has been confirmed, there being no difference between almitrine and doxapram. The haemodynamic effects were moderate, especially with almitrine. Both of these drugs, therefore, may be recommended for use after lung surgery.

Almitrine↗
PubMed1980

[Effects of a respiratory analeptic with peripheral action-almitrine on ventilation immediately after surgery].

After a brief review of the advantages and disadvantages of the postoperative administration of a respiratory analeptic with a central action, the authors study the effects of almitrine (respiratory analeptic with a peripheral action) on alveolar ventilation following thoracic surgery. Two groups of 10 patients were distinguished: the patients of the first group received almitrine (1.5 mg/kg-1 over a period of one hour) thirty minutes after their return from the operating room, whilst those of the second group received no respiratory analeptic. Blood gases were measured 30 minutes after the return from the operating room (immediately before the start of the infusion of almitrine) then 1 hour, 2 hours and 3 hours later. The improvement in blood gases after almitrine was significant: whilst arterial pCO2 was a mean of 5.78 kPa (44.46 mmHg) in the control subjects, it fell 4.99 kPa (38.4 mmHg) by the end of the infusion in the tested subjects and subsequently remained at a mean of 5.04 kPa (38.79 mmHg). Arterial pO2 measured with FIO2 in all patients remained stable in the control subjects during the three hours postoperatively (mean = 15.11 kPa (116.26 mmHg). In the tested subjects, it improved progressively and significantly, rising from 11.08 kPa (85.2 mmHg) before almitrine to 14.05 kPa (108 mmHg) at the end of the infusion, then to 15.95 kPa (122.7 mmHg) 1 hour later and to 16.51 kPa (127 mmHg) 2 hours later. The authors concluded that almitrine is effective in the treatment of early alveolar hypoventilation after thoracic surgery in patients receiving moderate doses of oxygen (FIO2 = 0.40).

Adult↗