Increased respiratory chemosensitivity induced by infusing almitrine intravenously in healthy man.

Stanley, N. N.; Galloway, James M.; Gordon, Ben; Pauly, N. C.

doi:10.1136/thx.38.3.200

Cited by 16 publications

(4 citation statements)

References 14 publications

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“…Mean plasma levels (325±9 ng•ml -1 ) (table 4) were the same as those obtained after 50 mg per os twice a day (between 214-387 ng•ml -1 ) which corresponds to the dose used in chronic studies in COPD patients [13]. At this dose, almitrine has little effect on ventilation [4,5,7,[14][15][16], although we did not measure this variable in the present study.…”

Section: Discussionsupporting

confidence: 56%

Effect of almitrine bismesylate on pulmonary vasoreactivity to hypoxia in chronic obstructive pulmonary disease

Saadjian¹,

Philip-Joel²,

Barret³

et al. 1994

Eur Respir J

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The aim of this double-blind, placebo-controlled study was to determine whether acute administration of almitrine enhances hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease (COPD). Haemodynamics and blood gases were studied at various inspiratory fractional concentrations of oxygen (FIO2): 0.15, 0.21, 0.30 and 1.0, randomly administered for 20 min periods under constant infusion of either placebo or almitrine (8 micrograms.kg-1.min-1) in 20 patients with COPD. The almitrine group exhibited a significant increase in mean pulmonary artery pressure, pulmonary vascular resistance and arterial oxygen tension (PaO2) at FIO2 0.15, 0.21 and 0.30. During hypoxia, the increase in mean pulmonary pressure and pulmonary vascular resistance was three times greater in the almitrine group than the placebo group. No significant difference in cardiac output and systemic haemodynamics was found. These results suggest that almitrine at the dose used, enhances pulmonary vasoconstriction in COPD patients.

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Section: Discussionsupporting

confidence: 56%

Effect of almitrine bismesylate on pulmonary vasoreactivity to hypoxia in chronic obstructive pulmonary disease

Saadjian¹,

Philip-Joel²,

Barret³

et al. 1994

Eur Respir J

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“…However, there are also circumstances where these slopes are not comparable. In sleeping dogs, Nakayama et al (17) showed that almitrine administration results in no change in the slope of the ventilatory response to CO 2 below eupnea, yet this drug is known to cause an increase in slope above eupnea (12,14,20,21,24). Furthermore, in the present study, we demonstrate that dopamine administration, despite its reported slope-decreasing properties above eupnea (1,2,4,9,19) results in an essentially normal slope below eupnea.…”

Section: Discussionsupporting

confidence: 55%

Increased propensity for apnea via dopamine-induced carotid body inhibition in sleeping dogs

Chenuel¹,

Smith²,

Henderson³

et al. 2005

Journal of Applied Physiology

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We determined the effects of specific carotid body chemoreceptor inhibition on the propensity for apnea during sleep. We reduced the responsiveness of the carotid body chemoreceptors using intravenous dopamine infusions during non-rapid eye movement sleep in six dogs. Then we quantified the difference in end-tidal Pco(2) (Pet(CO(2))) between eupnea and the apneic threshold, the "CO(2) reserve," by gradually reducing Pet(CO(2)) transiently with pressure support ventilation at progressively increased tidal volume until apnea occurred. Dopamine infusions decreased steady-state eupneic ventilation by 15 +/- 6%, causing a mean CO(2) retention of 3.9 +/- 1.9 mmHg and a brief period of ventilatory instability. The apneic threshold Pet(CO(2)) rose 5.1 +/- 1.9 Torr; thus the CO(2) reserve was narrowed from -3.9 +/- 0.62 Torr in control to -2.7 +/- 0.78 Torr with dopamine. This decrease in the CO(2) reserve with dopamine resulted solely from the 20.5 +/- 11.3% increase in plant gain; the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal. We conclude that specific carotid chemoreceptor inhibition with dopamine increases the propensity for apnea during sleep by narrowing the CO(2) reserve below eupnea. This narrowing is due solely to an increase in plant gain as the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal control. These findings have implications for the role of chemoreceptor inhibition/stimulation in the genesis of apnea and breathing periodicity during sleep.

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“…Levels were variable and were a little higher than those which caused little or no ventilatory change in man (Stanley et al 1983). This dose was found by Laubie and Schmidt (1980) to have a large but not maximal effect on ventilation in dogs.…”

Section: Alrnitrine and V/q Matching V Constantmentioning

confidence: 88%

“…The initial dose was high relative to those given recently in man but was designed to reach and with the subsequent infusions, sustain levels comparable to those achieved in man. Levels were variable and were a little higher than those which caused little or no ventilatory change in man (Stanley et al 1983). This dose was found by Laubie and Schmidt (1980) to have a large but not maximal effect on ventilation in dogs.…”

Section: Alrnitrine and V/q Matching V Constantmentioning

confidence: 88%

Action of Almitrine Bismesylate on Ventilation‐perfusion Matching in Cats and Dogs With Part of the Lung Hypoventilated

Wach

Gill

Suggett

et al. 1986

Clin Exp Pharma Physio

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Ventilation to one lobe of lung was reduced in anaesthetized open-chest cats and dogs to simulate the ventilation/perfusion (V/Q) mismatching of chronic lung disease. Blood flow to this lobe fell less than ventilation; thus lobar V/Q diminished. In seven cats almitrine (0.5 mg/kg + 10 micrograms/kg per min, i.v.) caused a rise in pulmonary artery pressure (PPA), increased flow through the hypoventilated lobe in six out of seven cats and both increased or decreased lobar vascular resistance (PVR); the lobar V/Q ratio therefore fell. Arterial and lobar venous oxygen tension (PO2) fell. In five dogs almitrine caused a rise in PPA and PVR but lobar flow changes were variable. Arterial and lobar venous PO2 fell. With fixed ventilation, almitrine failed to improve V/Q matching; there was no improvement in gas exchange in the hypoventilated lobe. In eight dogs the hypoventilated lobe was perfused at constant flow with right atrial blood (i.e. while V/Q was held constant). Almitrine caused a rise in perfusion pressure, vasoconstriction, followed, in five out of eight dogs, by vasodilatation. In six similar cat preparations, vasoconstriction but not vasodilatation was clearly shown. In two cats dilatation after almitrine was demonstrated during ventilation with Nitrogen. In all experiments there was no significant effect of the solvent. Thus the dual action of almitrine seen in other species was seen in a proportion of cats and dogs. Results do not support the view that improved arterial gas tensions in patients after almitrine are attributable to diversion of blood flow away from hypoxic lung. Alternative mechanisms are discussed.

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Increased respiratory chemosensitivity induced by infusing almitrine intravenously in healthy man.

Cited by 16 publications

References 14 publications

Effect of almitrine bismesylate on pulmonary vasoreactivity to hypoxia in chronic obstructive pulmonary disease

Effect of almitrine bismesylate on pulmonary vasoreactivity to hypoxia in chronic obstructive pulmonary disease

Increased propensity for apnea via dopamine-induced carotid body inhibition in sleeping dogs

Action of Almitrine Bismesylate on Ventilation‐perfusion Matching in Cats and Dogs With Part of the Lung Hypoventilated

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