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Respiration Physiology, 1988
Almitrine bismesylate (Aim) has been shown to increase arterial oxygen tension in patients with c... more Almitrine bismesylate (Aim) has been shown to increase arterial oxygen tension in patients with chronic obstructive pulmonary disease. This effect is thought to be attributable to the enhancement of hypoxic pulmonary vasoconstriction (HPV). We evaluated the effect of various doses of Alm on HPV in terms of blood flow diversion associated with anoxic challenge to the left lower lobe (LLL) in dogs with the LLL and the rest of the lung separately ventilated. The stimulus-response curve shifted to the right with increasing rate of Aim infusion, suggesting that Aim enhances the reactivity of the pulmonary vessels to hypoxia. Low doses of Aim enhanced HPV, while higher doses attenuated it. This suggests that the degree of vasoconstriction in hypoxic and non-hypoxic regions depends on the dose of Aim. The same effects of Alm were also observed in peripheral chemoreceptor denervated dogs. It is supposed that the vasoconstriction induced by Aim may be attributable to a direct effect on pulmonary vessels rather than to a nervous reflex effect. Almitrine; Dog; Hypoxic pulmonary vasoconstriction; Peripheral chemoreceptor Hypoxemia occurs in patients with chronic obstructive pulmonary disease (COPD) as a result of ventilation/perfusion ('V'A/t)) inequality (Wagner and West, 1980). Oxygen therapy and bronchodilators have been used in the treatment of this condition. Recently, almitrine bismesylate (Aim) which increases arterial oxygen tension (Pao2) has come into therapeutic use. This drug has been shown to stimulate peripheral chemoreceptors and increase ventilation (Laubie and Schmitt, 1980; de Backer et al., 1983). It has been shown, however, that Aim may increase Pao2 in patients with COPD at doses which do not induce an increase in ventilation (Rigaud etal., 1982; Mtlot etal., 1983; Simonneau etal., 1986) or in respiratory insufficiency with constant mechanical ventilation (Tenaillon et al., 1980; Castaing et aL, 1983). For this reason it has been suggested that the blood gas improvement may result from an improvement of VA/0 inequality due to an enhancement of hypoxic pulmonary vasoconstriction (HPV). The
Respiration Physiology, 1988
Almitrine bismesylate (Aim) has been shown to increase arterial oxygen tension in patients with c... more Almitrine bismesylate (Aim) has been shown to increase arterial oxygen tension in patients with chronic obstructive pulmonary disease. This effect is thought to be attributable to the enhancement of hypoxic pulmonary vasoconstriction (HPV). We evaluated the effect of various doses of Alm on HPV in terms of blood flow diversion associated with anoxic challenge to the left lower lobe (LLL) in dogs with the LLL and the rest of the lung separately ventilated. The stimulus-response curve shifted to the right with increasing rate of Aim infusion, suggesting that Aim enhances the reactivity of the pulmonary vessels to hypoxia. Low doses of Aim enhanced HPV, while higher doses attenuated it. This suggests that the degree of vasoconstriction in hypoxic and non-hypoxic regions depends on the dose of Aim. The same effects of Alm were also observed in peripheral chemoreceptor denervated dogs. It is supposed that the vasoconstriction induced by Aim may be attributable to a direct effect on pulmonary vessels rather than to a nervous reflex effect. Almitrine; Dog; Hypoxic pulmonary vasoconstriction; Peripheral chemoreceptor Hypoxemia occurs in patients with chronic obstructive pulmonary disease (COPD) as a result of ventilation/perfusion ('V'A/t)) inequality (Wagner and West, 1980). Oxygen therapy and bronchodilators have been used in the treatment of this condition. Recently, almitrine bismesylate (Aim) which increases arterial oxygen tension (Pao2) has come into therapeutic use. This drug has been shown to stimulate peripheral chemoreceptors and increase ventilation (Laubie and Schmitt, 1980; de Backer et al., 1983). It has been shown, however, that Aim may increase Pao2 in patients with COPD at doses which do not induce an increase in ventilation (Rigaud etal., 1982; Mtlot etal., 1983; Simonneau etal., 1986) or in respiratory insufficiency with constant mechanical ventilation (Tenaillon et al., 1980; Castaing et aL, 1983). For this reason it has been suggested that the blood gas improvement may result from an improvement of VA/0 inequality due to an enhancement of hypoxic pulmonary vasoconstriction (HPV). The