1989
DOI: 10.1007/bf01883865
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Peripheral hemodynamic effects of ibopamine in patients with congestive heart failure. A placebo-controlled, double-blind study

Abstract: Under double-blind conditions, 150 mg of ibopamine (di-isobutyric ester of N-methyldopamine) or placebo were given orally to 11 patients with congestive heart failure; after 3 hours, 50 mg of sulpiride were administered intramuscularly. Peripheral hemodynamics were evaluated at the level of the forearm using strain-gauge plethysmography. Ibopamine increased arterial blood flow and venous capacity and decreased arterial peripheral resistance; these effects were counteracted by sulpiride. No significant changes … Show more

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Cited by 3 publications
(4 citation statements)
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“…At an unchanged heart rate and mean arterial blood pressure, in accordance with the literature [4][5][6][7][8][9][10][11][12][13][14][15][16], the transient rise in arterial pulse pressure after IBO is probably caused by a rise in stroke volume and cardiac output rather than a fall in arterial compliance. Indeed, cardiac output may rise already = 0.5 h after a single oral dose of = 200 mg IBO, and this increase may be maintained for ~ 4 h, while, in some studies, systemic vascular resistance fell only -~ 1-2 h after administration following a transient rise in arterial pressure [4][5][6][7][8][9][10][11][12][13][14][15][16]. Hence, the early and transient rise in thoracic blood volume may have been caused by cardiac enlargement in response to a temporary increase in systolic blood pressure and, thus, left ventricular afterload in the absence of an effect on peripheral veins and in spite of the positive inotropic effect of the dose (200 mg) of IBO used [4][5][6][7][8][9][10][11][12][13][14].…”
Section: Discussionsupporting
confidence: 75%
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“…At an unchanged heart rate and mean arterial blood pressure, in accordance with the literature [4][5][6][7][8][9][10][11][12][13][14][15][16], the transient rise in arterial pulse pressure after IBO is probably caused by a rise in stroke volume and cardiac output rather than a fall in arterial compliance. Indeed, cardiac output may rise already = 0.5 h after a single oral dose of = 200 mg IBO, and this increase may be maintained for ~ 4 h, while, in some studies, systemic vascular resistance fell only -~ 1-2 h after administration following a transient rise in arterial pressure [4][5][6][7][8][9][10][11][12][13][14][15][16]. Hence, the early and transient rise in thoracic blood volume may have been caused by cardiac enlargement in response to a temporary increase in systolic blood pressure and, thus, left ventricular afterload in the absence of an effect on peripheral veins and in spite of the positive inotropic effect of the dose (200 mg) of IBO used [4][5][6][7][8][9][10][11][12][13][14].…”
Section: Discussionsupporting
confidence: 75%
“…This finding contrasts with studies in healthy volunteers and patients with CHF, as measured by strain-gauge plethysmography, the drug increased blood flow and dilated veins in the forearm, starting = 1.5 h after a single 150-rag dose; this could be prevented by prior blockade of dopamine receptors [15,16]. The discrepancy may relate to differences in methods, doses or both.…”
Section: Discussioncontrasting
confidence: 54%
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“…In patients with congestive heart failure, forearm arterial blood flow and venous capacity increased by 25 to 45% and 18%, respectively, and peripheral arterial resistance decreased by 35%, as assessed by strain-gauge plethysmography, in response to a single oral dose of ibopamine 150mg (Longhini et al 1989;Musacci et al 1986). These effects were significantly suppressed by sulpiride, a specific dopaminergic antagonist.…”
Section: Peripheral Haemodynamic Effectsmentioning
confidence: 99%