Cardiovascular Effects of KM-13, a New, Orally Effective, Cardiotonic Sympathomimetic Amine

Caldwell, Robert W.; Nash, Clinton B.; Smulkowski, M.; Tuttle, Ronald R.

doi:10.1097/00005344-198703000-00015

Cited by 4 publications

(1 citation statement)

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“…Dobutamine has relatively less chronotropic effect for a given inotropic effect [9]. In addition, dobutamine has been observed to decrease heart rate, to increase afterload, to increase left ventricular end-diastolic pressure, to reduce venous capacity, and to increase coronary perfusion pressue by stimulating alphaadrenergic receptors [14][15][16][17][18][19][20]. These effects result in a vagally mediated attenuation of the heart rate response.…”

Section: Discussionmentioning

confidence: 99%

A novel catecholamine, arbutamine, for a pharmacological cardiac stress agent

Nagarajan

Abou-Mohamed

Myers

et al. 1996

Cardiovasc Drug Ther

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Arbutamine, developed for use as a cardiac stress agent, was compared with isoproterenol and dobutamine in anesthetized dogs for cardiovascular actions prior to and after beta-adrenergic blockade with propranolol. The efficacy and safety of arbutamine were also evaluated in a canine model of myocardial ischemia obtained by partially occluding the left anterior descending coronary artery. Comparison of hemodynamic variables in normal dogs showed that arbutamine was approximately equipotent to isoproterenol in increasing heart rate and cardiac contractility, and in decreasing total peripheral vascular resistance and mean arterial blood pressure. Arbutamine was 210 times more potent than dobutamine in increasing cardiac contractility by 70%; however, at this dose dobutamine exhibited a negative chronotropic response. Beta-adrenergic blockade with propranolol shifted the agonist's dose-response curves for heart rate and contractility to the right; however, low doses of dobutamine exhibited a negative chronotropic effect and increased the total peripheral vascular resistance. In dogs subjected to partial left anterior descending coronary artery occlusion, arbutamine produced significant ST-segment deflections, beginning at a dose of 0.1 nmol/kg/min. Impairment of segment shortening, reflecting cardiac wall motion abnormality, was evident at a dose of 0.3 nmol/kg/min. Isoproterenol did not cause significant changes in these parameters. These results show that arbutamine is capable of producing graded increments in cardiac contractility and rate before and after beta-adrenergic blockage in normal dogs. In dogs subjected to coronary artery occlusion, it is capable of provoking myocardial ischemia at dose levels devoid of toxicity.

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