Cardiotonic and Coronary Vasodilatatory Effects of Amrinone in the Canine Heart-Lung Preparation with a Support Dog as Compared with Those of Dobutamine

Takeda, Kazuki; Matsui, Kazuki; Nakazawa, Makoto; Nakahara, Hiroyuki; Imai, Hirotatsu; Imai, Shoichi

doi:10.1254/jjp.40.381

Cited by 5 publications

(3 citation statements)

References 14 publications

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“…Rooney et al [16] have observed that amrinone did not increase coronary flow to a level greater than the metabolic requirement of the heart and that amrinone was not a direct coronary vasodilator. However, other studies have reported that amrinone caused direct coronary vasodilation and increased myocardial oxygen supply in excess of the increase in myocardial oxygen demand [13,17[. Milrinone, a bipyridine-positive inotropic agent that is closely related to amrinone, increased coronary blood flow without significant changes in systemic hemodynamics in the conscious rat [18].…”

Section: Discussionmentioning

confidence: 99%

Amrinone improves postischemic myocardial metabolism in the rat heart-lung preparation

et al. 1996

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Amrinone, a phosphodiesterase inhibitor, is a non-glycosidic noncatecholamine with both vasodilator and positive inotropic effects. We were interested in assessing the effect of amrinone on postischemic cardiac performance in the isolated heart-lung preparation. Twenty-four male Wistar-ST rats were used. They were randomly divided into three groups. Amrinone, 10 μg·ml or 100 μg·ml was administered 8 min after the start of perfusion except in the control group. Ten minutes after the start of perfusion, all hearts were made globally ischemic for 8 min. Subsequently, the preparations were reperfused for 10 min. At the end of the experimental period, the hearts were freeze-clamped, and then myocardial high-energy phosphates, lactate, pyruvate, and glycogen were measured. Hemodynamic parameters in all groups decreased significantly during ischemia. However, there were no significant differences among the groups. The myocardial ATP level in the 100 μg·ml group was significantly higher than that in the control group. Adenosine diphosphate (ADP) and adenosine monophosphate (AMP) levels in the 100 μg·ml group were significantly lower than those in the control group. Myocardial lactate, pyruvate, and glycogen levels were not significantly different among the groups. This result suggests that amrinone improves postischemic myocardial metabolism. Although we could not measure coronary flow, amrinone might increase coronary flow with direct coronary vasodilation which would have increased the myocardial ATP and energy charge levels.

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Section: Discussionmentioning

confidence: 99%

Amrinone improves postischemic myocardial metabolism in the rat heart-lung preparation

et al. 1996

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“…As described in the introduction amrinone is unique among newer PDE inhibitors in being more vasodilatory than positive inotropic (Firth 1984;Taira 1984Taira , 1987Wilmshurst et al 1984;Takeda et al 1986;Sate et al 1986). The mechanisms of its predominant vasodilator action, however, remained unsolved.…”

Section: Discussionmentioning

confidence: 99%

“…The prominent coronary vasodilator action of amrinone has also been demonstrated in canine heart-lung preparations with support dogs (Takeda et al 1986). In keeping with these results obtained from animal experiments, the salutary effect of amrinone in patients with congestive heart failure has been ascribed to its potent vasodilator effect (Firth et al 1984;Wilmshurst et al 1984).…”

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confidence: 91%

Vasodilator Mechanisms of Action of Amrinone Do Not Involve the Opening of Either ATP-Sensitive or Ca2+-Activated K+ Channels.

Orito

Satoh

Taira

1994

Tohoku J. Exp. Med.

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Amrinone is more coronary vasodilatory than positive inotropic compared with other newer phosphodiesterase inhibitors. In order to explore possible involvements of ATPsensitive K+ (KATP) and large-conductance Ca2~-activated K+ (Kca) channels in the vasodilator effect of amrinone, we investigated whether amrinone-induced vasodilation would be antagonized by glibenclamide, a blocker of KATP channels, or by charybdotoxin or tetraethylammonium, blockers of Kca channels. In isolated, blood-perfused canine papillary muscle preparations, the amrinone-induced increase in blood flow was not affected by glibenclamide given to support dogs. In canine large coronary arteries contracted with high (25 mM) KC1, amrinoneinduced relaxation was not affected by glibenclamide, charybdotoxin and tetraethylammonium. These results suggest that the vasodilator mechanisms of amrinone do not involve the opening of either KATP or Kca channels.

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Cardiotropic activity of pyridin-2(1H)-ones

et al. 1989

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Cardiotonic and Coronary Vasodilatatory Effects of Amrinone in the Canine Heart-Lung Preparation with a Support Dog as Compared with Those of Dobutamine

Cited by 5 publications

References 14 publications

Amrinone improves postischemic myocardial metabolism in the rat heart-lung preparation

Amrinone improves postischemic myocardial metabolism in the rat heart-lung preparation

Vasodilator Mechanisms of Action of Amrinone Do Not Involve the Opening of Either ATP-Sensitive or Ca2+-Activated K+ Channels.

Cardiotropic activity of pyridin-2(1H)-ones

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