Effect of Dopamine and Calcium on Lipolysis and Myocardial Ischemic Injury following Acute Coronary Occlusion in the Dog

Lekven, Jon; Semb, Gudmund

doi:10.1161/01.res.34.3.349

Cited by 18 publications

(7 citation statements)

References 55 publications

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“…Qualitatively we reached similar observations on the role of MVO2 as others (10,15,9,7). The difference to earlier studies lies in the quantitative approach and in the definition of known determinants of infarct size (myocardium at risk, collateral flow).…”

Section: Discussionsupporting

confidence: 90%

Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion

et al. 1982

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The influence of myocardial oxygen consumption (MVO2) at the moment of coronary occlusion on the size of the ensuing necrosis was investigated in 12 anaesthetised dogs. A two-infarction model was used with a sequential occlusion of two distant coronary branches in the same heart, however under different levels of MVO2. One group of occlusions was produced at a high MVO2 of 21.6 +/- 3.0 ml O2 . min-1 . 100 g-1. This group was compared with a second in which necrosis proceeded at a low MVO2 estimated to be 5.9 +/- 1.5 ml O2 . min-1 . 100 g-1 averaged over a 90-min occlusion period. Infarct size expressed as percentage of perfusion area was 43 +/- 28% in group 1 and 11 +/- 11% in group 2 (p less than 0.005). The mass of the perfusion area was equal in both groups (17 +/- 4 g, 19 +/- 6 g). The amount of myocardial necrosis, which after a 90-min occlusion depends on the acute collateral blood flow, was in every case greater under high MVO2. Thus a low MVO2 at the moment of occlusion can postpone myocardial necrosis.

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Section: Discussionsupporting

confidence: 90%

Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion

et al. 1982

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“…Such deleterious actions have been previously demonstrated for dopamine (Lekven and Semb, 1974) and isoproterenol (Vatner et al, 1974). Such deleterious actions have been previously demonstrated for dopamine (Lekven and Semb, 1974) and isoproterenol (Vatner et al, 1974).…”

Section: Discussionsupporting

confidence: 56%

“…By comparison, the sympathomimetic amine, dopamine induces systemic and local myocardial release of norepinephrine (Goldberg, 1972), as well as increasing arterial concentrations of free fatty acids through beta-adrenoreceptor-mediated activation of hormone-sensitive lipase (Lekven and Semb, 1974). These 2 effects, which serve to increase myocardial oxygen consumption, represent potential disadvantages of dopamine when compared to a non sympathomimetic inotropic agent such as in the treatment of postischemic ventricular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Myocardium During Reperfusion Injury by a New Inotrope‐vasodilator Agent, McI‐154

Wynsen

Shimshak

Preuss

et al. 1987

Fundamemntal Clinical Pharma

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The systemic and coronary hemodynamic actions of a newly synthesized inotropic agent structurally related to milrinone and amrinone, MCI-154 (0.5-4.0 micrograms/kg/min IV), were studied in 2 groups of conscious, chronically instrumented dogs with normal or depressed postischemic, reperfused myocardium after a 15-min coronary artery occlusion. In an additional group of control experiments, the time course of recovery of postischemic, reperfused myocardium was studied to verify the constancy of regional segment shortening in the previously ischemic zone during the time corresponding to drug infusion. Similar inotropic actions of MCI-154 were observed in both normal and postischemic, reperfused hearts, indicating significant contractile reserve to be present in 'stunned' myocardium. Global contractility as measured by peak positive dP/dt was significantly increased in both groups. In postischemic, reperfused myocardium 90 min after initiation of reflow, regional segment function remained depressed at 44% of control but improved to 93% of control after administration of MCI-154. In addition, MCI-154 produced significant dose-related decreases in mean arterial pressure, left ventricular end-diastolic pressure, end-diastolic segment length, and diastolic coronary vascular resistance. The data demonstrate that in addition to producing beneficial hemodynamic changes, MCI-154, a new non-sympathomimetic inotropic agent, markedly enhances regional contractility of postischemic, reperfused myocardium.

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“…The recent demonstration that the size of experimental infarcts may be altered favorably by therapeutic interventions (2)(3)(4)(5), which presumably change the rate at which ischemia progresses, has provided an impetus to define the metabolic and hemodynamic changes which occur following coronary artery occlusion.…”

Section: Introductionmentioning

confidence: 99%

“…The degree of S-T segment elevation has recently been used widely (2)(3)(4)(5) as an index of ischemic injury, so it was of particular interest to examine the relationship between epicardial S-T 6 9 8…”

Section: Introductionmentioning

confidence: 99%

Changes in myocardial blood flow and S-T segment elevation following coronary artery occlusion in dogs.

Smith¹,

Singh²,

Norris³

et al. 1975

Circulation Research

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The relationship between regional blood flow and epicardial S-T segment elevation was studied in 26 open-chest anesthetized dogs with left anterior coronary artery ligations. Changes in myocardial blood flow, measured with 15 plus or minus 5mu (diameter) microspheres labeled with 141-Ce, 85-Sr, and 169-Yb, were correlated with summated S-T segment elevations 15 minutes, 1 hour, and 2 hours after coronary artery occlusion. In normal areas, myocardial blood flow was 113 plus or minus 5 ml/min 100 g- minus 1 and summated S-T segment elevation was 0.3 plus or minus 0.2 mv. Fifteen minutes after coronary artery occlusion in 26 dogs, S-T segment elevation was 5.7 plus or minus 0.7 mv over the center of the infarct and myocardial blood flow was 10 plus or minus 1 ml/min 100 g- minus 1; over the border zone, myocardial blood flow was 63 plus or minus 4 ml/min 100 g- minus 1 and S-T segment elevation was 3.1 plus or minus 0.1 mv. One third of the areas with a myocardial blood flow of 10 ml/min 100 g- minus 1 or less had no S-T segment elevation. In the center and border zones of the infarct in 9 dogs, myocardial blood flow increased from 11 plus or minus 2 and 67 plus or minus 8 ml/min 100 g- minus 1 15 minutes after occlusion to 20 plus or minus 4 and 84 plus or minus 12 ml/min 100 g- minus 1, respectively, 2 hours after coronary artery occlusion. These increases were not associated with a significant reduction in summated S-T segment elevation. The results do not suggest a simple quantitative relationship between epicardial S-T segment elevation and myocardial blood flow following acute coronary artery occlusion.

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Effect of Dopamine and Calcium on Lipolysis and Myocardial Ischemic Injury following Acute Coronary Occlusion in the Dog

Cited by 18 publications

References 55 publications

Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion

Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion

Stimulation of Myocardium During Reperfusion Injury by a New Inotrope‐vasodilator Agent, McI‐154

Changes in myocardial blood flow and S-T segment elevation following coronary artery occlusion in dogs.

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