Effects of Catecholamines on the Coronary Circulation in the Unanesthetized Dog

Marchetti, G; Merlo, L; Noseda, V.

doi:10.1159/000388368

Cited by 4 publications

(2 citation statements)

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“…For example, propranolol reduces the myocardial uptake and utilization of free fatty acids (31,32) thereby making the heart more dependent on carbohydrates as a metabolic fuel (33). However, propranolol inhibits the y3-adrenergie activation of phosphorylase (34).…”

Section: Reimer Rasmussen Jenningsmentioning

confidence: 99%

Reduction by Propranolol of Myocardial Necrosis following Temporary Coronary Artery Occlusion in Dogs

Reimer

Rasmussen

Jennings

1973

Circulation Research

206

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The effect of propranolol on the severity of myocardial necrosis following 40 minutes of temporary coronary artery occlusion was assessed in dogs. The circumflex coronary artery was occluded 1-2 cm from the aorta in open-chest dogs anesthetized with sodium pentobarbital. One group of dogs was untreated and a second group received propranolol (5.0 mg/kg, iv) 10 minutes prior to the occlusion. After 40 minutes the clamp was removed and arterial perfusion was restored. Dogs which survived this procedure were killed 2-5 days later for gross and histologic assessment of the necrosis. The relative area of necrosis (percent of fibers involved) in the posterior papillary muscle of each heart was quantified from stained histologic sections prepared from serial longitudinal slices of each posterior papillary muscle. Dogs treated with propranolol showed significantly less necrosis than did untreated controls, but the mechanism of the drug's action remains unknown. During coronary artery occlusion, propranolol-treated dogs exhibited somewhat lower heart rates, systolic blood pressures , and S-T segment elevations than did untreated dogs. However, none of these latter differences between groups was significant. KEY WORDS infarction heart quantification of infarct size ventricular fibrillation cell death ^8-receptor blockade S-T segment elevation • In the past few years much attention has been directed toward various therapeutic interventions which slow or prevent the development of myocar-dial cell death following an acute coronary artery occlusion. Sommers and Jennings (1) have suggested that propranolol in some way alters the course of ischemic injury.-They observed that 17 of 31 untreated dogs subjected to a 20-minute temporary occlusion of the circumflex coronary artery showed foci of necrosis 24-48 hours later. Only 3 of 30 similar dogs treated prophylactically with proprano-lol showed any necrosis. The 20-minute occlusion, however, induced relatively mild injury even without treatment, since it caused only small islands of cell death in about half of the untreated dogs. The present study was undertaken to provide a more severe test of propranolol's efficacy against myocardial ischemic injury. A 40-minute period of temporary circumflex coronary artery occlusion was chosen for study; injury induced by this method causes necrosis in 100% of dogs in the absence of protective therapy, and the characteristics of this model have been described in considerable detail (2, 3). The posterior papillary muscle is in the center of the lesion and is the site of maximum, most predictable injury. The proportion of muscle fibers which become necrotic can readily be quantified and in a previous series of dogs was about 55% of the posterior papillary muscle projecting above the endocardial surface of the ventricle (4). Thus this model provides an appropriate injury in which either beneficial or deleteri-ous interventions can be observed. In this study our purpose was to determine whether propranolol could reduce the number of cells which ...

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Section: Reimer Rasmussen Jenningsmentioning

confidence: 99%

Reduction by Propranolol of Myocardial Necrosis following Temporary Coronary Artery Occlusion in Dogs

Reimer

Rasmussen

Jennings

1973

Circulation Research

206

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“…Other studies have reported that angiotensin has a dose dependent action on coronary arteries. Marchetti et al (22) showed that coronary flow is reduced by small doses of angiotensin and increased by large doses. These findings could be explained by the systemic pressure changes caused by angiotensin.…”

Section: Angiotensinmentioning

confidence: 99%

Effects of angiotensin and ergonovine on large and small coronary arteries in the intact dog

et al. 1985

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Angiotensin (ATN) and ergonovine (ERG) are known to cause vasoconstriction of the coronary bed. However, ATN effects have been described mainly on the coronary resistance vessels, while ERG effects have been described on proximal conductance vessels. Recent studies have shown that proximal and distal coronary arteries are regulated independently. To examine both proximal and distal effects of ATN and ERG on the same heart, we studied 7 intact dogs, anesthetized with Innovar (Fentanyl 0.4 mg, Droperidol 20 mg, in 1 ml) and nitrous oxide, which were subjected to direct left anterior (LAD) coronary infusion of angiotensin (0.1, 0.5 and 5 micrograms/min) and ergonovine (0.5, 5, and 25 micrograms/min). Using a quantitative angiographic technique to measure artery dimensions and microspheres to measure flow, ERG infusion showed significant large artery constriction at all doses (maximum: 38.9 +/- 7.8% area reduction), and a significant decrease in LAD coronary artery flow, while endocardial/epicardial flow ratio remained unchanged. ATN produced a biphasic effect on the large coronary arteries. The lowest dose produced constriction (12.3 +/- 3.7% area reduction), which returned toward control value with the 0.5 micrograms/min dose (6.0 +/- 1.0% area reduction), and the 5 micrograms/min dose (1.5 +/- 9.5% area reduction), and no significant changes were observed in LAD flow with ATN infusion. Endocardial/epicardial ratio was unchanged, but aortic pressure was significantly increased during 0.5 and 5 micrograms/min ATN infusion. Coronary resistance (pressure/flow) increased with both ERG and ATN. ERG and ATN produce large and small coronary artery constriction. The coronary response to ERG in dogs is similar to the human coronary response, even though previous data indicated a minimal constrictor response to ERG in canine coronary arteries.

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Adrenergic receptors in the coronary circulation

Parratt

1967

American Heart Journal

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Effects of Catecholamines on the Coronary Circulation in the Unanesthetized Dog

Cited by 4 publications

References 0 publications

Reduction by Propranolol of Myocardial Necrosis following Temporary Coronary Artery Occlusion in Dogs

Reduction by Propranolol of Myocardial Necrosis following Temporary Coronary Artery Occlusion in Dogs

Effects of angiotensin and ergonovine on large and small coronary arteries in the intact dog

Adrenergic receptors in the coronary circulation

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