Some similar effects after large doses of catecholamines and myocardial infarction in dogs∗

Maling, Harriet M.; Highman, Benjamin; Thompson, Elizabeth

doi:10.1016/0002-9149(60)90128-4

Cited by 63 publications

(22 citation statements)

References 13 publications

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“…In the present study, we administered 4 fig • kg" 1 • min" 1 of NE for 4 hours; an initial dose of propranolol was given before the onset of NE infusion and was followed by additional propranolol doses at hourly intervals to a total dose of 0.625 mg/kg. Although a number of investigators have observed some protection against catecholamine-induced myocardial lesions with a variety of alpha-receptor blocking agents (3, [11][12][13][14][15], the discrepancy in experimental design between those studies and the present investigation makes any comparison difficult.…”

Section: Discussionmentioning

confidence: 89%

Cardiovascular Effects of Sustained Norepinephrine Infusions in Dogs

Moss

Schenk

1970

Circulation Research

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Sustained infusions of norepinephrine (NE) are known to produce deleterious pathophysiologic effects on the circulatory system. The mechanisms responsible for these effects were investigated in 25 dogs; 17 were treated with selective block of alpha receptors by phenoxybenzamine or of beta receptors by propranolol, or by both agents, and then infused with NE (4 /ig-kg-1 -min-1 ) for 4 hours; 8 control animals were given only adrenergic blocking agents. Left ventricular and systemic pressure, cardiac output and arterial blood gases were measured at selected intervals throughout the infusion period, and histologic examinations of the heart and other vital organs were performed at the conclusion of each study. In animals with alpha-receptor blockade, NE infusions were associated with extensive subendocardial hemorrhage and focal myofiber fatty degeneration, yet blood pressure, cardiac output, and derived cardiac work parameters were well maintained. In animals with beta-receptor blockade, NE caused minimal pathologic changes in the heart despite significant reduction in cardiac output, minute and stroke work, and significant increase in left ventricular end-diastolic pressure (LVEDP) and peripheral vascular resistance. In animals receiving combined alpha-and beta-receptor blockade, NE infusions were not associated with significant hemodynamic or morphologic abnormality. These findings indicate: (1) the hemodynamic abnormalities are the result of the action of NE mediated primarily through alpha receptors; (2) the morphologic changes are produced by NE mediated mostly through beta receptors; and (3) the reductions in cardiac output and minute and stroke work and the increase in LVEDP produced by sustained NE infusions are not necessarily a consequence of the pathologic changes which develop in the heart muscle. This work was supported in part by U. S. Public Health Service Grants HE 10465-03 and HE 10251-05 from the National Heart Institute, a General Research Support grant and by the Ernest L. Woodward Research Fund.Received July 11, 1969; accepted for publication October 17, 1970. tory abnormalities were correlated with the development of extensive myocardial lesions (5, 6) and it was postulated that the myocardial lesions accounted in large part for the low cardiac output that developed during NE administration (4).Norepinephrine, by stimulating both alpha and beta receptors, produces constriction of the peripheral resistance vessels and a positive inotropic effect on the myocardium. To define more clearly the mechanisms responsible for the deterioration in cardiac function and for the cardiovascular lesions that develop during sustained NE infusions, selective adrenergic blocking agents were administered before NE

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Section: Discussionmentioning

confidence: 89%

Cardiovascular Effects of Sustained Norepinephrine Infusions in Dogs

Moss

Schenk

1970

Circulation Research

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“…4 Infusion of sympathetic catecholamines in experimental animals is known to produce widespread cardiac necrosis. [5][6][7][8] In man, patients with pheochromocytoma are frequently found at postmortem examination to have similar necrosis in the myocardium. 9 Patients who receive prolonged infusions of norepinephrine for the treatment of hypotension are also frequently seen to have similar lesions in their myocardium at autopsy.…”

mentioning

confidence: 99%

Intravascular Platelet Aggregation in the Heart Induced by Stress

Haft

Fani

1973

Circulation

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SUMMARYSixteen rats, stressed by immersion in ice-cold water for 25-45 min, were found to have platelet aggregates in myocardial small vessels on electron microscopic study. None of six similar nonstressed control rats had platelets in myocardial vessels. It XLVII, February 1973 intravascular aggregation of platelets in the heart. We have previously reported that pretreatment with the antiplatelet aggregating drugs aspirin and dipyridamole'6-18 will protect against the cardiac necrosis seen after epinephrine infusion,'9-20 and using the electron microscope we have demonstrated the presence of platelet aggregates in the small vessels of the heart in dogs infused with norepinephrine.20-22 It was the purpose of the present study to determine if stress alone, without the infusion of exogenous catecholamine, would also lead to intravascular platelet aggregation in the heart. Materials and MethodsTwenty-two 300-500-g rats were used for study. Sixteen rats were stressed by immersing them in 4-5 in. of ice-cold water in a glass bell jar. The level of the water was chosen such that the rats were able to keep their heads out of the water by balancing themselves to an upright position. The animals were kept in the water until they showed signs of marked fatigue, usually within 25-45 min. They were then sacrificed by a bl9w on the head followed by immediate removal. of their beating hearts and sections of the left ventricle were prepared for electron microscopy. Six similar rats were brought to the laboratory but kept at rest in their cages for the same period of time, then sacrificed and similar sections taken. The sections were prepared for electron microscopic study by fixing them in glutaraldehyde, postfixing with osmic acid, and staining with uranyl acetate and lead citrate. At least 20 blocks of tissue were prepared for each rat, and approximately 25 sections were taken from each block. ResultsAll 16 stressed rats were found to have myocardial small vessels that contained aggregated

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“…It is notable that even in defining the term infarction, as applied to the myocardium, recognition is now given to the fact that arterial obstruction or insufficiency is not the sole cause (47). Since the early study of Herrick (48), demonstrating the effects of coronary occlusion, and the subsequent emphasis by Keefer and Kesnik (49) on the role of myocardial oxygen deprivation in the symptoms of myocardium associated with elevated serum levels of several myocardial enzymes (59)(60)(61). These effects are prevented by the administration of an LY-receptor blocking agent (62-64').…”

Section: Sympathomimetic Aminesmentioning

confidence: 99%

Drug-induced cardiomyopathies

Wenzel

1967

Journal of Pharmaceutical Sciences

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Some similar effects after large doses of catecholamines and myocardial infarction in dogs∗

Cited by 63 publications

References 13 publications

Cardiovascular Effects of Sustained Norepinephrine Infusions in Dogs

Cardiovascular Effects of Sustained Norepinephrine Infusions in Dogs

Intravascular Platelet Aggregation in the Heart Induced by Stress

Drug-induced cardiomyopathies

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