The development of resistance to the ischemic cardiopathic effect of isoproterenol

Balázs, T.; Ohtake, Shigeaki; Noble, John F.

doi:10.1016/0041-008x(72)90063-4

Cited by 17 publications

(4 citation statements)

References 6 publications

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“…In fact, the lesions heal and may not recur during continuous dosing. A tolerance develops which lasts for a short period, even after discontinuation of the dosing (16). A decrease in the adrenergic receptor population may be surmised to be involved in the mechanism of the tolerance.…”

Section: Cardiac Lesions Due To Exaggerated Cardiovascular Effectsmentioning

confidence: 99%

Cardiac lesions induced by chemicals.

Balázs¹,

Ferrans²

1978

Environ Health Perspect

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Chemically induced cardiomyopathies are frequently the consequences of a cardiac metabolic imbalance brought about by exaggerated functional affects. The infarctlike lesions induced by adrenergic beta-receptor stimulants and the vasodilating antihypertensives serve as examples of this phenomenon. Direct cardiotoxic mechanisms not related to cardiovascular functional effects are responsible for another class of toxic cardiomyopathy. An example of this is the cardiomyopathy produced by the anthracycline antineoplastic agents. The pathogenesis, morphological changes and toxicologic features of these cardiomyopathies are described with particular reference to their detection in preclinical toxicity studies.

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Section: Cardiac Lesions Due To Exaggerated Cardiovascular Effectsmentioning

confidence: 99%

Cardiac lesions induced by chemicals.

Balázs¹,

Ferrans²

1978

Environ Health Perspect

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“…With minoxidil, the coronary arterial medial hemorrhage and necrosis seen at 3 d were not seen at 30 or 365 d because ofan apparent tolerance to injury after the first few days of treatment. Tolerance to subendocardial necrosis has been clearly shown to occur in dogs treated with several vasodilators (2,4,21). The left atrial lesions seen in pigs at 3 d (12,40), during the most profound pharmacologic response, were not evident at 32 dafter the pharmacologic effects had markedly subsided (Upjohn, unpublished data).…”

Section: Mechanism Ofright Atrial Lesions In Dogs Treated With Toxic mentioning

confidence: 99%

“…The microscopic appearance of the arterial lesions suggest that medial smooth muscle is the primary target of injury caused by minoxidil and other vasodilators. Coronary arterial injury, like papillary muscle necrosis (2,4,21), occurs only during the initial few days of treatment after which tolerance develops to further acute injury. The perivascular fibrosis, rare medial distortion, and subintimal thickening seen in dogs treated with minoxidil for 4 weeks would be consistent with responses to a previous acute vascular injury (28,32).…”

Section: Mechanism Ofright Atrial Lesions In Dogs Treated With Toxic mentioning

confidence: 99%

Pathogenesis of Cardiovascular Alterations in Dogs Treated with Minoxidil

et al. 1989

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Minoxidil and other potent vasodilators cause coronary arterial injury, right atrial hemorrhagic lesions, and subendocardial necrosis in dogs, This paper discusses the pathogenesis of coronary arterial and right atrial lesions associated with minoxidil in the dog, Acute coronary vascular injury characterized by segmental medial hemorrhage and necrosis and perivascular inflammation occurred only during the first few days of treatment, after which tolerance to further acute injury developed, At 30 d or more of treatment, coronary vascular injury was characterized by perivascular fibrosis rarely attended by medial distortion or hyperplasia and subintimal thickening, changes consistent with responses to previous injury, Right atrial hemorrhagic lesions, unlike coronary vascular injury, often became progressively more extensive with continued treatment. At 3 d, atrial hemorrhage and inflammation were confined to the subepicardium ofthe right atrium, evidently around affected subepicardial branches of the right coronary artery, At 30 d, fibrovascular proliferative right atrial lesions (granulation tissue with evidence of continual hemorrhage) extended from the epicardium to the myocardium, with eventual replacement ofthe atrial wall by mature connective tissue at I yr of treatment. Minoxidil-induced cardiovascular lesions were not prevented by treatment with a l3-blocker (propranolol), or an a-blocker (dibenzylene), or by sympathetic neural activity suppression (surgical sympathectomy or constant carotid sinus nerve stimulation), suggesting that the sympathetic response to the pharmacologic activity of minoxidil was not responsible for the induction of the cardiovascular lesions. Minoxidil-related vascular lesions were confined to the most pharmacologically responsive segment of the arterial system, the coronary arteries, suggesting that medial injury may have been associated with tensile changes in the arterial wall.

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“…Some investigators have reported that isoprenaline induces myocardial necrosis in experimental animals (Ferrans et al, 1964;Balazs, 1972), but at doses corresponding to 1 to 2 mg/kg, which are never used in medical treatment.…”

Section: Discussionmentioning

confidence: 99%

Comparative Haemodynamic Effects of Glucagon and Isoprenaline in the Early Postoperative Period in Cardiac Surgery

Goenen

Jaumin

Raveau

et al. 1975

Scandinavian Journal of Thoracic and Cardiovascular Surgery

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In order to study the haemodynamic effects of isoprenaline and glucagon in the immediate postoperative period, 16 patients who had single or multiple valve replacement or coronary artery bypass grafts were investigated. Measurements of cardiac index, stroke index, heart rate, arterial and right atrial mean pressures were made either before, during, or after the administration of both drugs. With the doses used, the inotropic effects of both drugs are similar, while the chronotropic action is statistically higher during isoprenaline infusion than after glucagon administration. This fact explains the greater increase in cardiac index after isoprenaline administration. Mean arterial pressure shows no significant changes after either drug, while right atrial mean pressure decreases significantly. Peripheral vascular resistance remained mostly constant. The activity of glucagon injected as a single bolus seems to be maximal 10 to 15 minutes after the injection and dissipates about 30 minutes later. The ideal dose of isoprenaline is between 0.8 and 2 mug/min. Within this range, the inotropic effect is maximal and the chronotropic and bathmotropic effects are limited. Above 2 mug/min, cardiac index and stroke index decrease, and arrhythmias become more frequent.

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The development of resistance to the ischemic cardiopathic effect of isoproterenol

Cited by 17 publications

References 6 publications

Cardiac lesions induced by chemicals.

Cardiac lesions induced by chemicals.

Pathogenesis of Cardiovascular Alterations in Dogs Treated with Minoxidil

Comparative Haemodynamic Effects of Glucagon and Isoprenaline in the Early Postoperative Period in Cardiac Surgery

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