Protection, by Coronary Ligature, Against Isoproterenol-Induced Myocardial Necroses.

Selye, Hans; Veilleux, R; Grasso, S

doi:10.3181/00379727-104-25830

Cited by 19 publications

(4 citation statements)

References 3 publications

(4 reference statements)

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“…Previous studies have shown that a number of treatments may protect the heart against isoproterenolinduced tissue injury, including prior exposure to lowdose isoproterenol (9) and prior ischemia-reperfusion (30). In the present study, we found that sepsis did not protect against isoproterenol-induced tissue injury.…”

Section: Isoproterenol and The Myocardium In Sepsiscontrasting

confidence: 56%

Effects of isoproterenol on myocardial structure and function in septic rats

Piper

Myers

et al. 1999

Journal of Applied Physiology

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In this study we sought to determine the effect of sepsis on two sequelae of prolonged (24-h) beta-agonist administration, myocardial hypertrophy and catecholamine-induced cardiotoxicity. Sprague-Dawley rats were randomized to cecal ligation and perforation (CLP) or sham study groups and then further randomized to receive isoproterenol (2.4 mg. kg-1. day-1 iv) or placebo treatment. At 24 h, myocardial function was assessed by using the Langendorff isolated-heart technique or the heart processed for plain light microscopy. We found that 1) sepsis reduced contractile function, indicated by a rightward shift in the Starling curve (ANOVA with repeated measures, sepsis effect, P < 0.002); 2) sepsis-induced myocardial depression was reversed by isoproterenol treatment (isoproterenol effect, P < 0.0001); 3) sepsis reduced, but did not block, isoproterenol-induced myocardial hypertrophy (isoproterenol effect, P < 0.0001); 4) sepsis did not protect the heart from catecholamine-induced tissue injury; 5) the septic heart was protected against the effects of ischemiareperfusion (decreased postreperfusion resting tension, ANOVA with repeated measures, P < 0.01), an effect attenuated by isoproterenol treatment (P < 0.005); and 6) sepsis reduced the incidence of sustained asystole or ventricular fibrillation after ischemia-reperfusion (P < 0.05), an effect also attenuated by isoproterenol treatment (P < 0.01). We conclude that, in sepsis, beta-agonists induce changes in myocardial weight and function consistent with acute myocardial hypertrophy. These changes occur at the expense of significant tissue injury and increased sensitivity to ischemia-reperfusion-induced tissue injury.

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Section: Isoproterenol and The Myocardium In Sepsiscontrasting

confidence: 56%

Effects of isoproterenol on myocardial structure and function in septic rats

Piper

Myers

et al. 1999

Journal of Applied Physiology

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“…In 1960, Selye et al (18) first showed that a preparatory procedure, coronary artery ligation, while itself causing myocardial necrosis, appeared to protect the rest of the myocardium against a subsequent challenging insult {toxic doses of ISO 1 week later). In 1960, Selye et al (18) first showed that a preparatory procedure, coronary artery ligation, while itself causing myocardial necrosis, appeared to protect the rest of the myocardium against a subsequent challenging insult {toxic doses of ISO 1 week later).…”

Section: Discussionmentioning

confidence: 99%

Experimental studies on cardiac muscle cell adaptation to insult

et al. 1977

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Studies were carried out in rats on myocardial adaptation to injury produced by left coronary artery ligation. In the ischemic zone, open collaterals were present as shown by studies using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). This phenomenon may explain the inhomogeneous cardiac muscle cell alteration in the early phase of coronarogenic myocardial injury. Reperfusion, as evidenced by the influx of HRP into the damaged cells, unmasked sarcolemmal membrane injury. Cardiac muscle cell stimulation modifies the binding of macromolecules to cell components and may influence the repair processes. In the surviving myocardium, correlative enzyme histochemical and ultrastructural studies demonstrated the development of alternative metabolic pathways and morphological signs of adaptation explaining increasing resistance of such cardiac muscle cells to subsequent insult.

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“…Released catecholamines may have produced myocardial lesions (Rosenblum, Wohl & Stein, 1965) and enhanced the arrhythmogenicity of isoprenaline. Although this possibility cannot be excluded a priori, available evidence suggests that the presence of myocardial damage induced by either coronary artery ligation (Selye, Veilleux & Grasso, 1960;Dusek, Rona & Kahn, 1970) or catecholamine administration (Balazs, Ohtake & Noble, 1972) does not increase the cardiotoxic nor the arrhythmogenic action of isoprenaline (Joseph, Bloom, Pledger & Balazs, 1983;Joseph, Jordan & Balazs, 1984).…”

Section: ?Iscussionmentioning

confidence: 99%

Doca‐salt Induced Myocardial Sensitization to Ventricular Fibrillation by Isoprenaline in Rats. Role of the Autonomic Nervous Systme

Healy

Guider

1985

Journal of Autonomic Pharmacology

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The possible role of the autonomic nervous system in the development of myocardial sensitization to isoprenaline produced by DOCA-salt pretreatment was evaluated in bilaterally unanaesthetized rats subject to chronic ganglionic blockade with chlorisondamine or hexamethonium and to treatment with 6-hydroxydopamine. Isoprenaline produced ventricular fibrillation and death in rats pretreated for 6 days with DOCA (20 mg pellet, s.c.) and 0.9% saline. The incidence of mortality was dose dependent and was 76.6% with 150 microgram/kg of isoprenaline. Adrenalectomy did not alter the mortality rate. The combination of adrenalectomy with concurrent chronic ganglionic blockade significantly decreased the incidence of mortality and delayed the time of death. In contrast, 6-hydroxydopamine treatment and adrenalectomy did not alter the incidence of mortality nor time of death. No differences in myocardial noradrenaline turnover were detected in rats susceptible and nonsusceptible to death in ventricular fibrillation. We conclude that myocardial sensitization to isoprenaline induced by DOCA-salt requires a neurogenic component, which is not, however, manifested by changes in myocardial noradrenaline turnover.

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Protection, by Coronary Ligature, Against Isoproterenol-Induced Myocardial Necroses.

Cited by 19 publications

References 3 publications

Effects of isoproterenol on myocardial structure and function in septic rats

Effects of isoproterenol on myocardial structure and function in septic rats

Experimental studies on cardiac muscle cell adaptation to insult

Doca‐salt Induced Myocardial Sensitization to Ventricular Fibrillation by Isoprenaline in Rats. Role of the Autonomic Nervous Systme

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