Extraordinary potentiation of isoproterenol cardiotoxicity by corticoid pretreatment

Guideri, Giancarlo; Barletta, Michael; Lehr, David

doi:10.1093/cvr/8.6.775

Cited by 35 publications

(10 citation statements)

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“…One explanation of this possible interaction would be increased cardiac automaticity due to an accumulation of deoxycortisol, produced when metyrapone blocks the enzyme 11b-hydroxylase which converts deoxycortisol into cortisol (Goldfien, 1995) Some corticosteroids potentiate isoproterenol-induced cardiotoxicity. Prednisone and desoxycorticosterone acetate potentiate the arrhythmogenic property (ventricular fibrillation) of isoproterenol in rats (Guideri et al, 1978). Deoxycortisol may have arrhythmogenic properties similar to desoxycorticosterone acetate and may potentiate arrhythmogenicity from methamphetamine.…”

Section: Discussionmentioning

confidence: 97%

Altering Cortisol Level does not Change the Pleasurable Effects of Methamphetamine in Humans

Harris

Reus

Wolkowitz

et al. 2003

Neuropsychopharmacol

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Preclinical studies have linked corticosteroid secretion and levels with drug self-administration by animals. In a double-blind, cross-over study, subjective, physiological, and endocrine responses to intravenous doses of methamphetamine 0.5 mg/kg or placebo were assessed in eight methamphetamine-experienced subjects after three cortisol-modifying premedication conditions: augmenting cortisol level with oral hydrocortisone 50 mg, blocking cortisol response with the corticosteroid synthesis inhibitor metyrapone 1500 mg orally, or no premedication. Although the pharmacologic manipulations produced the expected hormonal changes, subjective response to the methamphetamine showed few differences. Diminishing cortisol response by pharmacologic blockade did not alter the pleasurable effects of methamphetamine. Hydrocortisone did increase self-reported 'bad drug effect' and decreased craving after saline placebo relative to the period following methamphetamine. Metyrapone was associated with significant premature ventricular complexes in two subjects during methamphetamine administration and may not be safe for those who use methamphetamine.

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Section: Discussionmentioning

confidence: 97%

Altering Cortisol Level does not Change the Pleasurable Effects of Methamphetamine in Humans

Harris

Reus

Wolkowitz

et al. 2003

Neuropsychopharmacol

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“…Hypertrophy of severe degree is associated with depressed myocardial function possibly due to abnormal calcium activation and decreased contractile protein function (12)(13)(14). It has been shown by Lehr's group that steroids will potentiate arrhythmias and by others that hypertension (and associated myocardial hypertrophy) will result from steroidal treatment (22)(23)(24)(25)(26)(27). Steroidal-induced hypertension yields hypertrophied myocardial tissue that is more apt to undergo aftercontractions and afterpotentials (29)(30)(31)2).…”

Section: Discussionmentioning

confidence: 99%

Renal hypertensive hypertrophy in the rat: a substrate for arrhythmogenicity

et al. 1986

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We investigated the ability of ouabain to produce lethal arrhythmias in rats with myocardial hypertrophy resulting from chronic renal hypertension. A gradual pressure overload was produced in female Wistar rats by left renal artery stenosis (two kidney, one clip, Goldblatt hypertension). Hypertension (systolic blood pressure greater than 150 mm Hg) developed within three weeks after clipping of the left renal artery and blood pressure continued to increase for the next five weeks. At ten weeks after the onset of hypertension animals were anesthetized with sodium pentobarbital (40 mg/kg) and artificially ventilated with room air while ECG was continually monitored and recorded. Continuous infusion of ouabain was maintained (0.7 mg/kg/min) through the inferior vena cava. Body weight and heart rate of control animals (C) was not significantly different from hypertensive (H) values, while systolic blood pressure in animals hypertensive for ten weeks was considerably greater (187 +/- 8.4 mm Hg) than their age-matched normotensive counterparts (123 +/- 6.0 mm Hg). Heart weight in hypertensive animals was elevated by 69% +/- 2.5 by time of study. Serological evaluation of both groups of animals revealed no significant differences in electrolytes and blood gases while significant differences were noted in glucose, BUN and creatinine. The average time to the first premature ventricular contraction was significantly shorter in H animals (3.5 +/- 0.2 min) when compared to C rats (6.0 +/- 0.2 min). The average time to ventricular tachycardia, ventricular fibrillation and death were also significantly shorter in H rats when compared to C animals (7.5 +/- 0.6 vs. 13.5 +/- 0.3; 13.5 +/- 0.5 vs. 21.0 +/- 0.5; 15.6 +/- 0.4 vs. 24.0 +/- 0.6 min). Thus, the hypertensive hypertrophied myocardium displays an increased propensity for lethal cardiac arrhythmias due to ouabain.

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“…However, following exposure to isolation and cold stress [28] or to DOCA [13], rats appear more susceptible to the acute cardiotoxic effects of isoproterenol.…”

Section: Discussionmentioning

confidence: 99%

“…At the end of this period each rat of these subgroups was prepared for ECG recording, challenged with a single, subcutaneous (sc) dose of 150 Mg/kg of isoproterenol and monitored continuously for 80-90 min. This dose of isoproterenol was chosen because it elicits death in ventricular fibrillation within I hr in 80-100% of DOCA-saline-pretreated rats [14,18]. At the end of the observation period, rats surviving the isoproterenol challenge were anesthetized with…”

Section: Methodsmentioning

confidence: 99%

Enhanced Incidence of Isoproterenol-Induced Ventricular Fibrillation in the Magnesium-Deficient Rat

Guideri

Lehr

Horowitz

1985

Journal of the American College of Nutrition

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The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations.

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Extraordinary potentiation of isoproterenol cardiotoxicity by corticoid pretreatment

Cited by 35 publications

References 0 publications

Altering Cortisol Level does not Change the Pleasurable Effects of Methamphetamine in Humans

Altering Cortisol Level does not Change the Pleasurable Effects of Methamphetamine in Humans

Renal hypertensive hypertrophy in the rat: a substrate for arrhythmogenicity

Enhanced Incidence of Isoproterenol-Induced Ventricular Fibrillation in the Magnesium-Deficient Rat

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