Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

Fineschi, Vittorio; Baroldi, G; Centini, F.; Cerretani, Daniela; Fiaschi, Anna Ida; Micheli, Lucia; Parolini, Marina; Turillazzi, Emanuela; Giorgi, Giorgio

doi:10.1007/s004140000194

Cited by 57 publications

(48 citation statements)

References 35 publications

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“…Recent studies have shown that oxidation of catecholamines results in the formation of highly toxic substances such as aminochromes (e.g. adrenochrome) and free radicals and by virtue of the latter's actions on different types of heart membranes, which cause intracellular Ca 2+ overload and myocardial cell damage [38].…”

Section: Discussionmentioning

confidence: 99%

Sudden cardiac death in a child affected by Prader-Willi syndrome

et al. 2005

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A case of sudden cardiac death in a 3-year-old young male affected by Prader-Willi syndrome, clinically diagnosed and confirmed by means of DNA methylation, is presented. The infant suddenly collapsed at home and was taken apparently unconsciousness by his mother to the emergency clinic where he was pronounced dead. A complete postmortem examination was performed and the histological findings led to the definition of cardiac death with a typical picture of contraction band necrosis. Pulmonary hypoxic alterations are frequently reported as the primary cause of death in PWS cases. In this fatal case according to the macroscopic and microscopic findings, the cause of death was most likely cardiac and possibly related to contraction band necrosis linked with ventricular fibrillation and sudden death.

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Section: Discussionmentioning

confidence: 99%

Sudden cardiac death in a child affected by Prader-Willi syndrome

et al. 2005

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“…HSPs fulfill a range of functions, including cytoprotection and the intracellular assembly, folding, and translocation of oligomeric proteins, and represent a rapid response to altered redox states [23,26,27]. In addition to acting as cellular chaperones, HSPs mediate cytoprotection by associating with and hindering the action of key apoptotic proteins, and by facilitating the degradation of misfolded intracellular proteins by the ubiquitin/proteasome system, so-called protein triage [23].…”

Section: Discussionmentioning

confidence: 99%

Heat stroke in an incubator: an immunohistochemical study in a fatal case

et al. 2004

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The authors report the unique case of an 8-day-old infant succumbing to heat stroke caused by an abnormal increase of the environmental temperature in an incubator. At postmortem examination, second-degree burns were detected, and macroscopic and microscopic findings were typical for a heat-related death. An immunohistochemical study was performed. At the same time, a detailed examination of the incubator was conducted, revealing a malfunctioning of the temperature and relative humidity control system. We suggest that the diagnosis of heat stroke has to be confirmed on the basis of a detailed postmortem examination and a complete immunohistochemical investigation of heat shock proteins, molecules produced acutely in response to heat stress.

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“…Alternatively, chronic cocaine binging might alter signaling pathways downstream of NO production such as cyclic GMP. Finally, cocaine binging may alter nitroso-redox balance (Devi and Chan, 1996;Fineschi et al, 2001;Moritz et al, 2003aMoritz et al, , 2004Pacifici et al, 2003;Kovacic, 2005) by increasing oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Cocaine Binging Predisposes to an Accelerated Course of Dilated Cardiomyopathy in Conscious Dogs following Rapid Ventricular Pacing

Parikh

Nikolaidis²,

Stolarski³

et al. 2005

J Pharmacol Exp Ther

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Despite extensive study, the extent to which cocaine use predisposes to cardiac injury remains unknown. We hypothesized that chronic cocaine binging would increase susceptibility to a subsequent cardiac insult, even in the absence of demonstrable effects on baseline hemodynamics. We studied progression of dilated cardiomyopathy (DCM) induced by rapid ventricular pacing (240 beats per minute) in five conscious, chronically instrumented dogs, after exposure to repetitive cocaine binging (COC) in the form of four consecutive 1 mg/kg i.v. boluses daily for 8 days, to simulate human cocaine abuse. We compared the results with nine control dogs (CON) undergoing the exact pacing protocol, without prior cocaine exposure. Baseline hemodynamics were not significantly altered by chronic cocaine exposure. Following 2 weeks of pacing, COC dogs exhibited accelerated progression to DCM, depressed plasma nitric oxide levels (CON, 17 Ϯ 2 M; COC, 10 Ϯ 2 M, p Ͻ 0.05), and a significantly greater increase in plasma epinephrine (CON, 33 Ϯ 6 pg/ml; COC, 104 Ϯ 24 pg/ml). After only 2 weeks of pacing, COC dogs demonstrated progressive DCM of a magnitude comparable with end-stage pacing-induced DCM. Chronic cocaine binging increases susceptibility to a subsequent myocardial insult and accelerates progression of DCM in conscious dogs following rapid pacing. These data suggest that although chronic cocaine use alone may not affect myocardial function, it predisposes to greater susceptibility to a superimposed insult.Cocaine is responsible for the greatest number of hospitalizations in United States attributable to illicit drug use. According to a survey, it was reported that more than 25 million people had used cocaine at some time in their life, and 1.5 million were chronic users. The effects of cocaine on the cardiovascular system are multifaceted and remain incompletely understood. Cardiovascular manifestations of cocaine abuse include chest pain, myocardial ischemia and infarction, arrhythmias, infective endocarditis, aortic dissection and development of dilated cardiomyopathy, and heart failure (Wiener et al., 1986;Kloner et al., 1992;Mouhaffel et al., 1995). There have been increasing numbers of reports of dilated cardiomyopathy in cocaine abusers. Wiener et al. (1986) were the first to describe the occurrence of DCM in the absence of atherosclerotic coronary artery disease in two patients who were cocaine abusers.Chronic cocaine use in young men who were normotensive and had no symptoms or signs of heart diseases had electrocardiographic and echocardiographic abnormalities including LV hypertrophy (54%), LVEF Ͻ0.45 (4%), increased QRS voltage (23%), and episodes of ST-segment elevation on ambulatory monitoring (33%) (Chakko and Myerburg, 1995). However, the mechanism whereby chronic cocaine use predisposes to myocardial injury remains incompletely understood.There has been both confusion and controversy as to whether cocaine use predisposes to decreased myocardial contractility. Much of the evidence of cocaine-induced myoca...

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Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

Cited by 57 publications

References 35 publications

Sudden cardiac death in a child affected by Prader-Willi syndrome

Sudden cardiac death in a child affected by Prader-Willi syndrome

Heat stroke in an incubator: an immunohistochemical study in a fatal case

Chronic Exposure to Cocaine Binging Predisposes to an Accelerated Course of Dilated Cardiomyopathy in Conscious Dogs following Rapid Ventricular Pacing

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