Key result
Daily cocaine induces contraction band necrosis, mitochondrial dysfunction, and Connexin 43 dephosphorylation in rats.
Why the study?
Contraction band necrosis is common in cocaine abusers but rarely reported in experimental models, prompting exploration of cocaine effects on cardiac connexin 43 in vivo.
Cocaine may induce specific myocardial injury in rat models; leaves open human relevance and requires clinical validation.
Contraction band necrosis (CBN) is a common abnormality found in the myocardium of cocaine abusers, but is rarely reported in experimental models of cocaine abuse. Connexin 43 (Cx43) is essential for cardiac intercellular communication and the propagation of CBN. Under stress or injury, cardiac Cx43 is dephosphorylated, which is related to cardiomyocyte dysfunction and pathogenesis, whereas adiponectin exerts beneficial effects in the myocardium. In this study, we explore the effects of cocaine on cardiac Cx43 in vivo. Rats were administered cocaine via the tail vein at 20 mg/kg/day for 14 days, and showed widespread CBN, microfocal myocarditis and myocardial fibrosis, corresponding to a dysfunction of cardiac mitochondria under increased oxidative stress. The increase in dephosphorylated cardiac Cx43 and its negative correlation with the myocardial distribution of CBN after cocaine administration were determined. In addition, apoptosis and necroptosis, as well as increased adiponectin levels, were observed in the myocardium after cocaine exposure. Accordingly, we found altered profiles of cardiac Cx43, CBN and its negative correlation with dephosphorylated cardiac Cx43, and the possible involvement of adiponectin in the myocardium after 14 days of cocaine administration. The latter might play a protective role in the cardiotoxicity of cocaine. The current findings would be beneficial for establishing novel therapeutic strategies in cocaine-induced cardiac consequences.
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Wen et al. (2022) studied Cocaine-induced cardiotoxicity (n=7). Cocaine vs. Saline was evaluated on Myocardial contraction band necrosis, mitochondrial dysfunction, and Connexin 43 dephosphorylation (p=<0.05). Daily administration of cocaine for 14 days in rats induced widespread contraction band necrosis, mitochondrial dysfunction, increased dephosphorylation of cardiac Connexin 43, and upregulated adiponectin levels.
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