Experimental cobalt cardiomyopathy

Mohiuddin, Syed M.; Taskar, Pranali; Rheault, Michel; Roy, Paul‐Emile; Chenard, Jacques; Morin, Y

doi:10.1016/0002-8703(70)90202-4

Cited by 37 publications

(11 citation statements)

References 12 publications

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“…Excess amounts of Co 2ϩ are cardiotoxic in humans and animals, known as the cobalt cardiomyopathy [23]. Endoh et al [8] reported that the chronic (43 d) oral administration of 0.01% CoCl 2 , the same amounts as in the present study, showed normal weight gain and normal wet weight of the heart in rats.…”

Section: Discussionsupporting

confidence: 63%

Microvascular Remodelling after Endurance Training with Co2+ Treatment in the Rat Diaphragm and Hind-Leg Muscles.

Suzuki

2002

JJP

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Section: Discussionsupporting

confidence: 63%

Microvascular Remodelling after Endurance Training with Co2+ Treatment in the Rat Diaphragm and Hind-Leg Muscles.

Suzuki

2002

JJP

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“…Several investigators attempted to simulate this human pathological condition in the animal models of cobalt-induced cardiomyopathy (12,13,21,30). The remarkable individual variance of cobalt-induced cardiotoxicity was well recognized by several investigators (1,12,13,32).…”

Section: Discussionmentioning

confidence: 99%

Cobalt chloride induces delayed cardiac preconditioning in mice through selective activation of HIF-1α and AP-1 and iNOS signaling

Xi¹,

Taher²,

Yin³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

122

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Xi, Lei, Mohiuddin Taher, Chang Yin, Fadi Salloum, and Rakesh C. Kukreja. Cobalt chloride induces delayed cardiac preconditioning in mice through selective activation of HIF-1␣ and AP-1 and iNOS signaling. Am J Physiol Heart Circ Physiol 287: H2369 -H2375, 2004. First published July 29, 2004 doi:10.1152/ajpheart. 00422.2004.-Acute systemic hypoxia induces delayed cardioprotection against ischemia (I)-reperfusion (R) injury via inducible nitric oxide synthase (iNOS)-dependent mechanism. Because CoCl2 is known to elicit hypoxia-like responses, we hypothesized that this chemical would mimic the delayed preconditioning effect in the heart. Adult male mice were pretreated with CoCl2 or saline. The hearts were isolated 24 h later and subjected to 20 min of global I and 30 min of R in Langendorff mode. Myocardial infarct size (% of risk area; mean Ϯ SE, n ϭ 6 -8/group) was reduced in mice pretreated with 30 mg/kg CoCl2 (16.1 Ϯ 3.1% vs. 27.6 Ϯ 3.3% with saline control; P Ͻ 0.05) without compromising postischemic cardiac function. Higher doses of CoCl2 failed to induce similar protection. Electrophoretic mobility gel shift assay demonstrated significant enhancement in DNA binding activity of hypoxia-inducible factor 1␣ (HIF-1␣) and activator protein 1 (AP-1) in nuclear extracts from CoCl2-treated hearts. Activation of HIF-1␣ and AP-1 was evident at 30 min and sustained for the next 4 h after CoCl2 injection. In contrast, CoCl2-induced protection was independent of NF-B activation because no DNA binding or p65 translocation was observed in nuclear extracts. Also, CoCl2-induced cardioprotection was preserved in p50 subunit NF-B-knockout (KO) mice (11.1 Ϯ 3.0% vs. 25.1 Ϯ 5.0% in saline-treated p50-KO mice; P Ͻ 0.05). The infarct-limiting effect of CoCl2 was absent in iNOS-KO mice (20.9 Ϯ 3.0%). We conclude that in vivo administration of CoCl2 preconditions the heart against I/R injury. The delayed protective effect of CoCl2 is achieved through a distinctive signaling mechanism involving HIF-1␣, AP-1, and iNOS but independent of NF-B activation.ischemia-reperfusion injury; myocardial infarction; hypoxia; nitric oxide synthase; transcription factors INCESSANT OR INTERMITTENT chronic systemic hypoxia can elicit a complex adaptive response that leads to enhanced tolerance to myocardial ischemia-reperfusion (I/R) injury in immature or adult mammals (2,3,20,28). The myocardial endogenous adaptation to hypoxia leading to resistance against subsequent lethal injuries appears to be an inherent part of the so-called "late phase of preconditioning" (5), which may have great promise for eventual clinical applications. Most recently, we reported a similar protective effect by acute exposure to systemic hypoxia in adult mice (36), where the adverse effects of chronic hypoxia, such as pulmonary hypertension and right ventricular hypertrophy, can be effectively avoided. In these studies, inducible nitric oxide synthase (iNOS) played a pivotal role in triggering as well as mediating the hypoxia-induced late cardioprotection (36). Cai et al...

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“…As with many other health endpoints, cardiovascular effects were observed in all animal studies (i.e., there was no observed NOAEL). For example, Mohiuddin et al (1970) reported cardiac effects in guinea pigs dosed with approximately 7.7 mg of Co/kgday (HED = 2.2 mg Co/kg-day) in their diet or by oral gavage for five weeks. A substantial number of the animals reportedly developed tachypnea.…”

Section: Cardiovascular Toxicitymentioning

confidence: 99%