Impairment by cyclosporin A of reperfusion-induced arrhythmias

Arteaga, Diana; Odor, Alberto M; López, Rosa; Contreras, Gloria; Pichardo, Julieta; García, Elizabeth; Aranda, Alberto; Chávez, Edmundo

doi:10.1016/0024-3205(92)90514-p

Cited by 31 publications

(14 citation statements)

References 23 publications

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“…overload, inducing inner membrane leakage [19,22]. The latter brings about the opening of the nonspecific transmembrane pore, a process that leads to mitochondrial dysfunction, and underlies the pathogenesis of heart reperfusion damage [11,29,30]. From the above, it can be inferred that protection of mitochondria against Ca 2?…”

Section: Discussionmentioning

confidence: 99%

In hyperthyroid rats octylguanidine protects the heart from reperfusion damage

Pavón

Aranda

Garcı́a

et al. 2009

Endocr

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Hyperthyroidism sensitizes the heart for reperfusion injury. As known, mitochondrial permeability transition underlies reperfusion heart damage. This study was undertaken to explore the protective effect of octylguanidine (OG), an inhibitor of permeability transition, on hearts from hyperthyroid rats subjected to ischemia/reperfusion. Hyperthyroidism was induced by a daily injection of 2 mg T3/kg body weight for 5 days. OG was injected at a dose of 5 mg/kg body weight. It was found that the amine protects against reperfusion-induced permeability transition, i.e., mitochondria from hyperthyroid rats, treated with OG, retained accumulated Ca(2+), similarly to control mitochondria. OG maintained post reperfusion cardiac frequency in hyperthyroid rats at 429 +/- 16 in comparison to control and T3 treated rats (70 +/- 12 and 71 +/- 2, respectively). We also found that OG diminished the post reperfusion accumulation of IFNgamma from 34.3 +/- 2.5 to 18.7 +/- 1.35, IL-6 from 38.5 +/- 4.5 to 15.1 +/- 0.12, IL-1 from 16.78 +/- 0.73 to 12.19 +/- 1.54, and TNFalpha from 45.05 +/- 3.14 to 29.85 +/- 4.3 (pg/50 microg myocardial tissue). It is concluded that OG inhibits the hypersensitivity of the hyperthyroid myocardium to undergo reperfusion damage due to its inhibitory action on the permeability transition pore.

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Section: Discussionmentioning

confidence: 99%

In hyperthyroid rats octylguanidine protects the heart from reperfusion damage

Pavón

Aranda

Garcı́a

et al. 2009

Endocr

Self Cite

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“…However, the higher rate of hypertension associated with cyclosporine could conceivably be offset by other effects. For example, some reports have indicated that cyclosporine could actually be protective against reperfusion-associated dysrhythmias (16). Other reports have indicated that cyclosporine may also be protective against the development of left ventricular hypertrophy and cardiac enlargement (17), although tacrolimus appears to have at least an equivalent effect (18).…”

Section: Discussionmentioning

confidence: 99%

Hospitalized Atrial Fibrillation After Renal Transplantation in the United States

Abbott¹,

Reynolds²,

Taylor

et al. 2003

American Journal of Transplantation

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“…Then the clamp was released allowing the reestablishment of renal blood flow or reperfusion and 24 h after the rats were anesthetized and the kidney was excised. Cyclosporin A, at the dose of 20 mg/kg, was injected intraperitoneally to rats 30 min before inducing the reperfusion period (Arteaga et al, 1992). Cortex kidney mitochondria were prepared, following standard centrifugation procedures, in 0.25 M sucrose-1 mM EDTA, pH 7.3.…”

Section: Methodsmentioning

confidence: 99%

“…Several reports have pointed out that ischemia/reperfusion damage is circumvented by the immunosuppressant cyclosporin A (CSA) (Arteaga et al, 1992;Griffiths and Halestrap, 1993) that inhibits the opening of the non-specific pore (Broekemeier et al, 1995;Chávez et al, 2002). In recent years, our laboratory has been addressing the subject of the role of thyroid hormone as a regulator of reperfusion damage and mitochondrial permeability transition.…”

Section: Introductionmentioning

confidence: 99%