| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Faculte de Medecine Lyon-Nord, INSERM E 0226, Universite Claude Bernard Lyon I, Lyon cedex, France
2 INSA- Lyon, INSERM/INSA- UMR 585, Villeurbanne cedex, France
* To whom correspondence should be addressed. E-mail: ovize{at}rockefeller.univ-lyon1.fr.
Although the mechanism by which ischemic preconditioning (PC)inhibits myocardial apoptosis during ischemia- reperfusion is unclear,evidence indicates a role for the secondary messenger ceramide. We investigated in vivo whether PC may affect ceramide and sn-1,2-diacylglycerol (DAG)production,and attenuate apoptosis during ischemia. Rabbits underwent 30 minutes of ischemia followed by 4 hours of reperfusion. Prior to this,they received either no intervention (control group)or one episode of 5 minutes of ischemia followed by 5 minutes of reperfusion (PC group), or an IV administration of the sphingomyelinase inhibitor D609. Myocardial content of ceramide and DAG was measured using the DAG kinase assay at different time points of the experiment. Apoptosis was detected and quantified by Sandwich Enzyme Immunoassay.Area at risk and infarct size were measured using blue dye injection and tiphenyltrazolium chloride staining. Control hearts exhibited a peak of ceramide production at 5 minutes of the prolonged ischemia,with a mean value averaging 64± 5 ng/mg tissue (p<0.05 versus 48±4 ng/mg at baseline). In contrast, ischemic preconditioning and D609 prevented ceramide increase during the prolonged ischemia. Myocardial DAG content was increased only in PC hearts at 30 minutes of ischemia. Preconditioned and D609 groups developed less apoptosis, as well as a limited infarct size, when compared to the control group. These results suggest that the antiapoptotic effect of preconditioning may be due to a reduced ceramide production during sustained ischemia in the rabbit heart.
This article has been cited by other articles:
|
|
 |
|
  E. L. Smith and E. H. Schuchman The unexpected role of acid sphingomyelinase in cell death and the pathophysiology of common diseases FASEB J, October 1, 2008; 22(10): 3419 - 3431. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Argaud, O. Gateau-Roesch, L. Augeul, E. Couture-Lepetit, J. Loufouat, L. Gomez, D. Robert, and M. Ovize Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H386 - H391. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Pchejetski, O. Kunduzova, A. Dayon, D. Calise, M.-H. Seguelas, N. Leducq, I. Seif, A. Parini, and O. Cuvillier Oxidative Stress-Dependent Sphingosine Kinase-1 Inhibition Mediates Monoamine Oxidase A-Associated Cardiac Cell Apoptosis Circ. Res., January 5, 2007; 100(1): 41 - 49. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-s. Liang, W. Mao, C. Iwai, S. Fukuoka, and S. Y. Stevens Cardiac sympathetic neuroprotective effect of desipramine in tachycardia-induced cardiomyopathy Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H995 - H1003. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Labarthe, M. Khairallah, B. Bouchard, W. C. Stanley, and C. Des Rosiers Fatty acid oxidation and its impact on response of spontaneously hypertensive rat hearts to an adrenergic stress: benefits of a medium-chain fatty acid Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1425 - H1436. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
