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Ann Thorac Surg 2002;73:1245
© 2002 The Society of Thoracic Surgeons

Invited commentary

Hikaru Matsuda, MD, PhDa

a Department of Surgery, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 562-0027, Japan

e-mail: matsuda{at}surg1

It is a privilege to review and comment on this interesting article. The experimental study presented by Dr Munakata and coworkers demonstrates the role of phosphatidyl-inositol specific phospholipase C (PI-PLC) in the myocardium exposed to a short period of normothermic ischemia using an isolated rabbit heart model.

The authors used a specific inhibitor of PI-PLC, U73122 and its inactive analogue U73343 to modify the effect of PI-PLC to activate protein kinase C (PKC). The authors also were able to show reversal of the U73122 induced post-ischemic cardiac dysfunction by direct PKC activation with phorbol myristate acetate (PMA). This suggests that the myocardial protective effect of PI-PLC after ischemia occurs through PKC activation.

Many studies have shown a significant myocardial protective effect of ischemic preconditioning [1]. However, the mechanism and its clinical significance have been discussed for more than 10 years without a definitive answer. One promising candidate for the mechanism of ischemic preconditioning is activation of PKC by PI-PLC [2] to protect the heart against impairment in intracellular calcium flux. The authors’ observation in this article that PI-PLC inhibition impairs diastolic calcium flux without a significant decrease in cellular ATP level is new and important. Further investigation using modifications of the cellular calcium transport system, eg, sarcoplasmic reticulum inhibition and membrane L-type calcium channel inhibition would be interesting and may clarify the mechanism underlying the intrinsic, antiischemic property of myocardium [3].

Although the myocardial protective effect related to PKC activation during ischemia attracts much interest, many controversies remain. These controversies may due to the difference between species, experimental models, ischemic durations, and degree of ischemic insult. In addition, differences in the role of PKC-{varepsilon} and PKC-{alpha} during short periods of ischemia is not fully understood.

Researchers and clinicians must resolve these problems before this mechanism can be used to improve clinical myocardial protection. Further investigation is required.

I congratulate these investigators for stimulating our thinking about the mechanism of the intrinsic protective property of the myocardium against ischemic reperfusion damage.

References

  1. Murry C.E., Richard V.J., Reimer K.A., Jennings R.B. Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode. Circ Res 1990;66:913-931.[Abstract/Free Full Text]
  2. De Jonge H.W., Van Heugten H.A., Lamers J.M. Signal transduction by the phosphatidylinositol cycle in myocardium. J Mol Cell Cardiol 1995;27:93-106.[Medline]
  3. Liu D.M., Katnik C., Stafford M., Adams D.J. P2Y purinoceptor activation mobilizes intracellular Ca2+ and induces a membrane current in rat intracardiac neurones. J Physiol 2000;526(Pt 2):287-298.[Abstract/Free Full Text]




This Article
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