Developmental differences in the response of cytosolic free calcium to potassium depolarization and cardioplegia in cardiac myocytes.

Publication/Presentation Date

10-1-1992

Abstract

Several biochemical and functional characteristics of immature myocardium suggest a diminished capacity to regulate intracellular Ca2+ during stress. In particular, cellular calcium overload has been postulated as an important pathogenetic mechanism accounting for suboptimal functional recovery following cardioplegia in immature myocardium. Using intracellular Fura-2 fluorescence as Ca2+ indicator, we measured cytosolic free calcium ([Cai]) in single myocytes and cell suspensions derived from both juvenile (4 weeks post-partum) and mature (6-12 months post-partum) New Zealand white rabbits. Resting [Cai] in juvenile heart cells (26 +/- 3 nM) were approximately 50% of that found in adult myocytes (55 +/- 5 nM). In addition, on exposure to increasing concentrations of extracellular potassium ([Kex]), adult but not juvenile myocytes exhibited increases in [Cai]. These two observations underscore developmental differences in intracellular Ca2+ homeostasis. Of particular clinical relevance is the [Cai] response to cardioplegia containing 16 mM [Kex]: neither group demonstrated the expected [Cai] increase in response to potassium depolarization. The lack of [Cai] response to cardioplegia was most likely due to the high levels of Mg2+ (32 mM) contained in cardioplegic solutions. We conclude that cellular calcium overload does not occur following exposure to cardioplegia alone. Accordingly, these findings do not account for recognized developmental differences in functional recovery from "myocardial protection".

Volume

24

Issue

10

First Page

1167

Last Page

1177

ISSN

0022-2828

Disciplines

Medicine and Health Sciences | Pediatrics

PubMedID

1479617

Department(s)

Department of Pediatrics

Document Type

Article

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