An experimental model was developed to evaluate the effects of activators and inhibitors of K(ATP) channels on unidirectional K+ fluxes in the whole heart. Isolated rat hearts perfused in the Langendorff mode were equilibrated with Pi-free Krebs-Henseleit buffer (KH buffer) containing 0.94-2.14 mM R
Potassium transport in Langendorff-perfused mouse hearts assessed by 87Rb NMR spectroscopy
β Scribed by Olga Jilkina; Bo Xiang; Bozena Kuzio; John Rendell; Valery V. Kupriyanov
- Book ID
- 102532700
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 211 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0740-3194
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β¦ Synopsis
Abstract
We studied the fluxes of a potassium congener (Rb^+^) in mouse hearts by ^87^Rb MRS at 8.4T. The hearts were loaded with Rb^+^ by perfusion with KrebsβHenseleit buffer, in which 50% of K^+^ was substituted with Rb^+^. We initiated Rb^+^ efflux by changing the perfusion medium to Rb^+^βfree buffer. Spectra were acquired every 1.85 min, and the kinetics of Rb^+^ transport were analyzed by means of monoexponential fits. The rate constants of Rb^+^ uptake and efflux were 0.0680 Β± 0.0028 and 0.0510 Β± 0.0051 min^β1^, respectively (βΌ30% faster than in the rat heart). The ATPβsensitive potassium channel opener, Pβ1075 (5 ΞΌM), and mitochondrial uncoupler, 2,4βdintrophenol (50 ΞΌM), activated Rb^+^ efflux from mouse hearts by βΌ35%. The mechanisms responsible for the differences in Rb^+^ uptake and efflux under baseline conditions and stimulation, in comparison with rat hearts, are discussed. These data provide a background for studies of cardiac potassium transport in transgenic mouse strains. Magn Reson Med 53:1172β1176, 2005. Β© 2005 WileyβLiss, Inc.
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