Partial exposure of frog heart to high-potassium solution: an easily reproducible model mimicking ST segment changes

Author:

KON Nobuaki1,ABE Nozomu12,MIYAZAKI Masahiro1,MUSHIAKE Hajime1,KAZAMA Itsuro31

Affiliation:

1. Department of Physiology, Tohoku University Graduate School of Medicine, Seiryo-cho, Aoba-ku, Sendai, Miyagi 980-8575, Japan

2. Department of Anesthesiology, Tohoku University Hospital, Seiryo-cho, Aoba-ku, Sendai, Miyagi 980-8575, Japan

3. School of Nursing, Miyagi University, Gakuen, Taiwa-cho, Kurokawa-gun, Miyagi 981-3298, Japan

Publisher

Japanese Society of Veterinary Science

Subject

General Veterinary

Reference21 articles.

1. 1. Akao, M., Ohler, A., O’Rourke, B. and Marbán, E. 2001. Mitochondrial ATP-sensitive potassium channels inhibit apoptosis induced by oxidative stress in cardiac cells. Circ. Res. 88: 1267–1275.

2. 2. Bailey, J. J., Berson, A. S., Handelsman, H. and Hodges, M. 2001. Utility of current risk stratification tests for predicting major arrhythmic events after myocardial infarction. J. Am. Coll. Cardiol. 38: 1902–1911.

3. 3. Fuerstenwerth, H. 2014. On the differences between ouabain and digitalis glycosides. Am. J. Ther. 21: 35–42.

4. 4. Fuller, W., Parmar, V., Eaton, P., Bell, J. R. and Shattock, M. J. 2003. Cardiac ischemia causes inhibition of the Na/K ATPase by a labile cytosolic compound whose production is linked to oxidant stress. Cardiovasc. Res. 57: 1044–1051.

5. 5. Gong, B., Miki, T., Seino, S. and Renaud, J. M. 2000. A K(ATP) channel deficiency affects resting tension, not contractile force, during fatigue in skeletal muscle. Am. J. Physiol. Cell Physiol. 279: C1351–C1358.

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