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Ann Thorac Surg 2004;77:226-232
© 2004 The Society of Thoracic Surgeons
a Second Department of Cardiac Surgery, Katowice, Poland
b Department of Cardiology, Medical University of Silesia, Katowice, Poland
* Address reprint requests to Dr Deja, Second Department of Cardiac Surgery, Medical University of Silesia, Ul. Ziolowa 47, 40-635 Katowice, Poland.
e-mail: narizol{at}slam.katowice.pl
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
BACKGROUND: Diazoxide has been shown to confer significant myocardial protection in many experiments. This study was designed to assess its influence on the structural injury and functional recovery of human myocardium subjected to hypoxia/reoxygenation in vitro.
METHODS: The isolated electrically driven human right atrial trabeculae, obtained during cardiac surgery, were studied. The tissue bath was oxygenated with 95% oxygen and 5% carbon dioxide, hypoxia being obtained by replacing oxygen with argon. The influence of diazoxide on atrial contractility was studied first. Next, the two trabeculae from one atrial appendage were studied simultaneously, adding diazoxide to the tissue bath 10 minutes before hypoxia in one, with another serving as a control. We tested 10-4.5 mol/L and 10-4 mol/L diazoxide in three sets of experiments testing 30, 60, and 90 minutes of hypoxia. We continued reoxygenation for 120 minutes (in 60-minute and 90-minute hypoxia experiments) and subsequently tested reaction to 10-4 mol/L norepinephrine. Apart from continuous recording of the contraction force, we measured the troponin I release into the tissue bath after ischemia and reoxygenation.
RESULTS: Diazoxide exerted a negative inotropic effect in human atrial muscle (pD2=3.96 ± 0.18). Both concentrations of diazoxide studied resulted in better functional recovery of atrial trabeculae subjected to 30 minutes of hypoxia. With longer hypoxia, only the higher diazoxide concentration provided significant protection as assessed by contractility. After 120 minutes of reoxygenation, only diazoxide-treated muscle was viable enough to respond to norepinephrine. Only 10-4 mol/L diazoxide resulted in lower troponin I release during hypoxia and reoxygenation.
CONCLUSIONS: This study shows that diazoxide provides significant concentration-dependent protection against hypoxia/reoxygenation injury to human myocardium in vitro.
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  M. A. Deja, M. Malinowski, K. S. Golba, M. Kajor, T. Lebda-Wyborny, D. Hudziak, W. Domaradzki, D. Szurlej, A. Bonczyk, J. Biernat, et al. Diazoxide protects myocardial mitochondria, metabolism, and function during cardiac surgery: A double-blind randomized feasibility study of diazoxide-supplemented cardioplegia J. Thorac. Cardiovasc. Surg., April 1, 2009; 137(4): 997 - 1004. [Abstract] [Full Text] [PDF]
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 M. A. Deja, K. S. Golba, M. Malinowski, K. Widenka, J. Biernat, D. Szurlej, and S. Wos Diazoxide Provides Maximal KATP Channels Independent Protection if Present Throughout Hypoxia Ann. Thorac. Surg., April 1, 2006; 81(4): 1408 - 1416. [Abstract] [Full Text] [PDF]
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