Key result
2-APB triggers normoxic heart fibrillation but protects cardiac rhythm and vascular function during hypoxia/reoxygenation.
Why the study?
Intracellular calcium concentration changes play a pivotal role in hypoxia/reoxygenation injury, and 2-aminoethoxydiphenyl borate influences calcium currents and gap junctions.
Does 2-aminoethoxydiphenyl borate influence electrical activity and coronary blood flow in isolated rat hearts under hypoxia/reoxygenation conditions?
Does 2-aminoethoxydiphenyl borate influence electrical activity and coronary blood flow in isolated rat hearts under hypoxia/reoxygenation conditions?
p-value: p=<0.05
2-apb modulates electrical activity and vascular function in isolated rat hearts, attenuating hypoxia/reoxygenation injury effects but inducing fibrillation under normoxia.
The aim of the study was to apply the multi-electrode mapping method to investigate the effect of 2-aminoethoxydiphenyl borate (2-apb) on the electrical activity and vessels of the isolated rat heart under hypoxia/reoxygenation injury (H/R). To date, the ability to influence on the calcium currents and condition of gap junctions has been shown for 2-apb. Changes in the intracellular calcium concentration in the heart play the pivotal role in the development of H/R. As a result, it was shown that 2-apb influences on the myocardial conduction velocity, sinus rhythm and coronary blood flow in the isolated rat heart. 2-apb caused heart fibrillation during normoxia but not under hypoxia, and attenuated the effect of the H/R on heart rate and vascular function.
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Kharkovskaya et al. (2019) studied Hypoxia/reoxygenation injury (n=40). 2-aminoethoxydiphenyl borate (2-apb) vs. Standard perfusion (sKH) or H/R without 2-apb was evaluated on Myocardial conduction velocity (LATD), heart rate, and coronary blood flow (p=<0.05). 2-aminoethoxydiphenyl borate caused heart fibrillation during normoxia but not under hypoxia, and attenuated the effect of hypoxia/reoxygenation on heart rate and vascular function.
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