Reduced coronary reserve in response to short-term ischaemia and vasoactive drugs in ex vivo hearts from diabetic mice
Author:
Publisher
Wiley
Subject
Physiology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1748-1716.2006.01527.x/fullpdf
Reference37 articles.
1. Cardiac function and metabolism in Type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-α activator
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4. Blockade of the ATP-sensitive potassium channel modulates reactive hyperemia in the canine coronary circulation.
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1. Vasodilator Stress Echocardiography in the Assessment of Early Coronary Microvascular Function in Type II Diabetic Mice;Journal of Medical Imaging and Health Informatics;2018-08-01
2. Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure;Journal of Cardiovascular Pharmacology;2017-01
3. Enhanced A2A adenosine receptor-mediated increase in coronary flow in type I diabetic mice;Journal of Molecular and Cellular Cardiology;2016-01
4. Inhibition of cyclooxygenase-2 causes a decrease in coronary flow in diabetic mice. The possible role of PGE2 and dysfunctional vasodilation mediated by prostacyclin receptor;Journal of Physiology and Biochemistry;2015-05-05
5. Impaired cardiac functional reserve in type 2 diabetic db/db mice is associated with metabolic, but not structural, remodelling;Acta Physiologica;2010-03
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