Combination of miglitol, an anti‐diabetic drug, and nicorandil markedly reduces myocardial infarct size through opening the mitochondrial KATP channels in rabbits
暂无分享,去创建一个
M. Arai | G. Takemura | S. Minatoguchi | H. Fujiwara | Y. Uno | K. Hashimoto | Y. Hashimoto | N. Wang | X. H. Chen
[1] C. Spencer,et al. Miglitol , 2000, Drugs.
[2] M. Arai,et al. A novel anti‐diabetic drug, miglitol, markedly reduces myocardial infarct size in rabbits , 1999, British journal of pharmacology.
[3] HisatoTakatsu,et al. N-Methyl-1-Deoxynojirimycin (MOR-14), an α-Glucosidase Inhibitor, Markedly Reduced Infarct Size in Rabbit Hearts , 1998 .
[4] M. Arai,et al. N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly reduced infarct size in rabbit hearts. , 1998, Circulation.
[5] D. Yellon,et al. Myocardial protection afforded by nicorandil and ischaemic preconditioning in a rabbit infarct model in vivo. , 1998, Journal of cardiovascular pharmacology.
[6] M. Arai,et al. Nicorandil reduces myocardial infarct size by opening the K(ATP) channel in rabbits. , 1997, International journal of cardiology.
[7] E. Brendel,et al. Pharmacokinetics of miglitol. Absorption, distribution, metabolism, and excretion following administration to rats, dogs, and man. , 1997, Arzneimittel-Forschung.
[8] M. Karmazyn,et al. Transient ischemia in the presence of an adenosine deaminase plus a nucleoside transport inhibitor confers protection against contractile depression produced by hydrogen peroxide. Possible role of glycogen. , 1996, Journal of molecular and cellular cardiology.
[9] R. Sievers,et al. Loss of Myocardial Protection After Preconditioning Correlates With the Time Course of Glycogen Recovery Within the Preconditioned Segment , 1993, Circulation.
[10] R. Prager,et al. Effects of 8-Wk α-Glucosidase Inhibition on Metabolic Control, C-Peptide Secretion, Hepatic Glucose Output, and Peripheral Insulin Sensitivity in Poorly Controlled Type II Diabetic Patients , 1989, Diabetes Care.
[11] M. Bollen,et al. The antiglycogenolytic action of 1-deoxynojirimycin results from a specific inhibition of the alpha-1,6-glucosidase activity of the debranching enzyme. , 1989, European journal of biochemistry.
[12] G. Radda,et al. Determination of buffering capacity of rat myocardium during ischemia. , 1988, Biochimica et biophysica acta.
[13] Y. Yoshikuni. Inhibition of Intestinal α-Glucosidase Activity and Postprandial Hyperglycemia by Moranoline and Its N-Alkyl Derivatives , 1988 .
[14] J. R. Neely,et al. Role of Glycolytic Products in Damage to Ischemic Myocardium: Dissociation of Adenosine Triphosphate Levels and Recovery of Function of Reperfused Ischemic Hearts , 1984, Circulation research.
[15] J. Haselgrove,et al. Early ischemia after complete coronary ligation in the rabbit, dog, pig, and monkey. , 1981, The American journal of physiology.
[16] M. Fishbein,et al. Early phase acute myocardial infarct size quantification: validation of the triphenyl tetrazolium chloride tissue enzyme staining technique. , 1981, American heart journal.