Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia–reperfusion in a rat model

Ischaemia–reperfusion injury is associated with reduced bioavailability of nitric oxide (NO) and microvascular dysfunction. One emerging mechanism behind reduced NO bioavailability is upregulation of arginase, which metabolizes the NO synthase substrate l‐arginine. This study investigated the effects of arginase inhibition on coronary flow velocity and infarct size during reperfusion.

[1]  H. Westerblad,et al.  Local Arginase Inhibition during Early Reperfusion Mediates Cardioprotection via Increased Nitric Oxide Production , 2012, PloS one.

[2]  M. Nobilis,et al.  HPLC determination of arginases inhibitor N-(ω)-hydroxy-nor-L-arginine using core-shell particle column and LC-MS/MS identification of principal metabolite in rat plasma. , 2012, Journal of chromatography. B, Analytical technologies in the biomedical and life sciences.

[3]  C. Jung,et al.  Arginase inhibition restores in vivo coronary microvascular function in type 2 diabetic rats. , 2011, American journal of physiology. Heart and circulatory physiology.

[4]  P. Anversa,et al.  Mechanisms of Myocardial , 2011 .

[5]  Hua Qi,et al.  Predictors and Long‐term Prognosis of Angiographic Slow/No‐Reflow Phenomenon During Emergency Percutaneous Coronary Intervention for ST‐Elevated Acute Myocardial Infarction , 2010, Clinical cardiology.

[6]  Christian Jung,et al.  Arginase inhibition mediates cardioprotection during ischaemia-reperfusion. , 2010, Cardiovascular research.

[7]  J. Borén,et al.  Protein disulfide isomerase increases in myocardial endothelial cells in mice exposed to chronic hypoxia: a stimulatory role in angiogenesis. , 2009, American journal of physiology. Heart and circulatory physiology.

[8]  W. Durante,et al.  ARGINASE: A CRITICAL REGULATOR OF NITRIC OXIDE SYNTHESIS AND VASCULAR FUNCTION , 2007, Clinical and experimental pharmacology & physiology.

[9]  C. Gibson,et al.  Reperfusion strategies for ST-elevation myocardial infarction , 2007, Current cardiology reports.

[10]  J. Wikström.  Imaging of coronary artery function and morphology in living mice - applications in atherosclerosis research , 2007 .

[11]  Hiroshi Ito.  No-reflow phenomenon and prognosis in patients with acute myocardial infarction , 2006, Nature Clinical Practice Cardiovascular Medicine.

[12]  Michael V. Cohen,et al.  Nitric oxide is a preconditioning mimetic and cardioprotectant and is the basis of many available infarct-sparing strategies. , 2006, Cardiovascular research.

[13]  G. Bergström,et al.  Functional and morphologic imaging of coronary atherosclerosis in living mice using high-resolution color Doppler echocardiography and ultrasound biomicroscopy. , 2005, Journal of the American College of Cardiology.

[14]  L. Becker.  Myocardial Reperfusion Injury , 2004, Journal of Thrombosis and Thrombolysis.

[15]  M. Donato,et al.  Adenosine and cardioprotection during reperfusion – an overview , 2003, Molecular and Cellular Biochemistry.

[16]  R. Kloner,et al.  No-Reflow Phenomenon Persists Long-Term After Ischemia/Reperfusion in the Rat and Predicts Infarct Expansion , 2003, Circulation.

[17]  L. Kuo,et al.  Ischemia‐reperfusion selectively impairs nitric oxide‐ mediated dilation in coronary arterioles: counteracting role of arginase , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[18]  A. Shoukas,et al.  Arginase Reciprocally Regulates Nitric Oxide Synthase Activity and Contributes to Endothelial Dysfunction in Aging Blood Vessels , 2003, Circulation.

[19]  T. Ogihara,et al.  Two different coronary blood flow velocity patterns in thrombolysis in myocardial infarction flow grade 2 in acute myocardial infarction: insight into mechanisms of microvascular dysfunction. , 2002, Journal of the American College of Cardiology.

[20]  W. Schlack,et al.  Isoflurane Preconditions Myocardium against Infarction via Release of Free Radicals , 2002, Anesthesiology.

[21]  R. Kloner,et al.  The “no-reflow” phenomenon: basic science and clinical correlates , 2002, Heart.

[22]  伊藤浩.  no reflow 現象とは , 2000 .

[23]  B. Lucchesi,et al.  Mechanisms of myocardial reperfusion injury. , 1999, The Annals of thoracic surgery.

[24]  G. Ambrosio,et al.  Reperfusion injury: experimental evidence and clinical implications. , 1999, American heart journal.

[25]  Y. Taniyama,et al.  Alternation in the coronary blood flow velocity pattern in patients with no reflow and reperfused acute myocardial infarction. , 1996, Circulation.

[26]  Y. Muraoka,et al.  Impaired coronary flow reserve immediately after coronary angioplasty in patients with acute myocardial infarction. , 1993, British heart journal.

[27]  D. Larach,et al.  Direct vasodilation by sevoflurane, isoflurane, and halothane alters coronary flow reserve in the isolated rat heart. , 1991, Anesthesiology.

[28]  P. E. Parker,et al.  Coronary hemodynamics during reperfusion following acute coronary ligation in dogs. , 1975, American heart journal.