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10.1111/apha.12097 http://scihub22266oqcxt.onion/10.1111/apha.12097 C3756285!3756285 !23497275     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23497275 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Acta+Physiol+(Oxf) 2013 ; 208 (2 ): 172-9 Nephropedia Template TP {{tp|p=23497275 |t=2013. Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia-reperfusion in a rat model |pdf=|usr=}}{{23497275 }} gab.com Text Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia-reperfusion in a rat model JO: Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=23497275 #FOAvip AIM: 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. METHODS: Anaesthetized rats, subjected to 30-min coronary artery ligation and reperfusion up to 8 days, were treated with vehicle or the arginase inhibitor N(?) -hydroxy-nor-l-arginine (nor-NOHA; 100 mg kg(-1) ) intravenously 15 min before ischaemia. Coronary flow velocity was determined repeatedly during reperfusion. RESULTS: Arginase activity in the ischaemic-reperfused myocardium was increased already at 20 min of reperfusion and maintained at 8 days. Infarct size was reduced by arginase inhibition at 2 h (39 ± 3% of the area at risk (AAR) vs. 51 ± 2% in the vehicle group, P < 0.01) and at 8 days of reperfusion (13 ± 2% of the left ventricle (LV) vs. 22 ± 2%, P < 0.05). Basal coronary flow velocity was higher during reperfusion in the group given nor-NOHA, and it correlated inversely to infarct size (P < 0.01, r = -0.60). Hyperaemic coronary flow velocity was also increased in the nor-NOHA-treated group compared to vehicle at 24 h and at day 8 (P < 0.05). CONCLUSION: It is concluded that arginase activity is increased already during early reperfusion. Arginase inhibition increases coronary flow velocity and reduces infarct size that is sustained 8 days after reperfusion. Inhibition of arginase may thus be a promising therapeutic target to prevent the development of microvascular dysfunction and myocardial injury following ischaemia-reperfusion. Twit Text FOAVip Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia-reperfusion in a rat model ????Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=23497275 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23497275 #FOAvip English Wikipedia <ref>{{Cite pmid|23497275 }}</ref> Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia-reperfusion in a rat model #MMPMID23497275 Grönros J ; Kiss A ; Palmér M ; Jung C ; Berkowitz D ; Pernow J Acta Physiol (Oxf) 2013[Jun]; 208 (2 ): 172-9 PMID23497275 show ga AIM: 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. METHODS: Anaesthetized rats, subjected to 30-min coronary artery ligation and reperfusion up to 8 days, were treated with vehicle or the arginase inhibitor N(?) -hydroxy-nor-l-arginine (nor-NOHA; 100 mg kg(-1) ) intravenously 15 min before ischaemia. Coronary flow velocity was determined repeatedly during reperfusion. RESULTS: Arginase activity in the ischaemic-reperfused myocardium was increased already at 20 min of reperfusion and maintained at 8 days. Infarct size was reduced by arginase inhibition at 2 h (39 ± 3% of the area at risk (AAR) vs. 51 ± 2% in the vehicle group, P < 0.01) and at 8 days of reperfusion (13 ± 2% of the left ventricle (LV) vs. 22 ± 2%, P < 0.05). Basal coronary flow velocity was higher during reperfusion in the group given nor-NOHA, and it correlated inversely to infarct size (P < 0.01, r = -0.60). Hyperaemic coronary flow velocity was also increased in the nor-NOHA-treated group compared to vehicle at 24 h and at day 8 (P < 0.05). CONCLUSION: It is concluded that arginase activity is increased already during early reperfusion. Arginase inhibition increases coronary flow velocity and reduces infarct size that is sustained 8 days after reperfusion. Inhibition of arginase may thus be a promising therapeutic target to prevent the development of microvascular dysfunction and myocardial injury following ischaemia-reperfusion. |Animals [MESH] |Arginase/*antagonists & inhibitors [MESH] |Arginine/*analogs & derivatives/pharmacology [MESH] |Coronary Vessels/*drug effects/*physiology [MESH] |Myocardial Infarction/etiology/*pathology [MESH] |Nitric Oxide/metabolism [MESH] |Rats [MESH]Arginase inhibition improves coronary microvascular function and reduc(epmc).pdf DeepDyve Pubget Overpricing