Cardiac Adaptive Responses After Hypoxia in an Experimental Model
The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions...
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Veröffentlicht in: | Angiology 2010-02, Vol.61 (2), p.145-156 |
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creator | Bin-Jaliah, Ismaeel Ammar, Hania I. Mikhailidis, Dimitri P. Dallak, Mohammed A. Al-Hashem, Fahaid H. Haidara, Mohamed A. Yassin, Hanaa Z. Bahnasi, Abeer A. Rashed, Laila A. Isenovic, Esma R. |
description | The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (ΔP/Δt max ) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P < .001), RPP (P < .001), and ΔP/Δt max (P < .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms. |
doi_str_mv | 10.1177/0003319709352486 |
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Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (ΔP/Δt max ) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P < .001), RPP (P < .001), and ΔP/Δt max (P < .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.</description><identifier>ISSN: 0003-3197</identifier><identifier>EISSN: 1940-1574</identifier><identifier>DOI: 10.1177/0003319709352486</identifier><identifier>PMID: 19939823</identifier><identifier>CODEN: ANGIAB</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Adaptation, Physiological ; Animals ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Erythropoietin - metabolism ; Erythropoietin - physiology ; General and cellular metabolism. Vitamins ; Hypoxia - physiopathology ; Immunohistochemistry ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; Male ; Medical sciences ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - physiopathology ; Myocytes, Cardiac - metabolism ; Pharmacology. 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Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (ΔP/Δt max ) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P < .001), RPP (P < .001), and ΔP/Δt max (P < .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.</description><subject>Adaptation, Physiological</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Erythropoietin - metabolism</subject><subject>Erythropoietin - physiology</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Hypoxia - physiopathology</subject><subject>Immunohistochemistry</subject><subject>In Vitro Techniques</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Pharmacology. 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Vascular system</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Erythropoietin - metabolism</topic><topic>Erythropoietin - physiology</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Hypoxia - physiopathology</topic><topic>Immunohistochemistry</topic><topic>In Vitro Techniques</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascular Endothelial Growth Factor A - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bin-Jaliah, Ismaeel</creatorcontrib><creatorcontrib>Ammar, Hania I.</creatorcontrib><creatorcontrib>Mikhailidis, Dimitri P.</creatorcontrib><creatorcontrib>Dallak, Mohammed A.</creatorcontrib><creatorcontrib>Al-Hashem, Fahaid H.</creatorcontrib><creatorcontrib>Haidara, Mohamed A.</creatorcontrib><creatorcontrib>Yassin, Hanaa Z.</creatorcontrib><creatorcontrib>Bahnasi, Abeer A.</creatorcontrib><creatorcontrib>Rashed, Laila A.</creatorcontrib><creatorcontrib>Isenovic, Esma R.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Angiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bin-Jaliah, Ismaeel</au><au>Ammar, Hania I.</au><au>Mikhailidis, Dimitri P.</au><au>Dallak, Mohammed A.</au><au>Al-Hashem, Fahaid H.</au><au>Haidara, Mohamed A.</au><au>Yassin, Hanaa Z.</au><au>Bahnasi, Abeer A.</au><au>Rashed, Laila A.</au><au>Isenovic, Esma R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac Adaptive Responses After Hypoxia in an Experimental Model</atitle><jtitle>Angiology</jtitle><addtitle>Angiology</addtitle><date>2010-02-01</date><risdate>2010</risdate><volume>61</volume><issue>2</issue><spage>145</spage><epage>156</epage><pages>145-156</pages><issn>0003-3197</issn><eissn>1940-1574</eissn><coden>ANGIAB</coden><abstract>The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (ΔP/Δt max ) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P < .001), RPP (P < .001), and ΔP/Δt max (P < .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>19939823</pmid><doi>10.1177/0003319709352486</doi><tpages>12</tpages></addata></record> |
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subjects | Adaptation, Physiological Animals Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Erythropoietin - metabolism Erythropoietin - physiology General and cellular metabolism. Vitamins Hypoxia - physiopathology Immunohistochemistry In Vitro Techniques Ischemic Preconditioning, Myocardial Male Medical sciences Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Myocytes, Cardiac - metabolism Pharmacology. Drug treatments Rats Rats, Wistar Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor A - physiology |
title | Cardiac Adaptive Responses After Hypoxia in an Experimental Model |
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