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Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning
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Zeitschriftentitel: | American Journal of Physiology-Heart and Circulatory Physiology |
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Personen und Körperschaften: | , , , , |
In: | American Journal of Physiology-Heart and Circulatory Physiology, 279, 2000, 6, S. H2694-H2703 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Physiological Society
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Schlagwörter: |
author_facet |
Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. |
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author |
Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. |
spellingShingle |
Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. American Journal of Physiology-Heart and Circulatory Physiology Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
author_sort |
toyoda, yoshiya |
spelling |
Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2694 <jats:p>Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. The purpose of this study was to determine whether APC is modulated by ATP-sensitive potassium (K<jats:sub>ATP</jats:sub>) channels and to determine whether this modulation occurs before ischemia or during reperfusion. The role of K<jats:sub>ATP</jats:sub>channels before ischemia (I), during reperfusion (R), or during ischemia and reperfusion (IR) was investigated using the nonspecific K<jats:sub>ATP</jats:sub>blocker glibenclamide (Glb), the mitochondrial (mito) K<jats:sub>ATP</jats:sub>channel blocker 5-hydroxydecanoate (5-HD), and the sarcolemmal (sarc) K<jats:sub>ATP</jats:sub>channel blocker HMR-1883 (HMR). Infarct size was significantly increased ( P < 0.05) in APC hearts with Glb-I, Glb-R, and 5-HD-I treatment and partially with 5-HD-R. Glb-I and Glb-R treatment significantly decreased APC functional recovery ( P < 0.05 vs. APC), whereas 5-HD-I and 5-HD-R had no effect on APC functional recovery. HMR-IR significantly decreased postischemic functional recovery ( P < 0.05 vs. APC) but had no effect on infarct size. These data indicate that APC infarct size reduction is modulated by mitoK<jats:sub>ATP</jats:sub>channels primarily during ischemia and suggest that functional recovery is modulated by sarcK<jats:sub>ATP</jats:sub>channels during ischemia and reperfusion.</jats:p> Differential role of sarcolemmal and mitochondrial K<sub>ATP</sub>channels in adenosine-enhanced ischemic preconditioning American Journal of Physiology-Heart and Circulatory Physiology |
doi_str_mv |
10.1152/ajpheart.2000.279.6.h2694 |
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Online Free |
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American Physiological Society, 2000 |
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American Physiological Society, 2000 |
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American Physiological Society |
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American Journal of Physiology-Heart and Circulatory Physiology |
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title |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_unstemmed |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_full |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_fullStr |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_full_unstemmed |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_short |
Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_sort |
differential role of sarcolemmal and mitochondrial k<sub>atp</sub>channels in adenosine-enhanced ischemic preconditioning |
topic |
Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
url |
http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2694 |
publishDate |
2000 |
physical |
H2694-H2703 |
description |
<jats:p>Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. The purpose of this study was to determine whether APC is modulated by ATP-sensitive potassium (K<jats:sub>ATP</jats:sub>) channels and to determine whether this modulation occurs before ischemia or during reperfusion. The role of K<jats:sub>ATP</jats:sub>channels before ischemia (I), during reperfusion (R), or during ischemia and reperfusion (IR) was investigated using the nonspecific K<jats:sub>ATP</jats:sub>blocker glibenclamide (Glb), the mitochondrial (mito) K<jats:sub>ATP</jats:sub>channel blocker 5-hydroxydecanoate (5-HD), and the sarcolemmal (sarc) K<jats:sub>ATP</jats:sub>channel blocker HMR-1883 (HMR). Infarct size was significantly increased ( P < 0.05) in APC hearts with Glb-I, Glb-R, and 5-HD-I treatment and partially with 5-HD-R. Glb-I and Glb-R treatment significantly decreased APC functional recovery ( P < 0.05 vs. APC), whereas 5-HD-I and 5-HD-R had no effect on APC functional recovery. HMR-IR significantly decreased postischemic functional recovery ( P < 0.05 vs. APC) but had no effect on infarct size. These data indicate that APC infarct size reduction is modulated by mitoK<jats:sub>ATP</jats:sub>channels primarily during ischemia and suggest that functional recovery is modulated by sarcK<jats:sub>ATP</jats:sub>channels during ischemia and reperfusion.</jats:p> |
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author | Toyoda, Yoshiya, Friehs, Ingeborg, Parker, Robert A., Levitsky, Sidney, McCully, James D. |
author_facet | Toyoda, Yoshiya, Friehs, Ingeborg, Parker, Robert A., Levitsky, Sidney, McCully, James D., Toyoda, Yoshiya, Friehs, Ingeborg, Parker, Robert A., Levitsky, Sidney, McCully, James D. |
author_sort | toyoda, yoshiya |
container_issue | 6 |
container_start_page | 0 |
container_title | American Journal of Physiology-Heart and Circulatory Physiology |
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description | <jats:p>Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. The purpose of this study was to determine whether APC is modulated by ATP-sensitive potassium (K<jats:sub>ATP</jats:sub>) channels and to determine whether this modulation occurs before ischemia or during reperfusion. The role of K<jats:sub>ATP</jats:sub>channels before ischemia (I), during reperfusion (R), or during ischemia and reperfusion (IR) was investigated using the nonspecific K<jats:sub>ATP</jats:sub>blocker glibenclamide (Glb), the mitochondrial (mito) K<jats:sub>ATP</jats:sub>channel blocker 5-hydroxydecanoate (5-HD), and the sarcolemmal (sarc) K<jats:sub>ATP</jats:sub>channel blocker HMR-1883 (HMR). Infarct size was significantly increased ( P < 0.05) in APC hearts with Glb-I, Glb-R, and 5-HD-I treatment and partially with 5-HD-R. Glb-I and Glb-R treatment significantly decreased APC functional recovery ( P < 0.05 vs. APC), whereas 5-HD-I and 5-HD-R had no effect on APC functional recovery. HMR-IR significantly decreased postischemic functional recovery ( P < 0.05 vs. APC) but had no effect on infarct size. These data indicate that APC infarct size reduction is modulated by mitoK<jats:sub>ATP</jats:sub>channels primarily during ischemia and suggest that functional recovery is modulated by sarcK<jats:sub>ATP</jats:sub>channels during ischemia and reperfusion.</jats:p> |
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spelling | Toyoda, Yoshiya Friehs, Ingeborg Parker, Robert A. Levitsky, Sidney McCully, James D. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2694 <jats:p>Adenosine-enhanced ischemic preconditioning (APC) extends the protection afforded by ischemic preconditioning (IPC) by both significantly decreasing infarct size and significantly enhancing postischemic functional recovery. The purpose of this study was to determine whether APC is modulated by ATP-sensitive potassium (K<jats:sub>ATP</jats:sub>) channels and to determine whether this modulation occurs before ischemia or during reperfusion. The role of K<jats:sub>ATP</jats:sub>channels before ischemia (I), during reperfusion (R), or during ischemia and reperfusion (IR) was investigated using the nonspecific K<jats:sub>ATP</jats:sub>blocker glibenclamide (Glb), the mitochondrial (mito) K<jats:sub>ATP</jats:sub>channel blocker 5-hydroxydecanoate (5-HD), and the sarcolemmal (sarc) K<jats:sub>ATP</jats:sub>channel blocker HMR-1883 (HMR). Infarct size was significantly increased ( P < 0.05) in APC hearts with Glb-I, Glb-R, and 5-HD-I treatment and partially with 5-HD-R. Glb-I and Glb-R treatment significantly decreased APC functional recovery ( P < 0.05 vs. APC), whereas 5-HD-I and 5-HD-R had no effect on APC functional recovery. HMR-IR significantly decreased postischemic functional recovery ( P < 0.05 vs. APC) but had no effect on infarct size. These data indicate that APC infarct size reduction is modulated by mitoK<jats:sub>ATP</jats:sub>channels primarily during ischemia and suggest that functional recovery is modulated by sarcK<jats:sub>ATP</jats:sub>channels during ischemia and reperfusion.</jats:p> Differential role of sarcolemmal and mitochondrial K<sub>ATP</sub>channels in adenosine-enhanced ischemic preconditioning American Journal of Physiology-Heart and Circulatory Physiology |
spellingShingle | Toyoda, Yoshiya, Friehs, Ingeborg, Parker, Robert A., Levitsky, Sidney, McCully, James D., American Journal of Physiology-Heart and Circulatory Physiology, Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning, Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
title | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_full | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_fullStr | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_full_unstemmed | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_short | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
title_sort | differential role of sarcolemmal and mitochondrial k<sub>atp</sub>channels in adenosine-enhanced ischemic preconditioning |
title_unstemmed | Differential role of sarcolemmal and mitochondrial KATPchannels in adenosine-enhanced ischemic preconditioning |
topic | Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
url | http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2694 |