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 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 &lt; 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 &lt; 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 &lt; 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
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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 &lt; 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 &lt; 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 &lt; 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.
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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 &lt; 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 &lt; 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 &lt; 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 &lt; 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 &lt; 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 &lt; 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