Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.

BACKGROUND: We assess whether remote ischemic preconditioning (rIPC) of the recipient can modify ischemia-reperfusion (IR) injury in the donor heart following orthotopic heart transplantation from brain dead donors and to examine potential mechanisms of protection. METHODS: Sixteen pigs weighing fr...

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Główni autorzy: Konstantinov, I, Li, J, Cheung, M, Shimizu, M, Stokoe, J, Kharbanda, R, Redington, A
Format: Journal article
Język:English
Wydane: 2005
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author Konstantinov, I
Li, J
Cheung, M
Shimizu, M
Stokoe, J
Kharbanda, R
Redington, A
author_facet Konstantinov, I
Li, J
Cheung, M
Shimizu, M
Stokoe, J
Kharbanda, R
Redington, A
author_sort Konstantinov, I
collection OXFORD
description BACKGROUND: We assess whether remote ischemic preconditioning (rIPC) of the recipient can modify ischemia-reperfusion (IR) injury in the donor heart following orthotopic heart transplantation from brain dead donors and to examine potential mechanisms of protection. METHODS: Sixteen pigs weighing from 26 to 34.2 (mean 29.2) kg, randomized to control group (n=5), ischemic preconditioning (rIPC) group (n=6), and to receive rIPC with prior glibenclamide administration (Glib + rIPC) group (n=5) underwent orthotopic heart transplantation with the support of hypothermic (32 degrees C) cardiopulmonary bypass (CPB). The hearts were harvested from donor animal rendered brain dead by balloon compression via a craniotomy. Preconditioning of the recipients was induced by four 5-min cycles of lower limb ischemia. Myocardial infarction (MI) was induced following heart transplantation by 30 min of left anterior descending (LAD) artery occlusion following by 2 hr of regional reperfusion. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining. RESULTS: Preconditioning of the recipient reduced the mass of MI (6.75+/-6.3 g in rIPC vs. 18.1+/-5.8 g in control, P=0.01), MI to area at risk (ARR) mass ratio by 57% (15.6%+/-15.2% vs. 36.3%+/-13.4%, P=0.04). The protective effect of preconditioning was abolished by pretreatment with glibenclamide. CONCLUSIONS: Remote ischemic preconditioning of the recipient, decreases ischemia-reperfusion injury in the brain dead donor heart following orthotopic heart transplantation via a Katp channel-dependent mechanism. This study suggests that a circulating effector persists after the rIPC stimulus is applied, and excludes an ongoing afferent neurogenic mechanism of cardioprotection.
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spelling oxford-uuid:5eefa174-b45e-43c4-ad0d-f3465fb36be42022-03-26T17:43:53ZRemote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:5eefa174-b45e-43c4-ad0d-f3465fb36be4EnglishSymplectic Elements at Oxford2005Konstantinov, ILi, JCheung, MShimizu, MStokoe, JKharbanda, RRedington, A BACKGROUND: We assess whether remote ischemic preconditioning (rIPC) of the recipient can modify ischemia-reperfusion (IR) injury in the donor heart following orthotopic heart transplantation from brain dead donors and to examine potential mechanisms of protection. METHODS: Sixteen pigs weighing from 26 to 34.2 (mean 29.2) kg, randomized to control group (n=5), ischemic preconditioning (rIPC) group (n=6), and to receive rIPC with prior glibenclamide administration (Glib + rIPC) group (n=5) underwent orthotopic heart transplantation with the support of hypothermic (32 degrees C) cardiopulmonary bypass (CPB). The hearts were harvested from donor animal rendered brain dead by balloon compression via a craniotomy. Preconditioning of the recipients was induced by four 5-min cycles of lower limb ischemia. Myocardial infarction (MI) was induced following heart transplantation by 30 min of left anterior descending (LAD) artery occlusion following by 2 hr of regional reperfusion. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining. RESULTS: Preconditioning of the recipient reduced the mass of MI (6.75+/-6.3 g in rIPC vs. 18.1+/-5.8 g in control, P=0.01), MI to area at risk (ARR) mass ratio by 57% (15.6%+/-15.2% vs. 36.3%+/-13.4%, P=0.04). The protective effect of preconditioning was abolished by pretreatment with glibenclamide. CONCLUSIONS: Remote ischemic preconditioning of the recipient, decreases ischemia-reperfusion injury in the brain dead donor heart following orthotopic heart transplantation via a Katp channel-dependent mechanism. This study suggests that a circulating effector persists after the rIPC stimulus is applied, and excludes an ongoing afferent neurogenic mechanism of cardioprotection.
spellingShingle Konstantinov, I
Li, J
Cheung, M
Shimizu, M
Stokoe, J
Kharbanda, R
Redington, A
Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title_full Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title_fullStr Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title_full_unstemmed Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title_short Remote ischemic preconditioning of the recipient reduces myocardial ischemia-reperfusion injury of the denervated donor heart via a Katp channel-dependent mechanism.
title_sort remote ischemic preconditioning of the recipient reduces myocardial ischemia reperfusion injury of the denervated donor heart via a katp channel dependent mechanism
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