Comparison of 5 Different Remifentanil Strategies Against Myocardial Ischemia-Reperfusion Injury

Objective The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. Design An in vitro experimental study using the Langendorff system. Setting A university r...

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Published inJournal of cardiothoracic and vascular anesthesia Vol. 25; no. 6; pp. 926 - 930
Main Authors Chun, Kook Jin, MD, PhD, Park, Yong Hyun, MD, PhD, Kim, Jeong Su, MD, Jang, Youngho, MD, PhD, Kim, June Hong, MD, PhD, Kim, Jun, MD, PhD, Lee, Mi Young, MD, PhD
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Published United States Elsevier Inc 01.12.2011
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Abstract Objective The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. Design An in vitro experimental study using the Langendorff system. Setting A university research laboratory. Participants Male Sprague-Dawley rats (each n = 9). Interventions Five different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared. Measurement and Main Results The infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular–developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dtmax after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dtmax in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre ( p < 0.05). Conclusions Preconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.
AbstractList The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. An in vitro experimental study using the Langendorff system. A university research laboratory. Male Sprague-Dawley rats (each n = 9). Five different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared. The infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular–developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dt max after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dt max in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre ( p < 0.05). Preconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.
Objective The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. Design An in vitro experimental study using the Langendorff system. Setting A university research laboratory. Participants Male Sprague-Dawley rats (each n = 9). Interventions Five different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared. Measurement and Main Results The infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular–developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dtmax after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dtmax in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre ( p < 0.05). Conclusions Preconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.
OBJECTIVEThe purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury.DESIGNAn in vitro experimental study using the Langendorff system.SETTINGA university research laboratory.PARTICIPANTSMale Sprague-Dawley rats (each n = 9).INTERVENTIONSFive different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared.MEASUREMENT AND MAIN RESULTSThe infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular-developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dt(max) after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dt(max) in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre (p < 0.05).CONCLUSIONSPreconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.
The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against myocardial ischemia-reperfusion injury. An in vitro experimental study using the Langendorff system. A university research laboratory. Male Sprague-Dawley rats (each n = 9). Five different remifentanil strategies were performed in isolated rat hearts as follows: remifentanil preconditioning (R-Pre), remifentanil postconditioning (R-Post), ischemic targeting remifentanil (R1), reperfusion targeting remifentanil (R2), or both ischemic and reperfusion targeting remifentanil (R3). Infarct size and cardiodynamics were compared. The infarct-risk volume ratio in groups R-Pre (13.7% ± 9.9%), R-Post (13.7% ± 12.3%), and R3 (12.6% ± 6.1%) were decreased significantly compared with the untreated control hearts (32.9% ± 11.1%, p &lt 0.01). There was no significant difference in the left ventricular-developed pressure (LVDP) recovery after reperfusion between the control (43.6% ± 14.5%) and R-Pre (34.8% ± 12.9%, p > 0.05) groups after reperfusion. However, the LVDP recovery in R-Post (21.6% ± 7.7%, p < 0.05), R1 (16.7% ± 19.8%, p < 0.01), R2 (22.2% ± 13.9%, p < 0.05), and R3 (16.2% ± 7.8%, p < 0.01) was decreased significantly compared with control hearts. There was no significant difference in the recovery of dP/dt(max) after reperfusion between the R-Pre (42.0% ± 16.9%) and control groups (39.0% ± 15.4%, p > 0.05), whereas the dP/dt(max) in R3 group (16.9% ± 9.0%) was decreased significantly compared with R-Pre (p < 0.05). Preconditioning or postconditioning by remifentanil and the continuous infusion of remifentanil effectively reduce myocardial infarction, whereas reperfusion targeting ischemic targeting or reperfusion targeting remifentanil does not. Remifentanil preconditioning better preserves myocardial function, especially LVDP, than other remifentanil strategies.
Author Park, Yong Hyun, MD, PhD
Kim, Jun, MD, PhD
Kim, June Hong, MD, PhD
Lee, Mi Young, MD, PhD
Chun, Kook Jin, MD, PhD
Kim, Jeong Su, MD
Jang, Youngho, MD, PhD
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/21514843$$D View this record in MEDLINE/PubMed
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Keywords postconditioning
myocardial ischemia
remifentanil
cardiodynamics
preconditioning
Language English
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Snippet Objective The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous...
The purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous infusion) against...
OBJECTIVEThe purpose of this study was to investigate the effects of various remifentanil strategies (preconditioning, postconditioning, or continuous...
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SubjectTerms Anesthesia & Perioperative Care
Anesthetics, Intravenous - administration & dosage
Anesthetics, Intravenous - pharmacology
Animals
Body Weight - physiology
cardiodynamics
Cardiotonic Agents
Coloring Agents
Coronary Circulation - physiology
Critical Care
Heart - drug effects
Heart Function Tests
In Vitro Techniques
Ischemic Postconditioning - methods
Ischemic Preconditioning, Myocardial - methods
Male
Myocardial Infarction - pathology
Myocardial Infarction - prevention & control
myocardial ischemia
Myocardial Reperfusion Injury - prevention & control
Organ Size - physiology
Piperidines - administration & dosage
Piperidines - pharmacology
postconditioning
preconditioning
Rats
Rats, Sprague-Dawley
remifentanil
Reperfusion
Tetrazolium Salts
Ventricular Function, Left - physiology
Title Comparison of 5 Different Remifentanil Strategies Against Myocardial Ischemia-Reperfusion Injury
URI https://www.clinicalkey.es/playcontent/1-s2.0-S105307701100053X
https://dx.doi.org/10.1053/j.jvca.2011.02.019
https://www.ncbi.nlm.nih.gov/pubmed/21514843
https://search.proquest.com/docview/906559180
Volume 25
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