Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

Abstract Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome....

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Main Authors: Laura Ruggeri, Francesca Nespoli, Giuseppe Ristagno, Francesca Fumagalli, Antonio Boccardo, Davide Olivari, Roberta Affatato, Deborah Novelli, Daria De Giorgio, Pierpaolo Romanelli, Lucia Minoli, Alberto Cucino, Giovanni Babini, Lidia Staszewsky, Davide Zani, Davide Pravettoni, Angelo Belloli, Eugenio Scanziani, Roberto Latini, Aurora Magliocca
Format: Article
Language:English
Published: Nature Portfolio 2021-05-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-90202-w
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author Laura Ruggeri
Francesca Nespoli
Giuseppe Ristagno
Francesca Fumagalli
Antonio Boccardo
Davide Olivari
Roberta Affatato
Deborah Novelli
Daria De Giorgio
Pierpaolo Romanelli
Lucia Minoli
Alberto Cucino
Giovanni Babini
Lidia Staszewsky
Davide Zani
Davide Pravettoni
Angelo Belloli
Eugenio Scanziani
Roberto Latini
Aurora Magliocca
author_facet Laura Ruggeri
Francesca Nespoli
Giuseppe Ristagno
Francesca Fumagalli
Antonio Boccardo
Davide Olivari
Roberta Affatato
Deborah Novelli
Daria De Giorgio
Pierpaolo Romanelli
Lucia Minoli
Alberto Cucino
Giovanni Babini
Lidia Staszewsky
Davide Zani
Davide Pravettoni
Angelo Belloli
Eugenio Scanziani
Roberto Latini
Aurora Magliocca
author_sort Laura Ruggeri
collection DOAJ
description Abstract Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.
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spelling doaj.art-5f849f22a1b343d8bc393d3e5e1dc97a2022-12-21T23:38:32ZengNature PortfolioScientific Reports2045-23222021-05-0111111010.1038/s41598-021-90202-wEsmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrestLaura Ruggeri0Francesca Nespoli1Giuseppe Ristagno2Francesca Fumagalli3Antonio Boccardo4Davide Olivari5Roberta Affatato6Deborah Novelli7Daria De Giorgio8Pierpaolo Romanelli9Lucia Minoli10Alberto Cucino11Giovanni Babini12Lidia Staszewsky13Davide Zani14Davide Pravettoni15Angelo Belloli16Eugenio Scanziani17Roberto Latini18Aurora Magliocca19Istituto Di Ricerche Farmacologiche Mario Negri IRCCSIstituto Di Ricerche Farmacologiche Mario Negri IRCCSDepartment of Pathophysiology and Transplantation, University of MilanIstituto Di Ricerche Farmacologiche Mario Negri IRCCSDipartimento Di Medicina Veterinaria, University of MilanIstituto Di Ricerche Farmacologiche Mario Negri IRCCSIstituto Di Ricerche Farmacologiche Mario Negri IRCCSIstituto Di Ricerche Farmacologiche Mario Negri IRCCSIstituto Di Ricerche Farmacologiche Mario Negri IRCCSDipartimento Di Medicina Veterinaria, University of MilanDipartimento Di Medicina Veterinaria, University of MilanDepartment of Pathophysiology and Transplantation, University of MilanDepartment of Pathophysiology and Transplantation, University of MilanIstituto Di Ricerche Farmacologiche Mario Negri IRCCSDipartimento Di Medicina Veterinaria, University of MilanDipartimento Di Medicina Veterinaria, University of MilanDipartimento Di Medicina Veterinaria, University of MilanDipartimento Di Medicina Veterinaria, University of MilanIstituto Di Ricerche Farmacologiche Mario Negri IRCCSDepartment of Pathophysiology and Transplantation, University of MilanAbstract Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.https://doi.org/10.1038/s41598-021-90202-w
spellingShingle Laura Ruggeri
Francesca Nespoli
Giuseppe Ristagno
Francesca Fumagalli
Antonio Boccardo
Davide Olivari
Roberta Affatato
Deborah Novelli
Daria De Giorgio
Pierpaolo Romanelli
Lucia Minoli
Alberto Cucino
Giovanni Babini
Lidia Staszewsky
Davide Zani
Davide Pravettoni
Angelo Belloli
Eugenio Scanziani
Roberto Latini
Aurora Magliocca
Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
Scientific Reports
title Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
title_full Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
title_fullStr Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
title_full_unstemmed Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
title_short Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
title_sort esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest
url https://doi.org/10.1038/s41598-021-90202-w
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