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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Nature Portfolio
2021-05-01
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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. |
first_indexed | 2024-12-13T16:29:49Z |
format | Article |
id | doaj.art-5f849f22a1b343d8bc393d3e5e1dc97a |
institution | Directory Open Access Journal |
issn | 2045-2322 |
language | English |
last_indexed | 2024-12-13T16:29:49Z |
publishDate | 2021-05-01 |
publisher | Nature Portfolio |
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series | Scientific Reports |
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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