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Comparing anesthesia with isoflurane and fentanyl/fluanisone/midazolam in a rat model of cardiac arrest

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Comparing anesthesia with isoflurane and fentanyl/fluanisone/midazolam in a rat model of cardiac arrest. / Secher, Niels; Malte, Christian Lind; Tønnesen, Else; Østergaard, Leif; Granfeldt, Asger.

In: Journal of Applied Physiology, 2016, p. jap.00998.2015.

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@article{c8aac0b5b6a24950b1d44b320df78c23,
title = "Comparing anesthesia with isoflurane and fentanyl/fluanisone/midazolam in a rat model of cardiac arrest",
abstract = "BACKGROUND: Only one in ten patients survives cardiac arrest (CA), underscoring the need to improve CA management. Isoflurane has shown cardio- and neuroprotective effects in animal models of ischemia/reperfusion injury. Therefore, beneficial effect of isoflurane should be tested in an experimental CA model. We hypothesize that isoflurane anesthesia improves short-term outcome following resuscitation from CA compared with a subcutaneous fentanyl/fluanisone/midazolam anesthesia.METHODS: Male Sprague Dawley rats were randomized to anesthesia with isoflurane (n=11) or fentanyl/fluanisone/midazolam (n=11). After 10 min of asphyxial CA, animals were resuscitated by mechanical chest compressions, ventilations, and epinephrine and observed for 30 min. Hemodynamics including coronary perfusion pressure, systemic O2 consumption, and arterial blood gases were recorded throughout the study. Plasma samples for Endothelin-1 and cathecolamines were drawn before and after CA.KEY FINDINGS: Compared with fentanyl/fluanisone/midazolam anesthesia, isoflurane resulted in a shorter time to return of spontaneous circulation (ROSC), less use of epinephrine, increased coronary perfusion pressure during CPR, higher mean arterial pressure post ROSC, increased plasma levels of Endothelin-1 and decreased levels of epinephrine. The choice of anesthesia did not affect ROSC rate or systemic O2 consumption.CONCLUSION: Isoflurane reduces time to ROSC, increases coronary perfusion pressure, and improves hemodynamic function, all of which are important parameters in CA models.",
author = "Niels Secher and Malte, {Christian Lind} and Else T{\o}nnesen and Leif {\O}stergaard and Asger Granfeldt",
note = "Copyright {\circledC} 2015, Journal of Applied Physiology.",
year = "2016",
doi = "10.1152/japplphysiol.00998.2015",
language = "English",
pages = "jap.00998.2015",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "AMER PHYSIOLOGICAL SOC",

}

RIS

TY - JOUR

T1 - Comparing anesthesia with isoflurane and fentanyl/fluanisone/midazolam in a rat model of cardiac arrest

AU - Secher, Niels

AU - Malte, Christian Lind

AU - Tønnesen, Else

AU - Østergaard, Leif

AU - Granfeldt, Asger

N1 - Copyright © 2015, Journal of Applied Physiology.

PY - 2016

Y1 - 2016

N2 - BACKGROUND: Only one in ten patients survives cardiac arrest (CA), underscoring the need to improve CA management. Isoflurane has shown cardio- and neuroprotective effects in animal models of ischemia/reperfusion injury. Therefore, beneficial effect of isoflurane should be tested in an experimental CA model. We hypothesize that isoflurane anesthesia improves short-term outcome following resuscitation from CA compared with a subcutaneous fentanyl/fluanisone/midazolam anesthesia.METHODS: Male Sprague Dawley rats were randomized to anesthesia with isoflurane (n=11) or fentanyl/fluanisone/midazolam (n=11). After 10 min of asphyxial CA, animals were resuscitated by mechanical chest compressions, ventilations, and epinephrine and observed for 30 min. Hemodynamics including coronary perfusion pressure, systemic O2 consumption, and arterial blood gases were recorded throughout the study. Plasma samples for Endothelin-1 and cathecolamines were drawn before and after CA.KEY FINDINGS: Compared with fentanyl/fluanisone/midazolam anesthesia, isoflurane resulted in a shorter time to return of spontaneous circulation (ROSC), less use of epinephrine, increased coronary perfusion pressure during CPR, higher mean arterial pressure post ROSC, increased plasma levels of Endothelin-1 and decreased levels of epinephrine. The choice of anesthesia did not affect ROSC rate or systemic O2 consumption.CONCLUSION: Isoflurane reduces time to ROSC, increases coronary perfusion pressure, and improves hemodynamic function, all of which are important parameters in CA models.

AB - BACKGROUND: Only one in ten patients survives cardiac arrest (CA), underscoring the need to improve CA management. Isoflurane has shown cardio- and neuroprotective effects in animal models of ischemia/reperfusion injury. Therefore, beneficial effect of isoflurane should be tested in an experimental CA model. We hypothesize that isoflurane anesthesia improves short-term outcome following resuscitation from CA compared with a subcutaneous fentanyl/fluanisone/midazolam anesthesia.METHODS: Male Sprague Dawley rats were randomized to anesthesia with isoflurane (n=11) or fentanyl/fluanisone/midazolam (n=11). After 10 min of asphyxial CA, animals were resuscitated by mechanical chest compressions, ventilations, and epinephrine and observed for 30 min. Hemodynamics including coronary perfusion pressure, systemic O2 consumption, and arterial blood gases were recorded throughout the study. Plasma samples for Endothelin-1 and cathecolamines were drawn before and after CA.KEY FINDINGS: Compared with fentanyl/fluanisone/midazolam anesthesia, isoflurane resulted in a shorter time to return of spontaneous circulation (ROSC), less use of epinephrine, increased coronary perfusion pressure during CPR, higher mean arterial pressure post ROSC, increased plasma levels of Endothelin-1 and decreased levels of epinephrine. The choice of anesthesia did not affect ROSC rate or systemic O2 consumption.CONCLUSION: Isoflurane reduces time to ROSC, increases coronary perfusion pressure, and improves hemodynamic function, all of which are important parameters in CA models.

U2 - 10.1152/japplphysiol.00998.2015

DO - 10.1152/japplphysiol.00998.2015

M3 - Journal article

SP - jap.00998.2015

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

ER -