Ischemic Post-Conditioning in a Rat Model of Asphyxial Cardiac Arrest

Author:

Barajas Matthew B.12ORCID,Oyama Takuro2,Shiota Masakazu3,Li Zhu2ORCID,Zaum Maximillian24,Zecevic Ilija5,Riess Matthias L.126ORCID

Affiliation:

1. Department of Anesthesiology, Tennessee Valley Healthcare System, Veterans Affairs Medical Center, Nashville, TN 37212, USA

2. Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN 37212, USA

3. Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37212, USA

4. Department of Anesthesiology, University Medicine Greifswald, 17489 Greifswald, Germany

5. School of Medicine, Meharry Medical College, Nashville, TN 37212, USA

6. Department of Pharmacology, Vanderbilt University, Nashville, TN 37212, USA

Abstract

Background: Ischemic post-conditioning (IPoC) has been shown to improve outcomes in limited pre-clinical models. As down-time is often unknown, this technique needs to be investigated over a range of scenarios. As this tool limits reperfusion injury, there may be limited benefit or even harm after short arrest and limited ischemia-reperfusion injury. Methods: Eighteen male Wistar rats underwent 7 min of asphyxial arrest. Animals randomized to IPoC received a 20 s pause followed by 20 s of compressions, repeated four times, initiated 40 s into cardiopulmonary resuscitation. If return of spontaneous circulation (ROSC) was achieved, epinephrine was titrated to mean arterial pressure (MAP) of 70 mmHg. Data were analyzed using t-test or Mann–Whitney test. Significance set at p ≤ 0.05. Results: The rate of ROSC was equivalent in both groups, 88%. There was no statistically significant difference in time to ROSC, epinephrine required post ROSC, carotid flow, or peak lactate at any timepoint. There was a significantly elevated MAP with IPoC, 90.7 mmHg (SD 13.9), as compared to standard CPR, 76.7 mmHg (8.5), 2 h after ROSC, p = 0.03. Conclusions: IPoC demonstrated no harm in a model of short arrest using a new arrest etiology for CPR based IPoC intervention in a rat model.

Funder

U.S. Department of Veterans Affairs Biomedical Laboratory R&D Service

National Institutes of Health

Society of Cardiovascular Anesthesiologists

American Heart Association

Vanderbilt University Department of Anesthesiology Crawford Long Innovation

Foundation of Anesthesia Education and Research

Publisher

MDPI AG

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