Background: Anaesthetic postconditioning (APoC) attenuates myocardial injury following coronary ischaemia/reperfusion. We hypothesised that APoC at the initiation of cardiopulmonary resuscitation (CPR) will improve post resuscitation myocardial function along with improved mitochondrial function in a pig model of prolonged untreated ventricular fibrillation. Methods: In 32 pigs isoflurane anaesthesia was discontinued prior to induction of ventricular fibrillation that was left untreated for 15. min. At the initiation of CPR, 15 animals were randomised to controls (CON), and 17 to APoC with 2. vol% sevoflurane during the first 3. min CPR. Pigs were defibrillated after 4. min of CPR. After return of spontaneous circulation (ROSC), isoflurane was restarted at 0.8-1.5. vol% in both groups. Systolic and diastolic blood pressures were measured continuously. Of the animals that achieved ROSC, eight CON and eight APoC animals were randomised to have their left ventricular ejection fraction (LVEF%) assessed by echocardiography at 4. h. Seven CON and nine APoC were randomised to euthanasia 15. min after ROSC to isolate mitochondria from the left ventricle for bioenergetic studies. Results: ROSC was achieved in 10/15 CON and 15/17 APoC animals. APoC improved haemodynamics during CPR and post-CPR LVEF%. Mitochondrial ATP synthesis, coupling of oxidative phosphorylation and calcium retention capacity were improved in cardiac mitochondria isolated after APoC. Conclusions: In a porcine model of prolonged untreated cardiac arrest, APoC with inhaled sevoflurane at the initiation of CPR, is associated with preserved mitochondrial function and improved post resuscitation myocardial dysfunction.Approved by the Institutional Animal Care Committee of the Minneapolis Medical Research Foundation of Hennepin County Medical Center (protocol number 11-05).
|Original language||English (US)|
|Number of pages||7|
|State||Published - Dec 1 2014|
Bibliographical noteFunding Information:
Project-related funding was provided by institutional funds and by the National Institutes of Health (NIH; R01HL108926-01and R01HL123227 to DY). Further research funding was received from the Department of Veterans Affairs ( CARA-026-10F to MLR) and the NIH ( 5R01 HL098490-03 to MB and MLR). None of these entities had a role in the study design; the collection, analysis or interpretation of data; or the manuscript preparation.
- Cardiac arrest
- Cardiopulmonary resuscitation
- Ischaemia reperfusion injury