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Minocycline fails to improve neurologic and histologic outcome after ventricular fibrillation cardiac arrest in rats

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World Journal of Critical Care Medicine 2019年第7期8卷 106-119页

作者： Andreas Janata Ingrid AM Magnet Kristin L Schreiber Caleb D Wilson Jason P Stezoski Keri Janesko-Feldman Patrick M Kochanek Tomas Drabek Safar Center for Resuscitation Research University of Pittsburgh School of MedicinePittsburghPA 15224United States Department of Critical Care Medicine University of Pittsburgh School of MedicinePittsburghPA 15213United States Emergency Department KA RudolfstiftungVienna 1030Austria Department of Emergency Medicine Vienna General HospitalMedical University of ViennaVienna 1090Austria Department of Anesthesiology and Perioperative Medicine University of Pittsburgh School of MedicinePittsburghPA 15213United States Department of Anesthesiology Perioperative and Pain MedicineBrigham and Women’s HospitalHarvard Medical SchoolBostonMA 02115United States Wyoming Otolaryngology Wyoming Medical CenterCasperWY 82604United States

BACKGROUND Prolonged cardiac arrest(CA)produces extensive neuronal death and microglial proliferation and activation resulting in neuro-cognitive *** other potential mechanisms,microglia have been implicated as triggers of neuronal death after hypoxic-ischemic *** is neuroprotective in some brain ischemia models,either by blunting the microglial response or by a direct effect on *** To improve survival,attenuate neurologic deficits,neuroinflammation,and histological damage after ventricular fibrillation(VF)CA in *** Adult male isoflurane-anesthetized rats were subjected to 6 min VF CA followed by 2 min resuscitation including chest compression,epinephrine,bicarbonate,and *** return of spontaneous circulation(ROSC),rats were randomized to two groups:(1)Minocycline 90 mg/kg intraperitoneally(i.p.)at 15 min ROSC,followed by 22.5 mg/kg *** 12 h for 72 h;and(2)Controls,receiving the same volume of vehicle(phosphate-buffered saline).The rats were kept normothermic during the postoperative *** injury was assessed daily using Overall Performance Category(OPC;1=normal,5=dead)and Neurologic Deficit Score(NDS;0%=normal,100%=dead).Rats were sacrificed at 72 *** degeneration(Fluoro-Jade C staining)and microglia proliferation(anti-Iba-1 staining)were quantified in four selectively vulnerable brain regions(hippocampus,striatum,cerebellum,cortex)by three independent reviewers masked to the group *** In the minocycline group,8 out of 14 rats survived to 72 h compared to 8 out of 19 rats in the control group(P=0.46).The degree of neurologic deficit at 72 h[median,(interquartile range)]was not different between survivors in minocycline vs controls:OPC 1.5(1-2.75)vs 2(1.25-3),P=0.442;NDS 12(2-20)vs 17(7-51),P=0.328)or between all studied *** number of degenerating neurons(minocycline vs controls,mean±SEM:Hippocampus 58±8 vs 76±8;striatum 121±43 vs 153±32;cerebellum 20±7 vs 22

关键词： Heart arrest/pathology Cardiopulmonary resuscitation Survival rate neurons/drug effects Microglia/drug effects Minocycline/pharmacology

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