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1.
Brain Res ; 1648(Pt A): 345-355, 2016 10 01.
Artículo en Inglés | MEDLINE | ID: mdl-27495984

RESUMEN

In this study, we investigated the effects of remote ischemic preconditioning on post resuscitation cerebral function in a rat model of cardiac arrest and resuscitation. The animals were randomized into six groups: 1) sham operation, 2) lateral ventricle injection and sham operation, 3) cardiac arrest induced by ventricular fibrillation, 4) lateral ventricle injection and cardiac arrest, 5) remote ischemic preconditioning initiated 90min before induction of ventricular fibrillation, and 6) lateral ventricle injection and remote ischemic preconditioning before cardiac arrest. Reagent of Lateral ventricle injection is neuroglobin antisense oligodeoxynucleotides which initiated 24h before sham operation, cardiac arrest or remote ischemic preconditioning. Remote ischemic preconditioning was induced by four cycles of 5min of limb ischemia, followed by 5min of reperfusion. Ventricular fibrillation was induced by current and lasted for 6min. Defibrillation was attempted after 6min of cardiopulmonary resuscitation. The animals were then monitored for 2h and observed for an additionally maximum 70h. Post resuscitation cerebral function was evaluated by neurologic deficit score at 72h after return of spontaneous circulation. Results showed that remote ischemic preconditioning increased neurologic deficit scores. To investigate the neuroprotective effects of remote ischemic preconditioning, we observed neuronal injury at 48 and 72h after return of spontaneous circulation and found that remote ischemic preconditioning significantly decreased the occurrence of neuronal apoptosis and necrosis. To further comprehend mechanism of neuroprotection induced by remote ischemic preconditioning, we found expression of neuroglobin at 24h after return of spontaneous circulation was enhanced. Furthermore, administration of neuroglobin antisense oligodeoxynucleotides before induction of remote ischemic preconditioning showed that the level of neuroglobin was decreased then partly abrogated neuroprotection of remote ischemic preconditioning. These date suggested that neuroglobin involved in neuroprotective effect of remote ischemic preconditioning. In conclusion, remote ischemic preconditioning attenuated post resuscitation cerebral dysfunction and the neuroprotection was mediated partly by high level of neuroglobin in a rat model of cardiac arrest and resuscitation.


Asunto(s)
Encéfalo/fisiopatología , Reanimación Cardiopulmonar , Globinas/metabolismo , Paro Cardíaco/prevención & control , Precondicionamiento Isquémico/métodos , Proteínas del Tejido Nervioso/metabolismo , Animales , Región CA1 Hipocampal/metabolismo , Región CA1 Hipocampal/patología , Muerte Celular , Modelos Animales de Enfermedad , Paro Cardíaco/complicaciones , Masculino , Neuroglobina , Ratas , Ratas Sprague-Dawley
2.
Zhonghua Xin Xue Guan Bing Za Zhi ; 41(7): 590-3, 2013 Jul.
Artículo en Chino | MEDLINE | ID: mdl-24284188

RESUMEN

OBJECTIVE: To summarize the clinical experience of extracorporeal membrane oxygenation (ECMO) treatment for adult refractory cardiogenic shock. METHODS: From January 2003 to January 2011, patients with refractory cardiogenic shock required veno-arterial ECMO by failure of conventional therapy and intra-aortic balloon pump counterpulsation therapy were retrospectively studied. Patients with severe traumatic brain injury, advanced malignancies and multiple organ failure were excluded. Patients were divided into weaned group (n = 31) and not weaned group (n = 23) according to the ECMO weaning. RESULTS: The duration of ECMO was 24.16 (14.12, 56.75) hours. Twenty-two out of 31 patients in the weaned group survived and were discharged, 9 patients died after successfully weaned from ECMO (5 due to multisystem organ failure, 2 due to reoccurred cardiogenic shock, 1 due to infectious shock and 1 due to disseminated or diffuse intravascular coagulation). Pre-ECMO mean arterial pressure, ejection fraction, the duration of ECMO were significantly higher while pre-ECMO blood lactate [(8.64 ± 3.17) vs. (14.44 ± 2.52) , P < 0.01], the duration of ROSC [ (16.70 ± 5.29) vs. (35.64 ± 5.89), P < 0.01] and multisystem organ failure [0 vs. 17.4% (4/23) , P < 0.05] were lower in weaned group than in not wean group. CONCLUSIONS: ECMO is an effective mechanical assistant therapy strategy for adult refractory cardiogenic shock patients. Timely applying this strategy on suitable patients is crucial for the success of ECMO. Cardiac function and reversibility of heart failure are key factors determine the fate of weaned or not weaned ECMO in adult refractory cardiogenic shock patients.


Asunto(s)
Oxigenación por Membrana Extracorpórea , Choque Cardiogénico/terapia , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos
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