Effects of NLRP3 inflammasome blockade on postresuscitation cerebral function in a rat model of cardiopulmonary resuscitation

Aim. Intermittent positive pressure ventilation (IPPV) can adversely affect cardiopulmonary resuscitation outcomes by increasing the intrathoracic pressure. Continuous flow insufflation of oxygen (CFIO) has been investigated as a potential alternative, but evidence supporting its superiority over intermittent positive pressure ventilation in cases of cardiac arrest is scant. The aim of the current study was to compare the effects of continuous flow insufflation of oxygen using a one-way valve during cardiopulmonary-resuscitation with intermittent positive pressure ventilation in a rat model of respiratory arrest. Methods. Male Sprague-Dawley rats weighing 400∼450 g (from minimum to maximum) were randomly assigned to either a sham, IPPV, or CFIO group (n = 10 per group). Respiratory arrest was induced by blocking the endotracheal tube. Arterial blood gas analysis was performed during cardiopulmonary resuscitation to compare the oxygenation levels. Tissues were then harvested to compare the degrees of pulmonary barotrauma and ischemic brain injury. Results. Return of spontaneous circulation was observed in 6/10 rats in the IPPV group and 5/10 in the CFIO group. During cardiopulmonary resuscitation, the mean PaO2 was significantly higher in the CFIO group (83.10 mmHg) than in the IPPV group (56.10 mmHg). Lung biopsy revealed more inflammatory cells and marked thickening of the alveolar wall in the IPPV group; the group also exhibited a higher frequency of neuroglial cells and apoptotic bodies of pyramidal cells, resulting from ischemic injury. Conclusion. In a rat model of respiratory arrest, CFIO using a one-way valve resulted in a greater level of oxygenation and less lung and brain injuries than with IPPV.

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The Effects of Carvedilol Administration on Cardiopulmonary Resuscitation in a Rat Model of Cardiac Arrest Induced by Airway Obstruction

Anesthesia & Analgesia ◽

10.1213/ane.0b013e3181f1bd55 ◽

2010 ◽

Vol 111 (5) ◽

pp. 1207-1210 ◽

Cited By ~ 3

Author(s):

Akihide Kurita ◽

Takumi Taniguchi ◽

Ken Yamamoto

Keyword(s):

Cardiac Arrest ◽

Cardiopulmonary Resuscitation ◽

Airway Obstruction ◽

Rat Model

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Prolonged cardiopulmonary resuscitation with preservation of cerebral function in an elderly patient with asystole after electroconvulsive therapy

Journal of Clinical Anesthesia ◽

10.1016/s0952-8180(02)00344-6 ◽

2002 ◽

Vol 14 (3) ◽

pp. 234-240 ◽

Cited By ~ 12

Author(s):

Andrea Gabrielli ◽

A.J Layon ◽

Perry Cole ◽

Richard Holbert ◽

Jerome H Modell ◽

...

Keyword(s):

Elderly Patient ◽

Cardiopulmonary Resuscitation ◽

Electroconvulsive Therapy ◽

Cerebral Function

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Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation

BioMed Research International ◽

10.1155/2014/192769 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Jun Jiang ◽

Xiangshao Fang ◽

Yue Fu ◽

Wen Xu ◽

Longyuan Jiang ◽

...

Keyword(s):

Cardiac Arrest ◽

Ventricular Fibrillation ◽

Cardiopulmonary Resuscitation ◽

Oxidative Phosphorylation ◽

Mitochondrial Dysfunction ◽

Rat Model ◽

Mitochondrial Function ◽

High Energy ◽

Mitochondrial Morphology ◽

High Energy Phosphates

Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.

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