Effect of butylphthalide injection to mitochondrial function of porcine cerebral neuron after cardiopulmonary resuscitation
10.3760/cma.j.issn.1671-0282.2019.08.011
- VernacularTitle:丁苯酞注射液对猪心肺复苏后脑神经元线粒体功能的影响
- Author:
Xichao FAN
1
;
Ziren TANG
;
Peng XIAO
;
Xiaoping WANG
;
Caijing LIN
;
Shen ZHAO
Author Information
1. 齐齐哈尔医学院第一附属医院急诊科
- Keywords:
Cardiac arrest;
Cardiopulmonary resuscitation;
Butylphthalide injection;
Neurologic outcome;
Mitochondrial function
- From:
Chinese Journal of Emergency Medicine
2019;28(8):971-977
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of cerebral protection by treatment of butylphthalide (NBP) and its effect to mitochondria in a porcine model of cardiac arrest (CA) after cardiopulmonary resuscitation (CPR). Methods Healthy Wuzhishan pigs weighting (30±2) kg were divide into three groups randomly(random number): The sham group (n=6), the control group (n=12) and the NBP group (n=12). Operation was performed in the sham group. Cardiac arrest of ventricular fibrillation was induced by programed electrical stimulation in the control and NBP group. After CPR, asynchronous defibrillation of 150J was performed to achieve the restoration of spontaneous circulation. NBP was injected at the rate of 2.5 mg?kg-1 in the NBP group. Hemodynamics were recorded at baseline, 1 hr, 2 hr, 3 hr and 4 hr after CPR. The number of injured neurons, apoptosis index and evaluation of mitochondrial injury were calculated under light and electrical microscope respectively. Mitochondria were separated by differential centrifugation. Mitochondrial respiratory function was measured with oxygen consumption of R3 and R4, respiratory control rate (RCR), ADP/oxygen. Mitochondrial permeability transition pore (MPTP) open was tested by colorimetric. Results After CPR, the mean artery pressure, coronary perfusion pressure and cardiac output decreased significantly, whereas no significant differences were found between the control and NBPgroup (P>0.05). Significant cerebral injury was found after CPR. The number of injured neurons, apoptosis index and evaluation of mitochondrial injury were improved significantly by the NBP treatment (P<0.05). Compared with the sham group, oxygen consumption of R3 and R4, R3/R4 and ADP/O decreased significantly in the cerebral frontal cortex mitochondria of the control group (P<0.01), whereas they were increased in the NBP group (P<0.01). MPTP increased in the control group, which could be improved by the NBP treatment. Conclusions NBP can improve the neurologic outcome after CPR and decrease the apoptosis of neurons by improving the respiratory function of mitochondria and inhibiting the MPTPopening.
