Investigation of the Relationship Between Venticular Fibrillation Duration and Cardiac/Neurological Damage in a Rabbit Model of Electrically Induced Arrhythmia

Hu, Chunlin; H, Wei; Liu, Ziyou; Li, Xing; Liao, Xianghai; Li, Yujie; Zhan, Hong; Jing, Xiaoli; Xiong, Yan; Liu, Yanyan; Wu, Guifu

doi:10.1097/ta.0b013e3181dbbefc

Cited by 8 publications

(3 citation statements)

References 27 publications

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“…The methods for induction of ventricular fibrillation (VF) were described previously (20-22). Briefly, two acupuncture needles were trans-cutaneously inserted into the epicardium between the fourth rib of the left sternal border and the third rib of the right sternal border.…”

Section: Methodsmentioning

confidence: 99%

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Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

Hu¹,

Xia²,

Cai³

et al. 2013

Clinics

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OBJECTIVE:The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation.METHODS:Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL).RESULTS:Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation.CONCLUSIONS:Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde.

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Section: Methodsmentioning

confidence: 99%

“…Three sections from each animal and six standardized fields in each section were randomly selected and analyzed. The Nissl- and apoptotic-positive neurons in each cortex section were counted per 400 × 400-pixel area under 40X magnification by light microscopy (OLYMPUS BX51; OLYMPUS IMAGING CORP, Japan) (20). …”

Section: Methodsmentioning

confidence: 99%

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

Hu¹,

Xia²,

Cai³

et al. 2013

Clinics

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“…CTnI is a specific marker of myocardial injury ( 11 ). Early myocardial injury can be detected by serum cTnI levels ( 12 ). In the present study, serum cTnI was continuously elevated in both groups, but the level of UTI + CRRT was significantly lower than that of the control group.…”

Section: Discussionmentioning

confidence: 99%

Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation

et al. 2017

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The clinical efficacy of ulinastatin (UTI) combined with continuous renal replacement therapy (CRRT) in the treatment after early cardiopulmonary resuscitation (CPR) was evaluated. A total of 70 patients who were successfully treated with CPR in Ganzhou People's Hospital from October 2016 to March 2017 were selected as the subjects. The patients were randomly divided into control group (35 cases, conventional treatment) and UTI combined with CRRT group (35 cases, UTI + CRRT). The whole blood of patients was collected at 0, 3, 6 and 12 h after CPR. Reverse transcription-polymerase chain reaction assay was used to detect the changes of toll-like receptor 4 (TLR4) gene in mRNA levels between the two groups, i-STAT system 300 was used to analyze pH level, SO2, HCO3− and lactic acid (LAC) concentration; Abbott AXSYM system was used to detect the expression of cardiac troponin I (cTnI) in serum; the concentration of plasma malondialdehyde (MDA) was examined by a special kit; interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in patients was determined by enzyme-linked immunosorbent assay. The effect of UTI combined with CRRT in the early stage of CPR was analyzed. The levels of TLR4, cTnI, TNF-α, IL-6 and MDA in the plasma of patients in both groups were significantly increased (P<0.05), but the expression level in UTI + CRRT group was lower than that in control group (P<0.05). Compared with the control group, the HCO3− decreased significantly (P<0.05) in the UTI + CRRT group at 3 h, while the pH and SO2 did not change significantly. UTI + CRRT could significantly shorten the average recovery time of consciousness and the average recovery time of consciousness and spontaneous respiration in patients treated with CPR (P<0.05). Moreover, the score of APACHE II was significantly lower than that of control group (P<0.05). UTI combined with CRRT treatment can significantly improve the patient's condition after early CPR.

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Postreanimationssyndrom

et al. 2012

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Cardiac arrest with subsequent cardiopulmonary resuscitation causes an ischemic reperfusion syndrome of the whole body resulting in localized damage of particularly sensitive organs, such as the brain and heart, together with systemic sequelae. The main factor is a generalized activation of inflammatory reactions resulting in symptoms similar in many aspects to those of sepsis. Systemic inflammation strengthens organ damage due to disorders in the macrocirculation and microcirculation due to metabolic imbalance as well as the effects of direct leukocyte transmitted tissue destruction. The current article gives an overview on the role of inflammation following cardiac arrest and presents in detail the underlying mechanisms, the clinical symptoms and possible therapeutic approaches.

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Investigation of the Relationship Between Venticular Fibrillation Duration and Cardiac/Neurological Damage in a Rabbit Model of Electrically Induced Arrhythmia

Cited by 8 publications

References 27 publications

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation

Postreanimationssyndrom

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