Effects of hypothermia on brain injury assessed by magnetic resonance imaging after cardiopulmonary resuscitation in a porcine model of cardiac arrest

Tang, Ziren; Li, Chunsheng; Zhao, Hong; Gong, Ping; Zhang, Mingyue; Su, Zhiyu; Wang, Shuo

doi:10.1016/j.ajem.2012.06.008

Cited by 14 publications

(8 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the well-established pig CA model induced by VF [11], [15], [16], [17], [18], [19], [20], [21], [22], [23], we found that whole-body mild hypothermia prolonged APTT and PT, consistent with a previous report [24]. In addition, some studies have demonstrated that mild hypothermia resulted in mild platelet dysfunction, partial inhibition of the coagulation cascade, and decreased platelet count [9], [25], [26], [27].…”

Section: Discussionsupporting

confidence: 91%

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

et al. 2013

Self Cite

View full text Add to dashboard Cite

The aim of this study was to evaluate the effect of mild hypothermia on the coagulation-fibrinolysis system and physiological anticoagulants after cardiopulmonary resuscitation (CPR). A total of 20 male Wuzhishan miniature pigs underwent 8 min of untreated ventricular fibrillation and CPR. Of these, 16 were successfully resuscitated and were randomized into the mild hypothermia group (MH, n = 8) or the control normothermia group (CN, n = 8). Mild hypothermia (33°C) was induced intravascularly, and this temperature was maintained for 12 h before pigs were actively rewarmed. The CN group received normothermic post-cardiac arrest (CA) care for 72 h. Four animals were in the sham operation group (SO). Blood samples were taken at baseline, and 0.5, 6, 12, 24, and 72 h after ROSC. Whole-body mild hypothermia impaired blood coagulation during cooling, but attenuated blood coagulation impairment at 72 h after ROSC. Mild hypothermia also increased serum levels of physiological anticoagulants, such as PRO C and AT-III during cooling and after rewarming, decreased EPCR and TFPI levels during cooling but not after rewarming, and inhibited fibrinolysis and platelet activation during cooling and after rewarming. Finally, mild hypothermia did not affect coagulation-fibrinolysis, physiological anticoagulants, or platelet activation during rewarming. Thus, our findings indicate that mild hypothermia exerted an anticoagulant effect during cooling, which may have inhibitory effects on microthrombus formation. Furthermore, mild hypothermia inhibited fibrinolysis and platelet activation during cooling and attenuated blood coagulation impairment after rewarming. Slow rewarming had no obvious adverse effects on blood coagulation.

show abstract

Section: Discussionsupporting

confidence: 91%

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

et al. 2013

Self Cite

View full text Add to dashboard Cite

show abstract

“…13,14,17 Moreover, a lesser decrease in the apparent diffusion coefficient and N-acetyl aspartate/creatinine and a greater increase in choline/creatinine, which were detected by magnetic resonance spectroscopy, and an improvement in microscopic and ultrastructural abnormalities, and mitochondrial dysfunction in brain tissue after ROSC during mild hypothermia have been shown in our previous studies. 15,16,37 In the present study, we also observed a significant decrease in the brain contents of C1q, MBL, C3b, and C5a after treatment with mild hypothermia, which indicated inhibited complement activation through classic and MBL pathways, even at 24 hours after ROSC. Therefore, based on the above findings we speculate that inhibition of mild hypothermia on complement activation may be associated with postresuscitation ischemia/reperfusion injury, thus improving neurologic outcome after ROSC.…”

Section: Discussionsupporting

confidence: 73%

Mild Hypothermia Inhibits Systemic and Cerebral Complement Activation in a Swine Model of Cardiac Arrest

Gong,

Zhao,

Hua

et al. 2015

J Cereb Blood Flow Metab

Self Cite

View full text Add to dashboard Cite

Complement activation has been implicated in ischemia/reperfusion injury. This study aimed to determine whether mild hypothermia (HT) inhibits systemic and cerebral complement activation after resuscitation from cardiac arrest. Sixteen minipigs resuscitated from 8 minutes of untreated ventricular fibrillation were randomized into two groups: HT group (n=8), treated with HT (33°C) for 12 hours; and normothermia group (n=8), treated similarly as HT group except for cooling. Blood samples were collected at baseline and 0.5, 6, 12, and 24 hours after return of spontaneous circulation (ROSC). The brain cortex was harvested 24 hours after ROSC. Complement and pro-inflammatory markers were detected using enzyme-linked immunosorbent assay. Neurologic deficit scores were evaluated 24 hours after ROSC. C1q, Bb, mannose-binding lectin (MBL), C3b, C3a, C5a, interleukin-6, and tumor necrosis factor-α levels were significantly increased under normothermia within 24 hours after ROSC. However, these increases were significantly reduced by HT. Hypothermia decreased brain C1q, MBL, C3b, and C5a contents 24 hours after ROSC. Hypothermic pigs had a better neurologic outcome than normothermic pigs. In conclusion, complement is activated through classic, alternative, and MBL pathways after ROSC. Hypothermia inhibits systemic and cerebral complement activation, which may provide an additional mechanism of cerebral protection.

show abstract

“…Magnetic resonance spectroscopy (MRS) is a favorable advanced neuroimaging technique for assessing metabolite concentration alterations in ischemic brain injury. In means of CA brain injury, Tang and colleagues [ 102 ] analyzed brain metabolites after CA and exhibited lower levels of NAA/Cr (reduced N -acetyl aspartate (NAA)-to-creatine ratio) and NAA/Cho (reduced N -acetyl aspartate (NAA)-to-Cho ratio) at 6 h after spontaneous recirculation although Cho/Cr levels was found increased. Furthermore, in that study, hypothermia has a lessening effect on NAA/Cr decrease and Cho/Cr increase after CA.…”

Section: Metabolic Imaging Modalities For Cardiac Arrest Brain Injmentioning

confidence: 99%

“…Authors demonstrated the transient changes of glucose, choline, tau, myo-inositol, NAA and lactate in cerebral cortex and thalamus as a result of hypothermia [ 104 ]. More animal and clinical research with magnetic resonance spectroscopy are necessary in order to establish as a gold standard for monitoring the therapeutic effects of hypothermia and enhance the metabolic impacts of hypothermia during CA brain injury [ 102 ].…”

Section: Metabolic Imaging Modalities For Cardiac Arrest Brain Injmentioning

confidence: 99%

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Reis

Akyol

Araujo

et al. 2017

IJMS

View full text Add to dashboard Cite

Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians’ decision making in terms of which treatments to pursue.

show abstract

Effects of hypothermia on brain injury assessed by magnetic resonance imaging after cardiopulmonary resuscitation in a porcine model of cardiac arrest

Cited by 14 publications

References 32 publications

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model

Mild Hypothermia Inhibits Systemic and Cerebral Complement Activation in a Swine Model of Cardiac Arrest

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Contact Info

Product

Resources

About