Evaluation of cerebral metabolism by 1H-magnetic resonance spectroscopy for 4°C saline-induced therapeutic hypothermia in pig model of cardiac arrest

Su, Zhiyu; Li, Chunsheng; Han, Yi; Yin, Xi; Guo, Min

doi:10.1016/j.ajem.2010.04.001

Cited by 5 publications

(3 citation statements)

References 22 publications

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“…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

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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.

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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

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“…To mimic the clinical application of mild hypothermia in patients with cardiac arrest [7], by means of the CoolGard 3000 system, we intravascularly induced cooling, maintained mild hypothermia (32°C–34°C ) for 12 h, and then actively rewarmed (0.5°C/h) in a well established swine cardiac arrest model induced by VF [26], [27], [28], [29], [30], [31], [32], [33]. The results showed a significantly lower NDS in the HT group when compared with the NT group at 24 h or 72 h after ROSC, indicating mild hypothermia could improve neurological outcome.…”

Section: Discussionmentioning

confidence: 99%

Mild Hypothermia Attenuates Mitochondrial Oxidative Stress by Protecting Respiratory Enzymes and Upregulating MnSOD in a Pig Model of Cardiac Arrest

Gong

Hua

et al. 2012

PLoS ONE

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Mild hypothermia is the only effective treatment confirmed clinically to improve neurological outcomes for comatose patients with cardiac arrest. However, the underlying mechanism is not fully elucidated. In this study, our aim was to determine the effect of mild hypothermia on mitochondrial oxidative stress in the cerebral cortex. We intravascularly induced mild hypothermia (33°C), maintained this temperature for 12 h, and actively rewarmed in the inbred Chinese Wuzhishan minipigs successfully resuscitated after 8 min of untreated ventricular fibrillation. Cerebral samples were collected at 24 and 72 h following return of spontaneous circulation (ROSC). We found that mitochondrial malondialdehyde and protein carbonyl levels were significantly increased in the cerebral cortex in normothermic pigs even at 24 h after ROSC, whereas mild hypothermia attenuated this increase. Moreover, mild hypothermia attenuated the decrease in Complex I and Complex III (i.e., major sites of reactive oxygen species production) activities of the mitochondrial respiratory chain and increased antioxidant enzyme manganese superoxide dismutase (MnSOD) activity. This increase in MnSOD activity was consistent with the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA and protein expressions, and with the increase of Nrf2 nuclear translocation in normothermic pigs at 24 and 72 h following ROSC, whereas mild hypothermia enhanced these tendencies. Thus, our findings indicate that mild hypothermia attenuates mitochondrial oxidative stress in the cerebral cortex, which may be associated with reduced impairment of mitochondrial respiratory chain enzymes, and enhancement of MnSOD activity and expression via Nrf2 activation.

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“…Furthermore, in that study, hypothermia has a lessening effect on NAA/Cr decrease and Cho/Cr increase after CA. Parallel to their study, Su and colleagues used single voxel proton magnetic resonance spectroscopy in CA pig model and found lactic acid production was reduced in hypothermia group [ 103 ]. Chan K and colleagues designed an experimental rat study aimed to investigate the H-MRS efficacy for evaluating neuroprotective metabolic changes during hypothermia with CA.…”

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

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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.

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Evaluation of cerebral metabolism by 1H-magnetic resonance spectroscopy for 4°C saline-induced therapeutic hypothermia in pig model of cardiac arrest

Cited by 5 publications

References 22 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 Attenuates Mitochondrial Oxidative Stress by Protecting Respiratory Enzymes and Upregulating MnSOD in a Pig Model of Cardiac Arrest

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

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