Outcome effects of different protective hypothermia levels during cardiac arrest in rats

Yli‐Hankala, Arvi; Edmonds, H. L.; Jiang, Yi; Higham, Helen; Zhang, P. Y.

doi:10.1111/j.1399-6576.1997.tb04733.x

Cited by 12 publications

(5 citation statements)

References 24 publications

(12 reference statements)

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“…This finding is consistent with previous animal studies (28–30). A lower temperature of the central nervous system in ischemia has been correlated with a higher neuroprotective effect (31). However, deep hypothermia is associated with numerous side‐effects, such as arrhythmia, coagulation disorder and post‐operative infection at 32 °C or below (32, 33).…”

Section: Discussionsupporting

confidence: 91%

Effects of intrathecal bupivacaine in conjunction with hypothermia on neuronal protection against transient spinal cord ischemia in rats

Lee

Han

Leem

et al. 2006

Acta Anaesthesiol Scand

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Section: Discussionsupporting

confidence: 91%

Effects of intrathecal bupivacaine in conjunction with hypothermia on neuronal protection against transient spinal cord ischemia in rats

Lee

Han

Leem

et al. 2006

Acta Anaesthesiol Scand

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“…When several depths of TTM were tested, a lower temperature around 30 to 33°C was sometimes favoured compared to "milder" TTM around 34 to 35°C [2,[57][58][59], but just as often there was no significant difference between lower and "milder" TTM [60][61][62]. In the preclinical meta-analysis on TTM as treatment of ischemic stroke, efficacy was greater at temperatures below 31°C [40].…”

Section: Methodsmentioning

confidence: 99%

Meta-analysis of targeted temperature management in animal models of cardiac arrest

Olai

Thornéus

Watson

et al. 2020

ICMx

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Background: Targeted temperature management (TTM) of 32 to 34°C has been the standard treatment for out-of-hospital cardiac arrest since clinical trials in 2002 indicated benefit on survival and neurological outcome. In 2013, a clinical trial showed no difference in outcome between TTM of 33°C and TTM of 36°C. In this meta-analysis, we investigate the evidence for TTM in animal models of cardiac arrest. Methods: We searched PubMed and EMBASE for adult animal studies using TTM as a treatment in different models of cardiac arrest or global brain ischemia which reported neurobehavioural outcome, brain histology or mortality. We used a random effects model to calculate estimates of efficacy and assessed risk of bias using an adapted eight-item version of the Collaborative Approach to Meta-Analysis and Review of Animal Data from Experimental Studies (CAMARADES) quality checklist. We also used a scoring system based on the recommendations of the Stroke Treatment Academic Industry Roundtable (STAIR), to assess the scope of testing in the field. Included studies which investigated a post-ischemic induction of TTM had their treatment regimens characterized with regard to depth, duration and time to treatment and scored against the modified STAIR criteria. Results: The initial and updated search generated 17809 studies after duplicate removal. One hundred eighty-one studies met the inclusion criteria, including data from 1,787, 6,495 and 2,945 animals for neurobehavioural, histological and mortality outcomes, respectively. TTM was favoured compared to control for all outcomes. TTM was beneficial using short and prolonged cooling, deep and moderate temperature reduction, and early and delayed time to treatment. Median [IQR] study quality was 4 [3 to 6]. Eighteen studies checked seven or more of the eight CAMARADES quality items. There was no clear correlation between study quality and efficacy for any outcome. STAIR analysis identified 102 studies investigating post-ischemic induction of TTM, comprising 147 different treatment regimens of TTM. Only 2 and 8 out of 147 regimens investigated comorbid and gyrencephalic animals, respectively.

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“…We have previously established and validated a rodent model for global ischemic brain injury following CA (Geocadin et al, 2000b;Geocadin et al, 2000a). Neurological recovery is monitored using a standardized Neurological Deficit Scale (NDS) which relies on serial performance of a comprehensive behavioral examination (Ao et al, 2001;Xiao et al, 1998;Yli-Hankala et al, 1997;Zeiner et al, 2000). The NDS was patterned after the standard neurologic examination in humans, incorporating some elements from functional outcome scales developed for global cerebral ischemia in rats (Katz et al, 1995), dogs (Vaagenes et al, 1984;Woods et al, 2000), and piglets (Goel et al, 1996;Sherman et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Quantitative EEG and neurological recovery with therapeutic hypothermia after asphyxial cardiac arrest in rats

et al. 2006

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We test the hypothesis that quantitative electroencephalogram (qEEG) can be used to objectively assess functional electrophysiological recovery of brain after hypothermia in an asphyxial cardiac arrest rodent model. Twenty-eight rats were randomly subjected to 7-min (n = 14) and 9-min (n = 14) asphyxia times. One half of each group (n = 7) was randomly subjected to hypothermia (T = 33 degrees C for 12 h) and the other half (n = 7) to normothermia (T = 37 degrees C). Continuous physiologic monitoring of blood pressure, EEG, and core body temperature monitoring and intermittent arterial blood gas (ABG) analysis was undertaken. Neurological recovery after resuscitation was monitored using serial Neurological Deficit Score (NDS) calculation and qEEG analysis. Information Quantity (IQ), a previously validated measure of relative EEG entropy, was employed to monitor electrical recovery. The experiment demonstrated greater recovery of IQ in rats treated with hypothermia compared to normothermic controls in both injury groups (P < 0.05). The 72-h NDS of the hypothermia group was also significantly improved compared to the normothermia group (P < 0.05). IQ values measured at 4 h had a strong correlation with the primary neurological outcome measure, 72-h NDS score (Pearson correlation 0.746, 2-tailed significance <0.001). IQ is sensitive to the acceleration of neurological recovery as measured NDS after asphyxial cardiac arrest known to occur with induced hypothermia. These results demonstrate the potential utility of qEEG-IQ to track the response to neuroprotective hypothermia during the early phase of recovery from cardiac arrest.

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Outcome effects of different protective hypothermia levels during cardiac arrest in rats

Abstract: In this model, moderate (30 degrees C) cooling improved neurologic outcome. There was no additional benefit from more extreme hypothermia.

Cited by 12 publications

References 24 publications

Effects of intrathecal bupivacaine in conjunction with hypothermia on neuronal protection against transient spinal cord ischemia in rats

Effects of intrathecal bupivacaine in conjunction with hypothermia on neuronal protection against transient spinal cord ischemia in rats

Meta-analysis of targeted temperature management in animal models of cardiac arrest

Quantitative EEG and neurological recovery with therapeutic hypothermia after asphyxial cardiac arrest in rats

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