Induced hypothermia in experimental traumatic spinal cord injury: an update

Inamasu, Joji; Nakamura, Yoshiki; Ichikizaki, Kiyoshi

doi:10.1016/s0022-510x(02)00463-x

Cited by 44 publications

(35 citation statements)

References 30 publications

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“…However, its protective effect and mechanisms have not yet been fully elucidated. The start time, duration and specific temperature used when applying mild systemic and local hypothermia to the head remain debatable; a limited number of studies have challenged the protective effect of mild hypothermia on the brain (10)(11)(12)(13)(14). Therefore, further studies are required to verify the protective effect of mild hypothermia and its mechanism of action.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of mild hypothermia on oxygen-glucose deprivation injury in rat hippocampal neurons after hypoxia

Zhou

Jiang

Zhang

et al. 2013

Molecular Medicine Reports

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Abstract. The present study aimed to establish an oxygen-glucose deprivation (OGD) model of ischemic and hypoxic cerebral neurons to investigate the protective effect of mild hypothermia on neuronal OGD and its mechanisms. OGD injury was significantly mitigated in cells with 24 h of mild hypothermia compared with cells without mild hypothermia; cell morphology improved, the lactic acid dehydrogenase (LDH) release rate was decreased, cytoactivity was increased and the neuronal apoptotic rate was decreased. By contrast, no significant improvement in injury was observed after 6 h of mild hypothermia. This suggests that mild hypothermia treatment following OGD is effective only when implemented for 24 h. Additionally, the caspase-3 activity of neurons increased following OGD, which was positively associated with the neuronal apoptotic rate. However, the caspase-3 activity after 24 h of mild hypothermia was reduced. Simultaneously, the neuronal apoptotic rate was decreased, suggesting that mild hypothermia may inhibit neuronal apoptosis by reducing caspase-3 activity. Therefore, reducing caspase-3 activity potentially constitutes one of the protective mechanisms of mild hypothermia in neuronal OGD.

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Section: Introductionmentioning

confidence: 99%

Protective effect of mild hypothermia on oxygen-glucose deprivation injury in rat hippocampal neurons after hypoxia

Zhou

Jiang

Zhang

et al. 2013

Molecular Medicine Reports

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“…35 Temperature changes after SCI also modulate the release of excitatory amino acids, 36 leucocyte accumulation, 37 lipid peroxidation and the frequency of TUNEL-positive cells. 38 reported that after ischemia of the white matter, the intracellular accumulation of Ca 2 þ by way of the reverse operation of the Na þ /Ca 2 þ exchanger occurred.…”

Section: Discussionmentioning

confidence: 99%

Post-traumatic moderate systemic hyperthermia worsens behavioural outcome after spinal cord injury in the rat

Urdzíková

Vanický

2005

Spinal Cord

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Study design: A standardized rat model of compression spinal cord injury (SCI) was used to test the effect of transient systemic hyperthermia on long-term behavioural and morphometric outcomes. Objective: To determine the effect of hyperthermia on the development of spinal cord lesion after SCI. Setting: Institute of Neurobiology, Slovak Republic. Methods: Male Wistar rats (n ¼ 30) weighing between 300 and 330 g were used in the study. After incomplete spinal injury performed by balloon compression at the Th8-Th9 spinal level, rats were randomly divided into two groups. Rats in the treatment group were maintained hyperthermic for 3 h (rectal temperature at 40.570.51C), immediately after SCI; rats from the control group received exactly the same procedure except that their rectal temperature was maintained at 3770.51C. Results: The 3 h of post-traumatic hyperthermic treatment worsened behavioural outcome after SCI. Morphometric analysis showed that hyperthermia had a deleterious effect on white and grey matter, but the results did not reach statistical significance. Conclusion: These results indicate that systemic hyperthermia exacerbates secondary processes in the lesion and significantly worsens behavioural outcome after traumatic SCI in the rat. Sponsorship: Grant VEGA 2/3216/24.

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“…This has two components like a catabolic phase, which is characterized by excessive protein break down and a negative balance, followed by an anabolic phase, during which the body's stores are replenished (Inamasu et al, 2003).…”

Section: Convalescencementioning

confidence: 99%

“…In the human, 60-70% of the blood volume is contained in the veins and venules . Constriction of these vessels can readily increase the venous return to the heart; following a 10% blood loss, contraction of the venous reservoir can prevent any change occurring in the cardiac output and blood pressure (Inamasu et al, 2003). The arteriolar constriction is selective and the blood flow to the skin, skeletal muscle, salivary glands, intestines, liver, spleen and kidneys is reduced.…”

Section: The Phase Of Redistribution Of Available Blood To Vital Centmentioning

confidence: 99%

Pathophysiological Reaction of the Body to Trauma: A Review Update

Talukder

Quader²,

Momen

2016

J Sci Found

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Trauma to tissues can be of large magnitude (macrotrauma), such as the trauma that exists with crush injuries and both moderate and severe sprains or strains. The trauma can also be of small magnitude (microtrauma), such as the trauma that typically exists with stress fractures and other overuse syndromes. Regardless of magnitude, trauma exists in several forms, including physical, chemical, thermal, metabolic, and biological. Injury from any of these sources induces an inflammatory response whose magnitude largely depends on the severity of the injury and the degree of vascularization of the tissue. A local inflammatory response always occurs in relation to trauma. Severe injury or multiple trauma evoke a systemic inflammatory response. This systemic inflammatory response to major injury is caused by hormonal, metabolic and immunological mediators, and is associated with a haemodynamic response. Accidental unanaesthetised trauma is also to a larger extent associated with ischemia, ischemia/reperfusion injury, hypovolemia and the immunological reactions secondary to blood transfusion. The systemic inflammatory response is required for tissue repair and has evolved in all mammals to optimize the healing potential of an organism. In uncomplicated trauma patients the systemic inflammatory response is temporary, predictable and well balanced between pro-and antiinflammatory mediators. If the patient is exposed to severe major trauma an initial exaggerated proinflammatory response may be observed. In this review the pathophysiological changes have been described after trauma to the body. [Journal of Science Foundation, 2015;13(1):15-20]

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Induced hypothermia in experimental traumatic spinal cord injury: an update

Cited by 44 publications

References 30 publications

Protective effect of mild hypothermia on oxygen-glucose deprivation injury in rat hippocampal neurons after hypoxia

Protective effect of mild hypothermia on oxygen-glucose deprivation injury in rat hippocampal neurons after hypoxia

Post-traumatic moderate systemic hyperthermia worsens behavioural outcome after spinal cord injury in the rat

Pathophysiological Reaction of the Body to Trauma: A Review Update

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