Abstract

Through the years, the clinical application of mild hypothermia has been carried out worldwide and is built from the exploration and cognition of neuroprotection mechanisms by hypothermia. However, within the last decade, extensive and fundamental researches in this area have been conducted. In addition to aspects of the previous findings, scholars have discovered several new contents and uncertain results. This article reviews and summarizes this decade’s progression of mild hypothermia in lowering the cerebral oxygen metabolism, protecting the blood–brain-barrier, regulating the inflammatory response, regulating the excessive release of neurotransmitters, inhibiting calcium overload, and reducing neuronal apoptosis. In many aspects, particularly in regulating inflammatory reverse reaction, various results have been reported and therefore guide scholars to conduct more detailed analysis and investigation in order to discover the inherent theories surrounding the effect of mild hypothermia, and for better clinical services.

Highlights

  • Cold and humanity have a long-standing relationship

  • It is one of the most robust neuroprotectants studied to date, and recent clinical studies have established a role for therapeutic hypothermia in neuroprotection in some clinical conditions, including canoxic brain injury due to cardiac arrest (Bernard et al 2002), hypoxic ischaemic neonatal encephalopathy (Gluckman et al 2005; Shankaran et al 2005), stroke (Wu and Grotta 2013), brain (Dietrich and Bramlett 2010) and spinal cord trauma (Dietrich et al 2009)

  • This review focuses on the development of fundamental research on mild hypothermia neuroprotection over the past decade

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Summary

Introduction

Cold and humanity have a long-standing relationship. For the past twenty years, people have begun to recognize the protective effects of mild hypothermia on the body, especially on the brain. German scholars observed the effect of mild hypothermia on CMRO2 and cerebral function through an increase in intracranial pressure (ICP), and subsequent decrease in cerebral perfusion pressure (CPP) to reduce CBF (Bauer et al 2000).

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