Therapeutic hypothermia (TH) is a powerful neuroprotective strategy that has provided robust evidence for neuroprotection in pre-clinical studies of neurological disorders. Despite strong pre-clinical evidence, TH has not shown efficacy in clinical trials of most neurological disorders. The only successful trials employing therapeutic hypothermia were related to cardiac arrest in adults and hypoxic ischemic injury in neonates. Further investigations into the parameters of its use, and study design comparisons between pre-clinical and clinical studies, are warranted. This article demonstrates two methods of short-duration hypothermia induction. The first method allows for rapid hypothermia induction in rats using ethanol spray and fans. This method works by cooling the skin, which has been less commonly used in clinical trials and may have different physiological effects. Cooling is much more rapid with this technique than is achievable in human patients due to differences in surface area to volume ratio. Along with this, a second method is also presented, which allows for a clinically achievable cooling rate for short-duration hypothermia. This method is easy to implement, reproducible and does not require active skin cooling.
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http://dx.doi.org/10.3791/62325 | DOI Listing |
Cureus
October 2024
Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, USA.
Resuscitation
February 2023
Department of Emergency and Critical Care Medicine, St. Luke's International Hospital, Tokyo, Japan.
Aim: This study aimed to describe the characteristics of cases of out-of-hospital cardiac arrest (OHCA) with an initial asystole rhythm in which extracorporeal cardiopulmonary resuscitation (ECPR) was introduced and discuss the clinical indications for ECPR in such patients.
Methods: This was a secondary analysis of the SAVE-J II study, a retrospective, multicentre, registry study involving 36 participating institutions in Japan. Patients with an initial asystole rhythm were selected.
Brain Sci
November 2021
School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.
Background: Elevated intracranial pressure (ICP) occurs 18-24 h after ischaemic stroke and is implicated as a potential cause of early neurological deterioration. Increased resistance to cerebrospinal fluid (CSF) outflow after ischaemic stroke is a proposed mechanism for ICP elevation. Ultra-short duration hypothermia prevents ICP elevation 24 h post-stroke in rats.
View Article and Find Full Text PDFSci Rep
November 2021
The School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW, Australia.
Reperfusion therapies re-establish blood flow after arterial occlusion and improve outcome for ischaemic stroke patients. Intracranial pressure (ICP) elevation occurs 18-24 h after experimental stroke. This elevation is prevented by short-duration hypothermia spanning the time of reperfusion.
View Article and Find Full Text PDFFront Neurol
September 2021
The School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW, Australia.
There is a transient increase in intracranial pressure (ICP) 18-24 h after ischaemic stroke in rats, which is prevented by short-duration hypothermia using rapid cooling methods. Clinical trials of long-duration hypothermia have been limited by feasibility and associated complications, which may be avoided by short-duration cooling. Animal studies have cooled faster than is achievable in patients.
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