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Temperature is a fundamental factor that affects many functions and structural aspects of physiological systems. Despite its importance, few studies have been performed so far for investigating the compartments and mechanisms engaged in the response of cellular systems to temperature perturbation. In this review, focusing on stem cells, we tried to perform a literature review for investigating the possible ways through which the temperature reduction (hypothermia) affects stem cell function and behavior. Besides, using the obtained results of this investigation, the possible mechanisms are proposed. The survey indicates that profound hypothermia enhances cell adhesion by increasing the stability of E-cadherins. Furthermore, mild hypothermia increases stem cell survival by reducing oxidative stress and prevents apoptosis via the overexpression of anti-apoptotic heat shock proteins. Mild-hypothermia also promotes cell proliferation by affecting gene expression in several ways. Even though it seems that hypothermia generally reduced stem cell differentiation, some inconsistencies are observed between obtained results from the literature. Based on the obtained results, mechanisms responsible for the temperature effect of hypothermia in profound and mild ranges are given that might help the researcher in real experiments., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: Survival in exsanguinating cardiac arrest patients is poor, as is neurological outcome in survivors. Hypothermia has traditionally been seen as harmful to trauma patients and associated with increased mortality; however, there has been speculation that cooling to very low temperatures ( ≤ 20°C) could be used to treat haemorrhagic trauma patients by the induction of a suspended animation period through extreme cooling, which improves survival and preserves neurological function. This has been termed emergency preservation and resuscitation (EPR)., Methods: A systematic review of the literature was used to examine the evidence base behind the use of deep and profound hypothermia in haemorrhagic shock (HS). It included original research articles (human or animal) with cooling to ≤ 20°C after HS or an experimental model replicating it. Normovolaemic cardiac arrest, central nervous system injury and non-HS models were excluded., Results: Twenty articles using 456 animal subjects were included, in which 327 were cooled to ≤ 20°C. All studies describing good survival rates were possible using EPR and 19/20 demonstrated that EPR can preserve neurological function after prolonged periods of circulatory arrest or minimal circulatory flow. This additional period can be used for surgical intervention to arrest haemorrhage in HS that would otherwise be lethal., Conclusions: The outcomes of this review have significant implications for application to human patients and the ongoing human clinical trial (EPR for Cardiac Arrest from Trauma). Current evidence suggests that hypothermia ≤ 20°C used in the form of EPR could be beneficial to the HS patient., Competing Interests: Competing interests: None declared., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Background: The successful treatment of military combat casualties with penetrating injuries is significantly dependent on the time needed to get the patient to an adequate treatment facility. Profound hypothermia-induced suspended animation for delayed resuscitation (SADR) is a novel approach for inducing cardiac arrest and buying additional time for such injuries. However, the time used to safely administer circulatory arrest (CA) is controversial. The goal of this study was to evaluate the safety of hypothermia-induced SADR over 90 and 120 min time intervals., Methods: Sixteen male BAMA minipigs were randomized into two groups: CA90 group (90 min, n  = 8) and CA120 group (120 min, n  = 8). Cannulation of the right common carotid arteries and internal jugular veins was performed to establish cardiopulmonary bypass for each animal. Through the perfusion of cold organ preservation solution (OPS), cardioplegia and profound hypothermia (15 °C) were induced. After CA, cardiopumonary bypass (CPB) was restarted, and the animals were gradually re-warmed and resuscitated. The animals were assisted with ventilators until spontaneous breathing was achieved. The index of hemodynamic perioperative serum chemistry values [alanine transaminase (ALT), aspartate aminotransferase (AST), creatinine (CR), lactic dehydrogenase (LDH) and troponin T (TnT)] and survival were observed from pre-operation to 7 days post-operation., Results: Fifteen animals were enrolled in the experiment, while 1 animal in CA120 group died from surgical error. All 8 animals in CA90 group recovered, with only 1 animal displaying mild disability. However, in CA120 group, only 2 animals survived with severe disability, and the other 5 animals died after 2 days post-operation. In CA90 group, the perioperative serum chemistry values increased at 1 day post-operation (ALT 84.43 ± 18.65 U/L; AST 88.99 ± 23.19 U/L; Cr 87.90 ± 24.49 μmol/L; LDH 1894.13 ± 322.26 U/L; TnT 0.849 ± 0.135 ng/ml) but decreased to normal or almost normal levels at 7 days post-operation (ALT 52.48 ± 9.04 U/L; AST 75.23 ± 21.46 U/L; Cr 82.69 ± 18.41 μmol/L; LDH 944.67 ± 834.32 U/L; TnT 0.336 ± 0.076 ng/ml)., Conclusions: Profound hypothermia-induced SADR is an effective method for inducing cardiac arrest. Our results indicate that inducing CA for 90 min (at 15 °C) is safer than doing so for 120 min. Our results indicate that 120 min of CA at 15 °C is dangerous and can result in high mortality and severe neurological complications. Further experimentation is needed to determine whether 120 min of CA at temperatures lower than 15 °C can lead to safe recovery.

Objective: The primary focus of this study was to investigate the effects of local profound hypothermia and to explore the possible mechanism in adult rats with spinal cord injury., Study Design and Methods: Spinal cord injury models were established by placing aneurysm clips on T10. An epidural perfusion device was applied to maintain a steady temperature (18 °C) for 120 min with gradual rewarming to 37 °C Total hypothermic duration lasted up to about 170 min. The expression of axon regeneration inhibitors was tested by Western blot and real-time PCR. Luxol Fast Blue (LFB) stain and Bielschowsky silver stain were used to observe spinal cord morphology. Motor function of the hind limbs (BBB score) was monitored for 21 days., Results: The expressions of RhoA, ROCK-II, NG2, Neurocan, Brevican, and Nogo-A were downregulated by regional hypothermia (RH) after spinal cord injury. Subsequent observation showed that rats that had received RH had an alleviated demyelinating condition and a greater number of nerve fibers. Furthermore, the RH group achieved higher BBB scores than the spinal cord injury (SCI) group., Conclusions: Recovery of hind limb function in rats can be promoted by local profound hypothermia; this may be caused by the suppression of axon regeneration inhibitors.