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Nowadays, mild hypothermia is widely used in the fields of post-cardiac arrest resuscitation, stroke, cerebral hemorrhage, large-scale cerebral infarction, and craniocerebral injury. In this paper, a locally mixed sub-low temperature device is designed, and the cold and hot water mixing experiment is used to simulate the human blood transfer process. To set a foundation for the optimization of the heat transfer system, the static characteristics are analyzed by building the mathematic model and setting up the experimental station. In addition, the affection of several key structure parameters is researched. Through experimental and simulation studies, it can be concluded that, firstly, the mathematical model proved to be effective. Secondly, the results of simulation experiments show that 14.52 °C refrigeration can reduce the original temperature of 33.42 °C to 32.02 °C, and the temperature of refrigerated blood rises to 18.64 °C, and the average error is about 0.3 °C. Thirdly, as the thermal conductivity of the vascular sheath increases, the efficiency of the heat exchange system also increases significantly. Finally, as the input cold blood flow rate increases, the mass increases and the temperature of the mixed blood temperature decreases. It provides a research basis for subsequent research on local fixed-point sub-low temperature control technology.
Nowadays, mild hypothermia is widely used in the fields of post-cardiac arrest resuscitation, stroke, cerebral hemorrhage, large-scale cerebral infarction, and craniocerebral injury. In this paper, a locally mixed sub-low temperature device is designed, and the cold and hot water mixing experiment is used to simulate the human blood transfer process. To set a foundation for the optimization of the heat transfer system, the static characteristics are analyzed by building the mathematic model and setting up the experimental station. In addition, the affection of several key structure parameters is researched. Through experimental and simulation studies, it can be concluded that, firstly, the mathematical model proved to be effective. Secondly, the results of simulation experiments show that 14.52 °C refrigeration can reduce the original temperature of 33.42 °C to 32.02 °C, and the temperature of refrigerated blood rises to 18.64 °C, and the average error is about 0.3 °C. Thirdly, as the thermal conductivity of the vascular sheath increases, the efficiency of the heat exchange system also increases significantly. Finally, as the input cold blood flow rate increases, the mass increases and the temperature of the mixed blood temperature decreases. It provides a research basis for subsequent research on local fixed-point sub-low temperature control technology.
For years, moderate hypothermia (32 °C) has been proposed as an unorthodox therapy for liver injuries, with proven hepatoprotective potential. Yet, limited mechanistic understanding has largely denied its acceptance over conventional pharmaceuticals for hepatoprotection. Today, facing a high prevalence of acetaminophen-induced liver injury (AILI) which accounts for the highest incidence of acute liver failure, hypothermia was evaluated as a potential therapy to combat AILI. For which, transforming growth factor-α transgenic mouse hepatocytes (TAMH) were subjected to concomitant 5 mM acetaminophen toxicity and moderate hypothermic conditioning for 24 h. Thereafter, its impact on mitophagy, mitochondrial biogenesis, glutathione homeostasis and c-Jun N-terminal kinase (JNK) signaling pathways were investigated. In the presence of AILI, hypothermia displayed simultaneous mitophagy and mitochondrial biogenesis to conserve functional mitochondria. Furthermore, antioxidant response was apparent with higher glutathione recycling and repressed JNK activation. These effects were, however, unremarkable with hypothermia alone without liver injury. This may suggest an adaptive response of hypothermia only to the injured sites, rendering it favorable as a potential targeted therapy. In fact, its cytoprotective effects were displayed in other DILI of similar pathology as acetaminophen i.e., valproate- and diclofenac-induced liver injury and this further corroborates the mechanistic findings of hypothermic actions on AILI.
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