Hypothermia mechanisms

Hazards in addition to those taken for hydrogen gas should be taken when handling or storing LH2. Therefore, any LH2 splashed onto the skin or into the eyes can cause frostbite burns or hypothermia. Vents and valves in storage vessels and dewars may be blocked by accumulation of ice formed from moisture in the air. Excessive pressure may then result in mechanical failure with jet release of hydrogen and potentially in BLEVE. 

Although the precise mechanism for the hypothermia induced by chlordecone is unknown, data suggest a role of central nervous system (CNS) dopaminergic or a-noradrenergic activity in... 

The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support... 

Autonomic changes were quite prominent In DMHP-treated animals— hypothermia, mydriasis, hypersallvatlon, bradycardia, and reduced respiratory rate. Several experimental manipulations were undertaken to determine the mechanism of these autonomic changes. The tentative conclusion was that the drug was acting centrally to reduce sympathetic tone. 

Narcosis due lo CO is characterized by mental disturbances which may range from confusion, mania, or drowsiness to deep coma, headache, sweating, muscle twitching, increased intracranial pressure, pounding pulse, low blood pressure, hypothermia, and sometimes papilloedcina. The basic mechanisms by which carbon dioxide induces narcosis is probably through interference with the intracellular enzyme systems, which are all sensitive to pll changes. 

From Hypothermia and Cerebral Ischemia Mechanisms and Clinical Applications... 

The neuroprotective properties of mild hypothermia have been demonstrated in numerous experimental animal models. Research in this area has been conducted for many years, yet the mechanisms of cerebral protection by mild hypothermia remain unclear and continue to be the subject of intense investigation. The neuroprotective effects of mild hypothermia have been attributed to alterations in metabolic rate (24), neurotransmitter release (25-27), activity of protein kinases (28), resynthesis of cellular repair proteins (29), cerebral blood flow (30), preservation of the blood-brain barrier (BBB) (31), attenuation of inflammatory processes (32,33), and decreases in free radical production (34). Although these may all be components of a complex cascade leading to neurologic injury, it has become increasingly clear that the primary mechanism of action of hypothermia may be different at various temperatures as well as under different ischemic and traumatic conditions. 

Elucidate the cellular and molecular mechanisms of hypothermic neuroprotection to optimize the use of mild hypothermia as a neuro-protective strategy. 

From Hypothermia and Cerebral Ischemia Mechanisms and Clinical Applications Edited by C. M. Maier and G. K. Steinberg Humana Press Inc., Totowa, NJ... 

Inflammatory mechanisms involving polymorphonuclear leukocytes may, in part, mediate radical-induced pathology in ischemia. In focal ischemia, intraischemic hypothermia was shown to attenuate neutrophil infiltration (115). 

Early moderatepostischemic hypothermia attenuates the rise in excitotoxic index in the hippocampus—a possible mechanism for the beneficial effects of postischemic moderate cooBng. J. Cereb. Blood Flow Metab. 11, S10. 

The mechanisms whereby brain cells die during ischemia are not fully understood. Experimental evidence points to a complex array of parallel hemodynamic, biochemical, and electrophysiological events that combine to produce neuronal damage. In experimental cerebral ischemia, the severity of this damage can be significantly reduced by treatment with mild hypothermia (2-5°C below normal brain temperature). 

Although research in this area has been conducted for more than 40 yr, the mechanisms of cerebral protection by mild hypothermia remain unclear and are still a source of controversy. Proposed mechanisms of neuroprotection by mild hypothermia include suppression of neurotransmitter release (2,3), reduced free radical production (4), activity of protein kinases (5), resynthesis of cellular repair proteins (6),... 

The concept of neuroprotection relies on the fact that delayed neuronal injury occurs after ischemia, and each step along the ischemic cascade provides a target for therapeutic intervention. Thus, understanding the cellular and molecular mechanisms that underlie the development of neuronal and vascular injury is critical to optimize treatment. This chapter reviews experimental evidence from studies on focal cerebral ischemia and mild hypothermia, as well as the mechanisms involved in mild hypothermic neuroprotection. 

The main role of mild hypothermia against stroke may, perhaps, be to extend the therapeutic window of other treatment modalities. On the other hand, hypothermia is by far the most potent neuroprotectant available against experimental cerebral ischemia, and new technological advances are now facilitating its implementation in the clinical setting. Understanding the mechanisms by which mild hypothermia exerts its neuroprotective effects will allow us to optimize its use as a therapeutic strategy. 

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