Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The drugs used in frostbite injury care are: Plasma volume expanders (low molecular weight dextran); vasodilating agents (tolazoline hydrochloride); hypotensive agents (guanethidine monosulfate, reserpine); hemorrheologic agents (oxpentifylline); calcium blocking agents (nifedipine); sympatholytic agents (phenoxybenzamine hydrochloride); anticoagulating agents (heparin); thrombolytic enzymes (streptokinase, tissue plasminogen activator--TPA); an industrial solvent (dimethyl sulfoxide--DMSO); anti-inflammatory agents such as nonsteroidal drugs, and acetylsalicylic acid, Ibuprofen. As yet, no clear treatment policy has been determined for preventing injury secondary to the formation of oxygen free radicals, damaging neutrophils or reperfusion injury. The role of oxygen free radical scavengers and factors causing reperfusion injury is unclear at this date. Since that first reported series of 51 patients in 1960-61, 1,282 patients have been seen. Of that number, 1,026 had a diagnosis of frostbite; 151 were diagnosed as hypothermia; and 105 diagnosed as immersion injury.
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PMID:Comments on this issue of Alaska Medicine--from then (1960) until now (1993). 821 84

Whereas the efficacy of cold water cooling of horses has been demonstrated by several studies, the dynamics of temperature changes within and between compartments (primarily muscle, blood [core], skin and deep core [rectal]) have not been investigated. Changes in body temperature associated with cold water cooling were investigated in the hyperthermic horse. Muscle (TMU), pulmonary artery (TPA), rectal (TREC), tail-skin (TTSK) and coat surface (TCOAT) temperatures, were monitored continuously in 5 Thoroughbred horses during and after exercise in hot humid (30 degrees C and 80% RH) conditions on a treadmill. Horses were cooled in the hot humid environment with cold water (approximately 6 degrees C) for 6 30 s periods. Between each 30 s cooling period the horses stood for 30 s. A total of 180 l of cold water was applied. Horses were monitored for a further 4 min following the final cooling period. From the end of exercise to the end of the final cooling (6.5 min), mean (+/- s.e.) rates of decrease for TTSK and TPA were similar (0.8 +/- 0.1 and 0.8 +/- 0.1 degrees C/min, respectively). The effects on TMU and TREC were less marked, with average rates of 0.2 +/- 0.1 and 0.0 +/- 0.1 degrees C/min, respectively. During the first 4 min of cooling, TPA fell during the 30 s period of water application and rose during each 30 s period of standing. When TPA fell below approximately 36.5 degrees C, these variations were suppressed and TPA rose steadily, despite continued applications; TREC and TMU continued to fall, although less rapidly than before. These observations are consistent with the onset of skin vasoconstriction at low TPA. The mechanism is mediated through a cooling of circulating blood volume providing a greater capacity for heat transfer between muscle and circulation. Intermittent application of cold water (approximately 6 degrees C) improves heat removal without apparent deleterious effects and is well tolerated. Even when hypothermia develops (based on TPA), muscle and rectal temperatures continue to fall.
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PMID:Post exercise changes in compartmental body temperature accompanying intermittent cold water cooling in the hyperthermic horse. 945 96