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 influence of hypothermia on the development of the ischemic disorders was studied using allotransplantation of the rat skeletal muscle (m. lumbricalis) to the anterior chamber of the eye after different period of ischemia. The morphological and immunohistochemical (monoclonal antibodies to heavy chain of the fast myosin, PAP-method) data were found confirming that hypothermia (2-4 degrees C) prolongs the period of the ischemic disorders first appearance by 5 h (from 6 to 11 h) if compared with development of ischemia in the muscle at 21-23 degrees C.
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PMID:[Effects of hypothermia on the development of ischemic lesions of skeletal muscles in rats]. 139 78

Urinary excretion of the post-translationally modified amino-acid 3-methylhistidine, derived from the contractile proteins actin and myosin, was measured in patients with conditions associated with nitrogen loss. The ratio of 3-methylhistidine:creatinine excretion, a measure of the fractional catabolic rate of myofibrillar protein was increased in severe injury, thyrotoxicosis, neoplastic disease, prednisolone administration, and sometimes Duchenne muscular dystrophy. In myxoedema, osteomalacia, and hypothermia the ratio was decreased; and starvation, elective operations, and rheumatoid arthritis had little effect. Provided that the diet is meat free, measurement of urinary 3-methylhistidine may provide useful information on the cause of protein loss.
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PMID:Clinical usefulness of urinary 3-methylhistidine excretion in indicating muscle protein breakdown. 678 20

The purpose of this study was to examine the use of hypothermia to protect skeletal muscle from the effects of 4 hr of tourniquet ischemia. Muscle recovery was investigated at 6 weeks. Four hours of tourniquet ischemia was induced in two groups (n = 8 per group) of male, Wistar rats (344 +/- 15 g). In the ischemia-only group (IO), the ischemic leg was exposed to room temperature. In the ischemic-hypothermic group (IH), the ischemic leg was cooled to 5-8 degrees C throughout the ischemic period. The contralateral leg served as control. After 6 weeks, the isometric contractile function of the gastrocnemii of both the ischemic and nonischemic legs was determined. Following the functional assessment, the soleus and plantaris muscles were removed and weighed, and biopsies were taken for muscle fiber composition, mean fiber area, and myosin heavy chains (MHC) analysis. Differences between groups (P < 0.05) were determined using ANOVA. Muscle wet weight, tetanic forces, fiber area, fiber type, and MHC composition of IH group were the same as the control group. Yet, twitch tension and relaxation time were lower and longer in the IH group than control group. The tetanic force at 100 Hz of the IH group (12.62 +/- 0.73 N/g) was significantly greater than that of the IO group (2.12 +/- 0.84 N/g). The type 1 muscle fiber areas of plantaris in the IH (1.84 +/- 0.04 x 1000 microns 2) were significantly greater than those of the IO group (1.56 +/- 0.42 x 1000 microns 2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle form and function after 4 hr ischemia-hypothermia. 793 25

This study was aimed at elucidating whether ventricular hypothermia-induced dysfunction persisting after rewarming the unsupported in situ dog heart could be characterized as a systolic, diastolic, or combined disturbance. Core temperature of 8 mongrel dogs was gradually lowered to 25 degreesC and returned to 37 degreesC over a period of 328 min. Systolic function was described by maximum rate of increase in left ventricular (LV) pressure (dP/dtmax), relative segment shortening (SS%), stroke volume (SV), and the load-independent contractility index, preload recruitable stroke work (PRSW). Diastolic function was described by the isovolumic relaxation constant (tau) and the LV wall stiffness constant (Kp). Compared with prehypothermic control, a significant decrease in LV functional variables was measured at 25 degreesC: dP/dtmax 2,180 +/- 158 vs. 760 +/- 78 mmHg/s, SS% 20.1 +/- 1.2 vs. 13.3 +/- 1.0%, SV 11.7 +/- 0.7 vs. 8.5 +/- 0.7 ml, PRSW 90.5 +/- 7.7 vs. 29.1 +/- 5.9 J/m. 10(-2), Kp 0.78 +/- 0.10 vs. 0.28 +/- 0.03 mm-1, and tau 78.5 +/- 3.7 vs. 25.8 +/- 1.6 ms. After rewarming, the significant depression of LV systolic variables observed at 25 degreesC persisted: dP/dtmax 1,241 +/- 108 mmHg/s, SS% 10.2 +/- 0.8 J, SV 7.3 +/- 0.4 ml, and PRSW 52.1 +/- 3.6 m. 10(-2), whereas the diastolic values of Kp and tau returned to control. Thus hypothermia induced a significant depression of both systolic and diastolic LV variables. After rewarming, diastolic LV function was restored, in contrast to the persistently depressed LV systolic function. These observations indicate that cooling induces more long-lasting effects on the excitation-contraction coupling and the actin-myosin interaction than on sarcoplasmic reticulum Ca2+ trapping dysfunction or interstitial fluid content, making posthypothermic LV dysfunction a systolic perturbation.
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PMID:Left ventricular dysfunction following rewarming from experimental hypothermia. 984 36

Hypothermia is known to be a common feature of energy restriction (ER) and essential for a life-prolonging effect of ER. The heart is sensitive to hypothermia, but the heart in ER mice acquires some adaptation to hypothermia. The aim of the present study was to characterize the gene expression profile associated with ER-induced cold resistance of heart. We analyzed the expression of heart mRNA from ER (200 kJ/week) or control (400 kJ/week) B6 11-month-old male mice using cDNA array membranes including 588 genes. Eighty-eight out of 588 genes were expressed in the heart. mRNAs increased by ER were glutathion S-transferase Mu1, transcriptional factor 1 for heat shock gene (HSF1), and fetal myosin alkali light chain genes. mRNA decreased by ER were seven genes in four categories: (1). cell cycle or apoptosis-related proteins (cyclin G and nucleoside diphosphate kinase B); (2). stress response proteins (oxidative stress-induced protein); (3). DNA repair proteins (protein involved in DNA double-strand break repair, Rad23 UV excision repair protein homologue and ubiquitin-conjugating enzyme); and (4). cell-surface antigens (lamimin receptor 1). These data suggest that the heart of ER mice adapts to hypothermia involving heat shock proteins and their transcriptional factors and by changing structure and property of myofibrils. It is also suggested that ER induces protection against oxidative stress and inhibits cell proliferation of "nonmuscle cells" in the heart. Gene expression analysis using cDNA array was useful for screening genes associated with ER-induced cold adaptation.
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PMID:Characterization of gene expression profile associated with energy restriction-induced cold tolerance of heart. 1242 94