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 methylxanthine, theobromine (3,7-dimethylxanthine), was tested in mice, to determine whether theobromine could function in vivo as an adenosine receptor antagonist, in keeping with its reported in vitro effects as a blocker of agonist binding to the adenosine A-1 receptor. Theobromine doses, which themselves had no direct effects on spontaneous locomotor activity, completely blocked N6-cyclohexyladenosine-induced suppression of locomotor activity but were without effect on 5'-N-ethylcarboxamide adenosine (NECA)-induced decreases in motor activity. In contrast to the specific antagonism, theobromine blocked the hypothermia induced by both of these adenosine analogs. These results demonstrate that theobromine is an active in vivo adenosine receptor antagonist and that the antagonism of N6-cyclohexyladenosine sensitive systems occurs even though theobromine does not stimulate spontaneous locomotor activity. Thus, the behavioral stimulant effects of methylxanthines may be more related to effects on NECA-sensitive systems, which are not blocked by theobromine. The use of in vivo differences in the effects xanthine may provide a useful tool in the development of compounds to probe the mechanisms of caffeine induced CNS effects.
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PMID:Differential antagonism of the behavioral depressant and hypothermic effects of 5'-(N-ethylcarboxamide) adenosine by theobromine. 378 37

In a previous study of volume-controlled hemorrhagic shock (HS) in awake rats, without fluid resuscitation, either breathing of 100% oxygen or moderate hypothermia while breathing air, increased survival time. We hypothesized that combining oxygen and hypothermia can maximally extend the "golden hour" of HS from which resuscitation can be successful in terms of survival rate. Rats were prepared under light general anesthesia, breathing spontaneously via face mask, and then awakened for 2 h. Then, 3.25 ml arterial blood/100 g were withdrawn over 20 min. At the end of HS of 30, 60, 90 or 180 min duration, the shed blood was reinfused. Breathing was spontaneous. Survival endpoint was 24 h or earlier death. HS of 30 or 60 min was used for preliminary experiments; HS of 90 or 180 min for 35 definitive experiments. Control groups A-1 and B-1 had normothermia (rectal temperature 37.5 degrees C) and were breathing air. Treatment groups A-2 and B-2 had total body surface cooling during HS to rectal temperature 32 degrees C and were breathing 100% O(2). Arterial pressure during HS was higher in the hypothermia-O(2) groups. With HS of 90 min, in the normothermia-air group A-1 (n=10), none of the 10 rats survived to 3 h; while in the hypothermia-O(2) group A-2 (n=5), all rats survived to 24 h (P<0.001). With HS of 180 min, in the normothermia-air group B-1 (n=10), three of 10 rats survived to 3 h and 24 h (hypotension during HS in these three survivors was less severe than in the non-survivors); and in the hypothermia-O(2) group B-2 (n=10) all 10 rats survived to 24 h (P<0.003). We conclude that moderate hypothermia (32 degrees C) plus 100% oxygen inhalation during volume-controlled HS in awake rats mitigates hypotension and increases the chance of survival. It enables survival even after 3 h of moderate HS.
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PMID:Extending the golden hour of hemorrhagic shock tolerance with oxygen plus hypothermia in awake rats. An exploratory study. 1184 88