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)

Somatosensory evoked potential after posterior tibial nerve stimulation (PTN-SEP), as well as nasopharyngeal, bladder and plantar temperature were recorded in ten patients during cardiac surgery with hypothermic cardiopulmonary bypass. There was a best negative correlation between latencies (P27, P40 and the interpeak latency between P40 and P27 (P40-P27)) and nasopharyngeal temperature, but no correlation was found between latencies and plantar temperature during cooling and rewarming (27-37 degrees C) with cardiopulmonary bypass. No correlation was found between changes in amplitude and temperature. The slope of linear regression line of latencies versus nasopharyngeal temperature was -1.05 msec.degrees C-1 for P27 (r = -0.93), -1.47 msec.degrees C-1 for P40 (r = -0.95) and -0.43 msec.degrees C-1 for P40-P27 (r = -0.78). This study suggests that nasopharyngeal temperature measurement is required to aid the interpretation of PTN-SEP changes during hypothermia.
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PMID:[Effects of hypothermia with cardiopulmonary bypass on posterior tibial nerve somatosensory evoked potentials in man]. 149 79

Although nicotine and ethanol are often used together, little is known about their combined effects on visual system electrophysiology. This experiment examined the separate and combined effects of nicotine and ethanol on flash-evoked potentials (FEPs) recorded from both the visual cortex (VC) and superior colliculus (SC) of chronically implanted male Long-Evans rats. There were four treatment conditions administered on separate days: either saline or ethanol (2.0 g/kg, i.p.) was given 10 min before either saline or nicotine (1.0 mg/kg, s.c.). FEPs were recorded at 5, 20, and 40 min following the second injection. In the VC, ethanol significantly decreased the amplitude of most components, but increased P46. Peaks P22 and N53 were unchanged. Nicotine enhanced most component amplitudes, but decreased N29 and P234, while P22 and N139 were unchanged. In the SC, ethanol depressed the amplitude of all components studied. In contrast, nicotine significantly depressed only P27 and N48. Latencies of most components in both structures were increased by ethanol, nicotine, and the combination treatment, although a nicotine-induced enhancement of the effects of ethanol on latencies was not typically observed. Each drug treatment also produced significant hypothermia, with the combination treatment resulting in the greatest hypothermia. Ethanol, either alone or in combination with nicotine, significantly reduced body movements during the FEP recording sessions. In subsequent open-field observations, ethanol, but not nicotine, significantly increased the number of squares crossed, while the combination treatment produced the greatest increase in movement. Nicotine significantly increased rearing behavior, but both ethanol and the combination treatment eliminated rearings. Overall, data suggesting that nicotine can counteract some of the effects of ethanol was demonstrated in varying degrees in the amplitude of VC components N39, P46, N53, N65, and P88, the latency of VC component N53, the amplitude of SC component N59, and the latency of SC components N48 and N54. In contrast, a nicotine-induced enhancement of the effects of ethanol was found for only the latency of VC components N39, P88, and P234, body temperature, and open-field ambulation.
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PMID:Nicotine-ethanol interactions in flash-evoked potentials and behavior of Long-Evans rats. 1643 Sep 48

Term asphyxiated newborns remain at risk of developing brain injury despite available neuropreventive therapies such as hypothermia. Neurorestorative treatments may be an alternative. This study investigated the effect of sildenafil on brain injury induced by neonatal hypoxia-ischemia (HI) at term-equivalent age. Neonatal HI was induced in male Long-Evans rat pups at postnatal day 10 (P10) by left common carotid ligation followed by a 2-hour exposure to 8% oxygen; sham-operated rat pups served as the control. Both groups were randomized to oral sildenafil or vehicle twice daily for 7 consecutive days. Gait analysis was performed on P27. At P30, the rats were sacrificed, and their brains were extracted. The surfaces of both hemispheres were measured on hematoxylin and eosin-stained brain sections. Mature neurons and endothelial cells were quantified near the infarct boundary zone using immunohistochemistry. HI caused significant gait impairment and a reduction in the size of the left hemisphere. Treatment with sildenafil led to an improvement in the neurological deficits as measured by gait analysis, as well as an improvement in the size of the left hemisphere. Sildenafil, especially at higher doses, also caused a significant increase in the number of neurons near the infarct boundary zone. In conclusion, sildenafil administered after neonatal HI may improve brain injury recovery by promoting neuronal populations.
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PMID:Sildenafil Improves Brain Injury Recovery following Term Neonatal Hypoxia-Ischemia in Male Rat Pups. 2761 33