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951.
Cerebral Cortical Aquaporin-4 Expression in Brain Edema following Cardiac Arrest in Rats 总被引:14,自引:0,他引:14
Feng Xiao MD MS Thomas C. Arnold MD Shu Zhang MD Carlos Brown J. Steven Alexander PhD Donna L. Carden MD Steven A. Conrad MD PhD 《Academic emergency medicine》2004,11(10):1001-1007
OBJECTIVES: Brain edema occurs following clinical as well as experimental cardiac arrest (CA) and predicts a poor neurologic outcome. The objective of this study was to determine the expression of cerebral cortex aquaporin (AQP)-4, a member of a family of membrane water-channel proteins, in brain edema formation following normothermic or hypothermic CA. METHODS: Twenty-four rats were subjected to time-matched normothermic (N-Sham, 37.5 degrees C +/- 0.5 degrees C, n = 6) or hypothermic (H-Sham, 34 degrees C +/- 0.5 degrees C, n = 6) sham experiments and normothermic (N-CA, n = 6) or hypothermic (H-CA, n = 6) CA induced by asphyxiation for 8 minutes. Hypothermia was induced before CA. The animals were resuscitated with cardiopulmonary resuscitation, ventilation, and epinephrine administration. Brain edema was determined by brain wet-to-dry weight ratio at one hour of resuscitation. AQP4 immunoactivity in the cerebral cortex was determined using immunohistochemical staining and was semiquantified as an intensity of staining with an automated cell imaging system. RESULTS: Mild hypothermia in the sham experiments did not alter cerebral cortex AQP4 immunoactivity (mean +/- SD) (55.0 +/- 3.7 in H-Sham vs. 53.3 +/- 1.7 in N-Sham, p > 0.05). N-CA resulted in a significant increase in AQP4 immunoactivity (61.8 +/- 4.5) compared with N-Sham (p = 0.01) and H-Sham (p = 0.03). H-CA attenuated AQP4 compared with N-CA (53.4 +/- 1.3, p = 0.01). Brain wet-to-dry weight ratios were 4.41 +/- 0.07 in N-Sham, 4.40 +/- 0.08 in H-Sham (p > 0.05 vs. N-Sham), 4.55 +/- 0.04 in N-CA (p = 0.004 vs. N-Sham; p = 0.005 vs. H-Sham), and 4.43 +/- 0.09 in H-CA (p = 0.02 vs. N-CA; p > 0.05 vs. N-Sham and H-Sham). CONCLUSIONS: Cerebral cortical AQP4 expression is up-regulated after normothermic CA, which is attenuated by hypothermia induced before CA. 相似文献
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Carotid baroreflex function ceases
during vasovagal syncope 总被引:2,自引:0,他引:2
Shigehiko Ogoh PhD Stefanos Volianitis PhD Peter B. Raven PhD Niels H. Secher MD 《Clinical autonomic research》2004,14(1):30-33
Abstract. Despite the arterial baroreflex control of heart rate and
blood pressure, vasovagal syncope is a common cause of loss of
consciousness in people exposed to stimuli that reduce the
central blood volume, such as head-up tilt. Carotid baroreflex
function was evaluated using a rapid pulse train of neck
pressure and neck suction in three conscious volunteers who
developed a vasovagal episode during head-up tilt. The maximal
gain of the carotid-heart rate and carotid-blood pressure
baroreflex function curves were identified as measures of
carotid baroreceptor responsiveness. When presyncopal symptoms
developed, one further baroreflex assessment was obtained before
the subjects were returned to the supine position. The
bradycardia and hypotension exhibited during pre-syncope and
syncope reflected a leftward and downward relocation of both the
cardiac and vasomotor stimulusresponse curves. In addition,
during the vasovagal syncope, baroreflex control was suppressed
as blood pressure remained low during neck pressure stimuli. In
conclusion, arterial baroreflex function ceases during vasovagal
syncope. 相似文献
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Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity. Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets. Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms. It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues. Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity. Because Hg's binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis. This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm. However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern. Further studies of these relationships are needed to assist regulatory agencies in protecting and improving child health. 相似文献