Brain research
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Clinical Trial Controlled Clinical Trial
Correlation between local vascular and sensory changes following tissue inflammation induced by repetitive application of topical capsaicin.
The aim of the present study was to investigate local vascular and sensory changes and their correlation in order to obtain a better understanding of the mechanisms of allodynia, hyperalgesia and vascular changes following tissue inflammation induced by repetitive application of capsaicin cream. This type of application was utilized as a controlled model of inflammation which was altered in intensity due to its repetitive applicability. Ten healthy volunteers participated in two experiments separated by at least five days. ⋯ Compared to placebo, the first application of capsaicin cream also resulted in an increased blood-flow, elevated temperature and visible flare. The highest values of these sensory and vascular parameters were reached after the third application. A direct correlation between visible flare, secondary mechanical hyperalgesia and allodynia following repetitive application of capsaicin indicates that both common central and peripheral mechanisms were involved in these changes.
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The objective of this study was to determine whether the duration of an ischemic insult effects the activity of the mitochondrial enzyme pyruvate dehydrogenase (PDH) in relation to the recovery of metabolites and regional cerebral blood flow (rCBF) immediately after ischemia and during reperfusion in gerbil cortex. Cerebral ischemia was induced, using the bilateral carotid artery occlusion method, for 20 or 60 min, followed by reperfusion up to 120 min. Immediately after ischemia PDH activity increased threefold regardless of ischemic duration. ⋯ Recovery of metabolism after reperfusion did not parallel the changes in rCBF in either group, most noticeably in the 60-min ischemic group. The slow normalization of PDH activity reflected the poor recovery of metabolites in the 60-min ischemic group, indicating that PDH activity is important in the resynthesis of energy metabolites during reperfusion. In conclusion, prolonging the ischemic insult effected PDH activity during reperfusion, impaired recovery of energy metabolites, and worsened the recovery of rCBF.