Change of extracellular ascorbic acid in the brain cortex following ice water vestibular stimulation： an on-line electrochemical detection coupled with in vivo microdialysis sampling for guinea pigs

Background Ascorbic acid （AA） represents one of the most important enzyme co-factors, antioxidants and neuromodulators and plays an important role in the cerebral system. Increasing evidence has suggested that AA could treat certain kinds of vertigo diseases such as Meniere＇s disease. To elucidate the neurochemical functions associated with AA in vertigo, the change of extracellular AA in the brain cortex following caloric vestibular stimulation （CVS） was evaluated.Methods An on-line electrochemical detection was coupled with in vivo microdialysis to continuously monitor the change of extracellular AA in the primary somatosensory （SI） area of guinea pigs following a caloric vestibular stimulation. Sixteen guinea pigs were divided into three groups, i.e., experimental group with irrigation of the ear canal with ice water （0℃） （n=-8）, and two control groups, one with irrigation of the ear canal with warm water （38℃） （n=-4） and the other with irrigation of the auricle with ice water （n=-4）.Results In the experimental group, the ice water irrigation of the left external ear canal induced a horizontal nystagmus towards the right side lasting about 45 seconds. No nystagmus was induced by warm water irrigation of the external ear canal or by ice water irrigation of the auricle. The extracellular AA concentration significantly increased following the ice water vestibular stimulation, reaching a maximum of （130±20）% （n=8） of the basal dialysate level （2.61±0.92） μmol/L （n=8）, lasting at least for an hour. AA level did not change distinctly after the irrigation of the left external ear canal with warm water or the irriclation of the auricle with ice water.Conclusions The concentration of extracellular AA in the brain cortex of the SI area increased following the ice water vestibular stimulation. This demonstration may be useful for the investigation of the neurochemical processes associated with AA in the process of vertigo.

Effect of 17β-estradiol on the Brain Damage and Metabolic Changes in Rats

An in vivo model of glutamate excitotoxicity in which glutamate is applied to the cortex of rats through a microdialysis probe has been used to investigate the neuroprotective processes initiated by 17β estradiol. Rats were pre treated with 17β estradiol i.v. before local application of glutamate. The experimental results showed that pre treatment with 17β estradiol significantly reduced the size of the glutamate induced lesion. In the microdialysates, the peak of lactate observed immediately after glutamate application was significantly higher and longer lasting after 17β estradiol pre treatment. The level of extracellular glucose was markedly decreased concomitantly to the increase in lactate, but no difference could be observed with and without 17β estradiol pre treatment. These suggest a new neuroprotective mechanism of 17β estradiol by activating glutamate induced lactate production. This effect on lactate production and lesion reduction is estrogen receptor dependent and is abolished totally by estrogen antagonist tamoxifen. It was also demonstrated here that high lactate subserves estrogen neuroprotection during glutamate toxicity.

In vivo electrochemical recording of continuous change of magnesium in medial vestibular nucleus following vertigo induced by ice water vestibular stimulation

Vertigo is one of the most common clinical symptoms. However, the chemical processes involved in the pathological mechanism of vertigo remain to be fully understood. In this study, we investigate the dynamic changes in the magnesium (Mg 2+ ) concentration in medial vestibular nucleus (MVN) of guinea pigs following vertigo induced by vestibular ice water stimulation with an electrochemical detection method consisting of in vivo microdialysis and on-line selective electrochemical detection. Electrochemical detection of Mg 2+ was accomplished based on the current enhancement of Mg 2+ towards the electrocatalytic oxidation of NADH at the electrodes modified with the polymerized film of toluidine blue O (TBO). Selectivity for the on-line electrochemical detection against Ca 2+ was achieved by using ethyleneglcol-bis(2-aminoethylether) tetraacetic acid (EGTA) as the selective masking agent for Ca 2+ . The basal level of the extracellular Mg 2+ in the MVN of guinea pigs was determined to be 759.7 ± 176.2 M(n = 16). Upon ice water irrigation of the left external ear canal, the concentration of Mg 2+ in the MVN decreases significantly, reaches 72 ± 6% (n = 8) of the basal level, and maintains for at least 1000 s. Control experiments reveal that neither warm water irrigation of the external ear canal nor ice water irrigation of the auricle induces the decrease in the concentration of Mg 2+ in the MVN. These results demonstrate that the extracellular Mg 2+ in the MVN decreases significantly following vertigo induced by vestibular ice water stimulation. This demonstration suggests that Mg 2+ might play an important role in the pathological mechanism of vertigo.

Extracellular ascorbic acid fluctuation during the protective process of ischemic preconditioning in rabbit renal ischemia-reperfusion model measured

Background Ascorbic acid has important antioxidant ischemic preconditioning on later ischemia-reperfusion ascorbic acid in ischemic preconditioning in the kidney. properties, and may play a role in the protective effects of Herein, we examined the role of endogenous extracellular Methods We developed a solitary rabbit kidney model where animals received ischemia-reperfusion only （ischemia-reperfusion group, n=-15） or ischemic preconditioning followed by ischemia-reperfusion （ischemic preconditioning group, n=15）. Ischemia-reperfusion was induced by occluding and loosening of the renal pedicle. The process of ischemic preconditioning included 15-minute brief ischemia and 10-minute reperfusion. In vivo microdialysis coupled with online electrochemical detection was used to determine levels of endogenous extracellular ascorbic acid in both groups. The extent of tissue damage was determined in kidney sections stained with hematoxylin and eosin. Serum creatinine and urea nitrogen were also detected to assess renal function. Results During ischemia-reperfusion, the extracellular ascorbic acid concentration during ischemia increased rapidly to the peak level （（130.01±9.98）%）, and then decreased slowly to near basal levels. Similar changes were observed during reperfusion （peak level, （126.78±18.24）%）. In the ischemic preconditioning group there was a similar pattern of extracellular ascorbic acid concentration during ischemic preconditioning. However, the ascorbic acid level was significantly lower during the ischemia and early reperfusion stage compared to the ischemia-reperfusion group. Additionally, the extent of glomerular ischemic collapse, tubular dilation, tubular denudation, and loss of brush border were markedly attenuated in the ischemic preconditioning group. Levels of serum creatinine and urea nitrogen were also decreased significantly in the ischemic preconditioning group. Conclusions Ischemic preconditioning may protect renal tissue against ischemia-reperfusion injury via use of extracellular ascorbic acid. In vivo microdialysis coupled with online electrochemical detection is effective for continuous monitoring extracellular ascorbic acid in the renal cortex.