Effect of hyperbaric oxygen treatment on mitochondrial free radicals after transient focal cerebral ischemia in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of hyperbaric oxygen(HBO)therapy on mitochondrial free radicals after transient focal cerebral ischemia in rats.</p><p><b>METHODS</b>The male SD rats were randomly assigned into two groups, control and HBO groups. All animals were subjected to 90 min intra-luminal middle cerebral artery occlusion (MCAO) with the regional cerebral blood flow monitored in vivo by laser Doppler flowmetry. HBO treatment was performed in a pressure chamber with 100% O(2)(3 ATM 1 h) 3 h after ischemia. Twenty-four hours after ischemia, mitochondria in the ischemic core and penumbra were isolated and the contents of H(2)O(2), O(2)(*-), MDA, SOD, GSH-PX and GSH in mitochondria were measured respectively.</p><p><b>RESULT</b>After cerebral ischemia-reperfusion, contents of mitochondrial H(2)O(2), O(2)(*-), MDA increased, while the SOD, GSH-PX and GSH in the mitochondria decreased significantly both in the ischemic core and the ischemic penumbra, compared with those in the normal controls(P<0.05). In the ischemic penumbra, HBO therapy increased significantly the content of O(2)(*-)(P<0.05), enhanced the activity of SOD, and decreased the level of MDA (P<0.05). However, HBO therapy did not change the level of MDA, though it also increased the content of O(2)(*-) and the activity of SOD in the ischemic core. HBO therapy had no significant effect on the contents of H(2)O(2), GSH-PX and GSH in the ischemic mitochondria.</p><p><b>CONCLUSION</b>HBO therapy initiated early after acute transient cerebral ischemia in rats can increase the mitochondrial free radicals level, but also increase the activity of the anti-radical enzymes. HBO treatment inhibits the lipid peroxidation damage of mitochondria in the ischemic penumbra, but not in the ischemic core, which indicates that the mitochondrial function plays a role in the reaction of the free radical in the ischemic area after HBO therapy.</p>

An insulinoma with clinical and electroencephalographic features resembling complex partial seizures / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

We described a female patient with insulinoma who experienced recurrent episodes of automatism, confusion and convulsion. Furthermore, her electroencephalography (EEG) findings resembled the pattern in complex partial seizures with secondary generalization. The interictal EEG showed spikes and sharp waves, as well as focal slowing over the left temporal lobe, and the ictal EEG revealed generalized spikes and sharp waves associated with diffused slowing. She was initially misdiagnosed as pharmacoresistant epilepsy. After the insulinoma was found and surgically removed, her EEG turned normal and she was seizure-free during the 4-year follow-up. This report highlights the need for careful reassessment of all seizures refractory to medication, even for the patients associated with epileptiform discharges on EEG.

Effect of hyperbaric oxygenation treatment on the apoptotic cell death pathway after transient focal cerebral ischemia / 中国应用生理学杂志

<p><b>AIM</b>To evaluate the effects of administration of hyperbaric oxygenation(HBO) when initiated at different time after acute transient ischemia. Apoptosis in the ischemic penumbra was further investigated to search for the possible mechanism.</p><p><b>METHODS</b>The male SD rats were randomly assigned to the following groups: control, HBO therapy initiated 3 h after ischemia, HBO therapy initiated 6 h after ischemia, HBO therapy initiated 12 h after ischemia. All animals were subjected to 90 min intraluminal middle cerebral artery occlusion (MCAO) with the regional cerebral blood flow monitored in vivo by laser Doppler flowmetry. HBO treatment was performed in a pressure chamber with 100% O2, 3 arm for 1 h. Neurological deficits and infarct volumes were assessed at 24 hours after ischemia. The immunohistochemical changes of apoptosis in the penumbra were evaluated by detecting the expression of cleaved Caspase-3, cleaved Caspase-9, Bcl-2, Bax and TUNEL staining.</p><p><b>RESULTS</b>HBO therapy initiated at 3 and 6 hours after ischemia significantly improved the neurological function and reduced infarct volume. Meanwhile, it increased the expression of Bcl-2 protein and decreased the expression of activated Caspase-3, activated Caspase-9 and TUNEL-positive cells. However, HBO therapy administrated 12 hours after ischemia aggravated the neurological deficits and enlarged infarct volume, while it showed no significant reduction of apoptotic change compared with control.</p><p><b>CONCLUSION</b>There is a therapeutic window for the use of HBO in acute transient cerebral ischemia in rats. HBO-treatment is highly effective in reducing infarct volume when initiated up to 6h after the onset of ischemia. Inhibition of apoptotic cell death in the penumbra appears to be the underlying protective effect of early therapy.</p>

Effect of irbesartan on focal cerebral ischemia in rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate whether the selective AT1 receptor antagonist irbesartan exerts neuroprotective effect on focal cerebral ischemia in normotensive rats.</p><p><b>METHODS</b>Cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion, with the monitoring of laser Doppler flowmetry. To avoid the interaction with peripheral AT1 receptors, irbesartan was infused intracerebroventricularly (ICV) at a dose which effectively inhibited brain- but not vascular AT1 receptors. Neurological status was evaluated daily after MCAO. Rats were killed and brain samples were collected for the measurement of infarct size and immunohistochemical evaluation of apoptosis by deoxynucleotidyltransferase-mediated biotinylated UTP nick end labeling (TUNEL) and expression of activated Caspase-3 and the cleavage fragment of poly (ADP-ribose) polymerase (PARP).</p><p><b>RESULTS</b>Treatment with irbesartan improved significantly the neurobehavioral functions after cerebral ischemia. The infarct size was reduced about 42% on day 7 after MCAO (P < 0.05). Meanwhile,irbesartan treatment significantly decreased the number of TUNEL-positive cells in the penumbra. The expression of activated Caspase-3 and the downstream cleavage fragment of poly (ADP-ribose) polymerase in the penumbra were also inhibited by irbesartan therapy on day 3 after transient cerebral ischemia.</p><p><b>CONCLUSION</b>Angiotensin AT1 receptor antagonist exhibits neuroprotection against transient cerebral ischemia in the brain. The neuroprotective effects in ischemic tissue may be associated with its inhibition of apoptotic cell death in the penumbra.</p>

Serum levels of soluble intercellular adhesion molecule-1 in patients with cerebral infarct / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To observe the changes of the levels of soluble intercellular adhesion molecule-1(sICAM-1) in serum of patients with cerebral infarct and to explore the effect of sICAM-1 on cerebral infarct.</p><p><b>METHODS</b>The serum levels of sICAM-1 in 55 patients with cerebral infarct both in acute stage(within 2 days) and convalescence(2 weeks after attack) were detected by using ELISA. At the same time, we compare the results with those of 32 patients having other neurologic diseases(20 patients with sciatica, 12 with trigeminal neuralgia) and 30 healthy subjects.</p><p><b>RESULTS</b>(1) The serum levels of sICAM-1 of patients with cerebral infarct (acute stage: 766+/-179 microgram/L, convalescence: 602+/-155 microgram/L, respectively) were significantly higher than those of the control groups(530+/-77 microgram/L and 521+/-116 microgram/L, respectively, P<0.01). (2)There was a positive correlation of SICAM levels with the amount of leukocytes in acute stage(r=0.285,P<0.05), but negative correlation to clinical severity of cerebral infarct(r= 0.333,P<0.05). And there was no significant correlation between the level of sICAM-1 and the levels of cholesterol and triglyceride in serum(r= 0.042 and r=0.061, respectively, P>0.05). (3)There was no significant difference between sICAM levels of patients of cerebral cortex infarct and those of patients with basal ganglia infarct(773+/-178 microgram/L and 758+/-183 microgram/L, respectively, P>0.05). (4)The levels of sICAM-1 between patients of cerebral infarct with or without hypertension were no significant difference(774+/-189 microgram/L and 754+/-165 microgram/L, respectively, P>0.05).</p><p><b>CONCLUSION</b>The levels of sICAM-1 increase significantly in patients with cerebral infarct. sICAM-1 may participate in the pathophysiologic process through inflammatory mechanism.</p>