Objective To investigate the effects of clonidine on the visceral pain induced by acute myocardial ischemia. Methods Male SD rats weighing 250-280 g were operated upon under general anesthesia with intraperitoneal methane 1.2 g/kg and local infiltration of the skin incision. After tracheal intubation, the animals were mechanically ventilated (VT = 5-7 ml/kg, RR = 75 bpm). The anterior descending branch of left coronary artery was occluded with a snare through the left 4 th intercostal space. The animals were then fastened to a brain stereotaxic instrument and a burr hole was made in the skull. A glass micro-electrode was inserted into the brain. The discharges of noxious stimulation responding neuron (NSRN) in parafascicular nucleus were recorded. Twenty-four rats detected NSRN showed response to coronary artery occlusion (CAO) were randomly divided into 4 groups (n =6 each): group Ⅰ CAO + normal saline 0.1 ml; group Ⅱ CAO + elonidine 30 μg; group Ⅲ CAO + clanidine 100 μg; group Ⅳ CAO + clonidine 100 μg + yohimbine (an α2-adrenergic receptor antagonist) 200 μg. In group Ⅳ , clonidine was administered intravenously 15 min after CAO, and then yohimbine was injected intravenously 15 min later. The discharges of NSRN were recorded every 5 min for 60 min from the beginning of CAO. Results Clonidine 100 μg significantly inhibited the increased frequency of nociceptive discharge rate of NSRN after CAO. However, this effect could be blocked by the α2-adrenergic receptor antagonist yohimbine.Conclusion Clonidine 100 μg can reduce the visceral pain induced by acute myocardial ischemia through activiting α2-adrenergic receptor.

Objective To investigate the effect of propofol pretreatment on hippocampal monocyte chemotactic protein-1 ( MCP-1 ) and CC-chemokine receptor type 2 (CCR2) expression following forebrain ischemiarepcrfusion (I/R) in rats. Methods Twenty-four male SD rats weighing 250-300 g were randomly divided into 3 groups ( n = 8 each): group Ⅰ control; group Ⅱ I/R and group Ⅲ propofol pretreatment. Cerebral I/R was induced by clamping bilateral common carotid arteries for 10 min combined with hypotension ( MAP was maintained at 35-45 mm Hg) induced by exsanguinations in group Ⅱ and Ⅲ. In group Ⅲ propofol 50 mg/kg was injected into femoral vein immediately before cerebral ischemia. The animals were sacrificed at 6 h of reperfusion. Hippocampal tissue was obtained for detection of MCP-1 mRNA and CCR2 mRNA and their protein expression by RT-PCR and Western blot technique. Results I/R significantly increased the expression of MCP-1 and CCR2 in hippoeampal tissue as compared with control group. Propofol pretreatment significantly attenuated cerebral I/R induced increase in MCP-1 and CCR2 expression. Conclusion Propofol pretreatment can significantly inhibit forebrain I/R-induced hippocampal MCP-1 and CCP2 expression.

Automatic detection of epileptic events is of significance in clinical application. It is helpful to reduce the electroencephalogram analysts' workload. This paper summarizes and analyzes the detection of epileptic events by traditional and especially advanced methods, including nonlinear filtering, template matching, mimetic, wavelet transform and artificial neural network.
Electroencephalography ; Epilepsy ; diagnosis ; Humans ; Neural Networks (Computer) ; Signal Processing, Computer-Assisted ; Wavelet Analysis