AIM: To study the chloride channel activity [ICl_(Ca)] in vascular smooth cells of the spontaneously hypertensive rats (SHR). METHODS: The vascular beds of mesenteric arteries were isolated from the pentobarbital anesthetized rats and perfused with 37 ℃ PSS at a constant flow rate. The vasoconstriction response to norepinphrine (NE) was determined by changes in perfused pressure. The strips of the rat arteries were mounted in an organ chamber filled with 37 ℃ PSS and the vascular tension was measured. RESULTS: (1) The contractile responses of mesenteric arteries to NE in SHR were greater than that in Wistar rats. (2) The inhibitory magnitude of the contractile response by niflumic acid in SHR was significantly less than that in Wistar rats and showed dose-dependent manner. (3) Decreasing the extracellular Cl~- concentration increased the contractile response to NE significantly and the amplitude of enhanced contractile response in SHR was greater than that in Wistar rats. CONCLUSION: It can be concluded that NE-induced contraction is enhanced in SHR, which is partly due to an increase in Cl~- efflux through the Ca~(2+)-activated Cl~- channels. The chloride channel activity may increase in association with the elevation of vascular tone and blood pressure.

AIM: To investigate the changes of bcl-2, bax expression and neuron apoptosis of cerebral cortex in lymphostatic encephalopathy of rats. METHODS: The model of lymphostatic encephalopathy was established by occluding and removing both the shallow and deep cervical lymph nodes in rats. The animals were sacrificed at 1, 2, 3, 5, 7 and 14 days after operation. HE staining was used to observe the structure of brain tissues and TUNEL staining was used to detect in situ cell apoptosis. The expressions of bcl-2 and bax were examined by RT-PCR. RESULTS: Cerebroedema appeared at the second day and was the most serious at the 5th day after blockage of cervical lymphatics. The number of TUNEL positive cells and the expression of bax began to increase at the 2nd day, reached a peak at the 5th day and dropped to control level at the 14th day. The expression of bcl-2 began to increase at the 1st day, reached a peak at the 5th day and dropped to control level at the 7th day. The increasing extent of bax was higher than that of bcl-2. CONCLUSION: The blockage of cervical lymphatics can lead to lymp[JP2]hostatic encephalopathy. Apoptosis is the main form of neuron death in the cortex and has relation to the increasing expression of bcl-2 and bax. [JP]

AIM: To examine whether ischemic preconditioning (IPC) can protect against apoptosis in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats and explore the role of IPC by inhibiting the expression of p53 in this process. METHODS: Wistar rats were used in the experiment. A global ischemia/reperfusion model was induced by 4-vessel occlusion. The rats were divided into the following three groups randomly: (1) ischemic preconditioning group (IPC group); (2) ischemia/reperfusion group (IR group); (3) control group. The histopathological changes, the percentage of apoptosis and the expression of p53 gene in CA1 region of rat hippocampus were examined by HE staining, FCM, RT-PCR and immunohistochemistry techniques. RESULTS: The neuronal density of CA1 region in IPC group [(217?9)/0.72 mm2] was significantly higher than that in IR group [(29?5)/0.72 mm2, P

Objective To explore the effect of oxygen inhalation on auditory sensory gating P50 in healthy human brain. Methods 28 healthy male academician right-handed were included. They were divided into control group (n=12) and experiment group (n=16) according to the random numerical table, and blinded about groups. The subjects inhaled pure oxygen in the experiment group, and air in the control group through a mask for 60 min. The electroencephalograph was recorded while an auditory paired-click sensory gating test was conducted during 4 study periods: before inhalation (pre0), inhale for 20 min (Oxy20) and 50 min (Oxy50), and 30 min after inhalation (post30). The latency and amplitude (S1-S2) of auditory sensory gating P50 were calculated. Results The latencies of P50 from S1 were stable in each group (P>0.7), and the latency of Oxy50 was shorter in the experiment group than in the control group (P<0.05). The latencies from S2 were stable in each group (P>0.30), and there was no significant difference between groups in all the time points (P>0.05). The amplitudes of (S1-S2) of P50 were stable in the control group (P=0.70), and was higher on Oxy20 (P=0.04) and Oxy50 (P=0.02) than post30 in the experiment group. There was no difference between the groups in all the time points (P>0.05). Conclusion Oxygen inhalation may be helpful to shorten the active time to stimulate, and trend to enhancing the amplitude of P50.

Objective To observe the change of the latency and amplitude of auditory-evoked potential P300 after oxygen inhalation.Methods 27 healthy male academicians were included. They were divided into control group (n=12) and experiment group (n=15) according to the random numerical table, and they were blinded about groups. All subjects in the experiment group inhaled pure oxygen while air in the control group through a mask for 60 minutes. EEG was recorded when an auditory Oddball paradigm was performed during following 4 periods: before oxygen inhalation (pre0), inhale oxygen (air in control) for 20 minutes (Oxy20) and 50 minutes (Oxy50), 30 minutes after oxygen inhaled (post30). The latency and amplitude of P300 from target stimuli were calculated. Results The latency of P300 was longer at Oxy20 as (358.58±15.32) ms, Oxy50 as (353.42±9.41) ms and post30 as (354.10±10.42) ms than at pre0 as (335.91±15.40) ms in the control group (P<0.01). The latency of P300 was shorter at Oxy50 as (319.17±14.34) ms, and post30 as (318.50±13.87) ms than at pre0 as (332.98±14.63) ms in the experiment group (P<0.05). The latency was shorter in the experiment group than in the control group at Oxy20,Oxy50 and post30 (P<0.01). The amplitudes were stable in the control group (P<0.05). The amplitude was lower at post30 as (2.41±0.64) μV than at pre0 as (5.49±0.89) μV in the experiment group (P<0.05). Conclusion Oxygen inhalation shortens the latency of P300, and decreases the amplitude in the similar trend with the prolongation of oxygen inhalation.