Rat colitis induced by intrathecal injection of substance P / 生理学报

The aim of this study was to, from the point of neurogenic inflammation, explore the pathogenesis of colitis and to provide direct evidence for the neurogenic colitis hypothesis. Male Sprague-Dawley rats (180-220 g) anesthetized with chloral hydrate were intrathecally (ith) implanted with polyethylene-10 (PE-10) catheter to reach the spinal cord T₁₂-L₅ level. Substance P (SP) was ith injected once a day for 14 d. The disease active index (DAI) score was calculated by rat body weight and stool. The macroscopic and HE staining-microscopic pathologies of colon/spinal tissue were evaluated. By immunofluorescence staining, the protein expression of a pro-inflammatory cytokine, migration inhibitory factor (MIF), in colon tissue was detected and was semi-quantitatively analyzed. The results showed that in the colon tissue, inflammation was dose-dependently aggravated by ith SP 10 μ and 20 μ, whereas in the spinal tissue, only slight edema and congestion were seen in SP 20 μ group. The MIF protein of colon tissue was increased in ith SP 10 μ and 20 μ groups (P<0.05, P<0.01 as compared to normal saline group respectively), but in the spinal tissue, there was no obvious MIF protein expression either in SP groups or in normal saline group. Pretreatment with neurokinin-1 (NK₁) receptor antagonist ([D-Pro2, D-Trp7, 9] -SP, 22.4 μ, ith, 10 min before ith SP) prolonged the latency of DAI rising and reduced the DAI amplitude, as well as prevented the high MIF expression induced by ith SP. These results suggest that rat colitis can be induced by direct SP stimulation in lumbar spine via activating central NK₁ receptor; and that colonic MIF is possibly one of the inflammatory factors involved in this pathogenesis. These data provide a reasonable support to the hypothesis of colitis being a neurogenic inflammation. In addition, a potential clinical significance for the finding that higher concentration of spinal SP can induce colitis via NK₁ receptor is discussed.

Migration inhibitory factor is involved in experimental colitis induced by intrathecal injection of haptten to rat / 生理学报

In recent years, there has emerged academic tendency towards the neurogenic mechanism of ulcerative colitis (UC). As one of the supports to the hypothesis of UC being a neurogenic inflammation, we have built a colitis model by intrathecal (ith) injection of a haptten 2,4-dinitrochlorobenzene (DNCB) to DNCB-sensitized rats. In order to explore further the neuroimmunal mechanism of this colitis model, we here focused on a pro-inflammatory cytokine, migration inhibitory factor (MIF), to observe its expression in rat colon nervous tissue and spinal cord in the colitis induced by ith injection of DNCB. At the same time we also observed the effect of MIF antibody pretreatment on the disease active index (DAI) score and the colon pathology by HE staining in the colitis rats. The results obtained showed that the immunofluorescence intensity of double staining of MIF protein in colon nervous tissue and spinal cord was increased in 0.8% and 1.6% DNCB-induced colitis groups than that in the control (60% ethanol) group. Both the colon pathology and the DAI score were significantly reduced by MIF antibody ith pretreatment. Ith injection of 0.8% DNCB after MIF antibody (1:10, 1:5) pretreatment could only induce lower DAI score (P<0.01 as compared, respectively, to the IgG pretreatment group). The colon pathological changes in ith 0.8% DNCB rats were mild, even little after MIF antibody (1:10, 1:5) pretreatment. These results suggest that MIF in spinal cord and enteric nervous system is possibly involved in the rat colitis induced by ith injection of DNCB, which reflects a neuroimmunal mechanism underlying this kind of colitis. MIF is possibly one of the important neurochemical factors in this experimental colitis, even in the UC.

The effect of changing body posture on thrombin activity and concentration / 中国应用生理学杂志

<p><b>AIM</b>To provide proof for Evidence-based Medicine as well quality control, our laboratory detected the thrombin activity on various body position.</p><p><b>METHODS</b>By autogenous contrast and cross matched survey, 105 volunteers divided into 3 season patches of winter, spring and summer, blood samples were drawn from the same part in both standing and lying position. Both samples and the quality control were detected to investigate the effect of the body position to thrombin activity's changing. The data were analyzed by SPSS 10.0.</p><p><b>RESULTS</b>Taking the lying's data as baseline, the average changing on all those the "5" index was 7.07% and the highest changing reached 9.33%. This kind changing had great significant differences (P < 0.01). According to the t value, sequences ranged: FIB > TT > PT > INR > APTT. FIB, TT and APTT's values slowly raised, adversely PT and INR slowly went down. While sitting for 15 min after lying, these indices returned to 95.2% of the original value in sitting position in addition. Season, age and device had no relationship with body position.</p><p><b>CONCLUSION</b>Changing body position can result in obvious physiological variation of thrombin activity.</p>

Effects of simulated high altitude hypoxia on cognitive performance / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of mild and moderate hypoxia on human cognitive performance.</p><p><b>METHODS</b>Eighteen healthy young male volunteers performed a set of tests of human ergonomics at sea level (300 m in Xi'an) and simulated high altitude of 2 800 m, 3 600 m and 4 400 m for 1 h in hypobaric chamber, respectively.</p><p><b>RESULTS</b>The performance of continuous recognition memory tests compared with the controls' was deteriorated significantly (P < 0.01) after exposure to 2 800 m for 1 h. After exposure to 3 600 m for 1 h, in all test, the reaction time was much longer, the accurate rates were lower and the performance was worse than that of control (P < 0.05). All the parameters were deteriorated with the increment of altitude and the performance of all tests were much worse at 4 300 m for 1 h (P < 0.01).</p><p><b>CONCLUSION</b>Different parameters of human cognitive performance may have different susceptible thresholds to hypoxia according to the results from our studies. The cognitive performance after exposure to 3 600 m for 1 h was not sufficiently effective for the demands of human ergonomics due to its significant deteriorating changes. However, the performance can be effectively restored after exposure to enough oxygen supply for 1 h.</p>