| Objective To build up the PFIB Inhalation-induced ALI model of rabbit and then research on its mechanisms.Methods We operated tracheotomy and trachealcannula on the anesthetic rabbit, jointed the rat dynamic exposure system to a breathing apparatus, cascaded it to the trachealcannula and then did machine ventilate. 25 New Zealand famale rabbits were divided into 5 groups at random according to the PFIB exposure time (0, 10, 20, 27, 33min), and PFIB exposure concentration was 0.3mg/L. The respiratory rate, heart rate, MAP, blood gas analysis (PaO2, PaCO2) were monitored per 2h after PFIB exposure. Leukocyte of whole blood was counted and the level of IL-8 in the serum was detected at the 2, 4, 8 and 12h after PFIB exposure. Rabbits were killed at 12h after exposure. The protein concentration, the level of IL-8 and the NE concentration in BALF were calculated. The MDA and MPO level, the wet/dry ratio and water-bearing rate of lung, the pulmonary microvascular permeability index were detected. Pathologic examination was done with right inferior lobe of lung for 3 animals in every group. Results (1) The exposure concentration of PFIB was stable during the period of exposure time in 33min(P>0.05). (2)The PaC>2 and respiratory frequency began to decrease and increase notably in the group III at 8h and the groupIV at 4h respectively(P<0.05). (3) The count of WBC in the group II, III and IV rose significantly compared with that in the controlgroup in 8h and began to decrease in 12h in the group II and III(P<0.05). (4) the serum levels of IL-8 after 8h and IL-8 levels of the BALF in the group II, III and IV were notably higher than those in the control group separately (except for the group IV) (P<0.05). (5) The total protein , NE concentration in BALF, and the parameters of MDA concentration (except for the group II ) , MPO concentration, the wet/dry ratio and the water-bearing rate of lung, the pulmonary microvascular permeability index, which were all higher strikingly in the group II ,111 and IV than that of the control group respectively(P<0.05). (6)A11 rabbits in the the groupIV died within 9h after PFIB exposure. (7) In the control group, there was't obviously pathologic changes of lung, but which appeared in all trial groups and the severity of lesion was parallel with the PFIB exposure time.Conclusion The PFIB Inhalation-induced ALI model of rabbit was built up successfully. PMN and IL-8 both play very important roles in the whole period of PFIB-induced ALI. The suitable exposure exposure time of rabbit is 20~27min(exposure concentration 0.3mg/L ), within which the animal's physiological conditions are stable relatively in 10 hours, and the parameters such as the protein concentration, IL-8 levels, the NE concentration in BALF, MPO concentration, wet/dry ratio and water-bearing rate of lung, and the pulmonary microvascular permeability index are all valuable to judge the severity of ALI.ABSTRACT (Chapter 2)Studies on the protective effect of charcoal hemoperfusion onPFIB inhalation -induced ALI of rabbitObjective To Study on the protective effect of CHP on PFIB inhalation-induced ALI of rabbitMethods 31 rabbits were divided into 5 the groups at random according to the different treatment: group A (adopt the data of the control group in the chapter 1, n=5); group B (with Artio to venous bypass, n=7); group C (with exposure to PFIB, adopt the data of the group II in the chapter 1, n=5); group D (with A-V bypass after exposure to PFIB, n=7); group E (with CHP after exposure to PFIB, n=7). The PFIB Inhalation -induced ALI model of rabbit was built up (exposure time 20min, exposure concentration 0.3mg/L). The CHP was began at 4h after the PFIB exposure (2 hours, perfusion flow rate 50~100ml/min). The collection and examination of the sample were done similar with the charpter 1 (except the respiratory rate and MDA concentration of lung tissue). Pathologic examination was done with right inferior lobe of lung for 3 animals in every group, and the heart, liver and kidney in the group B and E... |
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