ABSTRACT
Objective To establish an animal model of neurogenic pulmonary edema (NPE),and to study the role of catecholamine and beta receptors in the occurrence of NPE. Methods The NPE model was established by injecting fibrinogen and thrombin into the cerebellum medullary pool of the rabbits. Twenty-four rabbits were divided into the control group,the saline group and the experimental group by random num-ber table. In the control group,only cerebellar medullary cistern puncture was carried out,and no drug was in-jected. Cerebrospinal fluid was drew out and the same amount of saline was injected into the cerebellum me-dullary pool in the saline group. Fibrinogen and thrombin were injected into the cerebellum medullary pool in the experimental group. The animals were intubated by tracheotomy,the femoral artery and the internal jugu-lar vein were dissected and connected with the PiCCO instrument to detect the blood pressure,heart rate,and respiratory rate before puncture and at 1 min,10 min,30 min after puncture. Serum samples were collected for the determination of epinephrine,norepinephrine,acetylcholine,endothelin-1,cardiac troponin I,brain natri-uretic peptide and neuropeptide Y levels before puncture and at 1 min,10 min after puncture. The rabbits weresacrificed at 3 hours after successful modeling,the pathological examination of lung was performed. Myocar-dial samples were taken to detect adrenergic beta receptors mRNA. Results (1)The heart rate,respiratory rate and mean arterial pressure at 1 min and 10 min after puncture in experimental group were significantly higher than those in control group and saline group. (2) The pathological examination of the rabbits′ lungs in experimental group found that the lung tissue was swollen and dark red in appearance with large areas of con-gestion. Under the microscope,the lung tissue was edema,bleeding,and inflammatory cells were infiltrated in the alveolar cavity,which was consistent with characteristics of NPE. (3)There was no difference in epineph-rine and norepinephrine concentration in all groups before the cerebellar medullary pool puncture. The concen-tration of epinephrine and norepinephrine at 1 min after puncture time were (200. 0 ± 251. 7)μg/ L,(448. 9 ± 356. 7)μg/ L in the experimental group,whcih were significantly higher than those of control group[(15. 4 ± 3. 4)μg/ L,(15. 9 ± 9. 7)μg/ L] and saline group[(17. 1 ± 3. 8) μg/ L,(29. 6 ± 18. 4) μg/ L] (P < 0. 05). The concentration of epinephrine and norepinephrine at 10 min after puncture were (397. 0 ± 797. 7)μg/ L, (221. 4 ± 173. 7)μg/ L in the experimental group,whcih were significantly higher than those of control group [(23. 3 ± 6. 4) μg/ L,(18. 8 ± 3. 9) μg/ L] and saline group[(16. 7 ± 9. 1) μg/ L,(20. 3 ± 6. 5) μg/ L] (P < 0. 05). (4)There was no significant difference in the levels of serum neuropeptide Y,acetylcholine and endothelin-1 among the three groups. (5)The mRNA of adrenergic beta-1 receptor in the experimental group was 0. 37 ± 0. 12,which was significantly lower than those in the control group (0. 54 ± 0. 13) and saline group (0. 56 ± 0. 14) (P < 0. 05). There was no significant difference in adrenergic beta-3 receptor mRNA among the three groups. Conclusion The NPE animal model was constructed by injecting fibrinogen and thrombin into the cerebellum medullary pool of the rabbits. Catecholamine and beta-1 receptor play a role in the occurrence of NPE rabbit model. There is no significant correlation between neuropeptide Y,acetylcholine,en-dothelin-1 and the occurrence of NPE in rabbits.
ABSTRACT
Objective To investigate the changes of cellular immunity and humoral immunity in children with acute or critical illness. Methods Seventy-three critically ill children admitted to PICU of Chil-dren′s Hospital Affiliated to Fudan University during the period from April,2015 to September,2015 were the objects of study. Blood samples were collected within 48 hours after admition. The lymphocyte subpopulation was measured by flow cytometry,and the level of humoral immunity was measured by rate immune scatter turbidimetry,and the neutrophil function was measured by flow cytometry-DHR analysis. Twenty-three cases from 73 cases were detected the second time after admitted to hospital for seven days. Ten health children be-fore elective surgery were selected as control. Results (1) Compared with the control,the percentages of CD3 +T cells and CD8 +T cells were significantly decreased in critically ill children within 48 hours of admis-tion[(57. 43 ± 13. 46)%,(21. 26 ± 7. 87)% vs. (66. 24 ± 5. 27)%,(26. 82 ± 7. 63)%,P<0. 05]; At the same time,CD4 +T cells and NK cells had no significant change[(33. 42 ± 11. 29)%,(8. 83 ± 7. 77)% vs. (34. 89 ± 4. 94)% (11. 34 ± 5. 60)%,both P<0. 05]; While B cells were significantly increased[(31. 69 ±13. 83)% vs. (21. 08 ±7. 24)%,P<0. 05]. Neutrophil activation rate[(14. 32 ±14. 81)%] was signifi-cantly higher than the normal reference value ( 0 -10%) and the activation rate was more than 90% after stimulated by PMA. The plasma level of complement C3[(0. 88 ± 0. 31) g/L] was lower than that of the control group[(1. 19 ± 0. 18)g/L,P<0. 05]. (2) Compared with the first time,the percentages of CD3 +cells and CD4 + cells were increased after treated for one week in 23 patients[(61. 20 ± 13. 56)%,(36. 79 ± 9. 95)% vs. (56. 80 ± 13. 99)%,(32. 86 ± 10. 87)%,both P<0. 05]. No significant difference in neutrophil activation and activation rate after PMA stimulation was found compared with admition. IgA,IgM and comple-ment C3 were significantly increased[(0. 98 ± 0. 75) g/L,(1. 00 ± 0. 39) g/L,(1. 15 ± 0. 34) g/L vs. (0. 80 ± 0. 69) g/L,(0. 86 ± 0. 48) g/L,(0. 93 ± 0. 23) g/L,all P<0. 05]. Conclusion Immune disorders occur in critically ill children in the early stage of illness,the most obvious change is cellular immune response,and im-mune function starts to recover after one week.