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To investigate the epithelial growth factor (EGF) expression of EGF gene-transfected keratinocytes and its effect on cell proliferation after grafting.Newborn Balb/c mouse keratinocytes and gene transfected keratinocytes were seeded on the surface of acellular dermal matrix and cocultured in different ratios as follows: 1:1, 1:3, or 1:5 1 week after culture. The composite skin was grafted onto the full-thickness wound in Balb/c mouse. Specimen was harvested at interval after grafting and underwent the immunohistochemistry staining for EGF and proliferating cell nuclear antigen (PCNA).Immunohistochemical staining showed EGF was expressed in the newly generated epidermis 1-2 week after grafting of the composite skin comprising Balb/c mouse keratinocytes and gene-transfected keratinocytes (at the ratio of 1:5). One week after surgery, Anti-PCNA positive basal cells were more than that in composite skin containing Balb/c mouse keratinocytes alone (P0.01).The gene-transfected keratinocytes expresses EGF and promotes the proliferation of keratinocytes in the early stage after transplantation.

To investigate the changes in myocardial dynamics in early phases of burn shock of dogs and the effects of rapid fluid infusion in delayed resuscitation.Twelve mongrel dogs were randomly divided into control (n=6) and burn (n=6) groups. The dogs in burn group were subjected to 35% total body surface area (TBSA) III degree burn and were resuscitated with lactate Ringer's solution 6 hours postburn. The volumes and rates of fluid infusion were controlled basically on the urinary output of 1.0 mlxkg(-1)xh(-1) and cardiac output (CO) of 70%-80% of pre-burn values. The mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximum rate of intraventricular pressure rise/down (+/-dp/dt max) and cardiac index (CI) were determined at 0.5, 1,2, 6, 7, 8, 10 and 24 hours postburn.The MAP, LVSP, +/-dp/dt max and CI were significantly lowered from their baseline and those of control group at 0.5 hour postburn, and they kept declining until 6 hours postburn. They showed a tendency of elevation and reached or approached the levels of that in control group within 2 hours of resuscitation, and the differences were not significant between the two groups 4 hours after burn (all P0.05). The amount of infusion fluid within the first 4 hours of resuscitation was (3.63+/-0.99) ml/kg per 1% TBSA.The myocardial dynamics is depressed in the early stage of burn, the effective way to improve it is to infuse a large amount of fluid rapidly when resuscitation is delayed.

To study whether nimodipine, a dihydropyridine-type calcium channel blocker, can inhibit the production of interleukin-1beta(IL-1beta), interleukin-6(IL-6) by Kupffer cells(KC) and down-regulate its level of plasma after severe burn injury.KC of normal rats were isolated with portal vein catheter, intrahepatic digestion and density gradient centrifugation. Intracellular calcium concentration ([Ca2+]i) in individual KC after stimulated with postburn serum was assessed fluorometrically with microspectrofluorimeter. Level of IL-1beta and IL-6 in the supernatant of KC cultured with postburn serum were detected by enzyme-linked immunosorbent assay(ELISA). SD rats underwent 30% total body surface area(TBSA) full thickness burn 6 hours later, KCs was isolated and their mRNA were extracted. Level of IL-1beta mRNA and IL-6 mRNA were detected by ribonuclease protection assay(RPA). Levels of plasma IL-1beta and IL-6 were also detected. Role of nimodipine on above-mentioned effects were observed.Compared with that of control group, levels of [Ca2+]i of KCs and IL-1beta and IL-6 supernatant in burn group increased significantly(all P0.01). At present of 1 micromol/L nimodipine, however, the [Ca2+]i, IL-1beta, IL-6 values decreased significantly(all P0.01). The level of plasma cytokines and KC mRNA in burn group also increased significantly. After intravenously injection with nimodipine (40 microg x kg(-1) x h(-1)), the numerical values decreased significantly(all P0.01).Kupffer cells of rats are activated to secret IL-1beta and IL-6 after severe burn injury and this process is realized through calcium ion signal transduction channel. Nimodipine can inhibit IL-1beta and IL-6 production of KC by preventing its mRNA transcription, down-regulating its level of plasma.