ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of dosages of total body irradiation on the healing process of cutaneous wounds and to observe the changes of wound area at different periods after injury.</p><p><b>METHODS</b>The entire body irradiation from a (60)Co gamma-ray source was performed on Wistar rats. The single dosage varied from 1 to 8 Gy. Within 1 h after irradiation, two whole thickness circular cutaneous wounds corresponding to 2.5% of total body surface area (Phi = 22 mm) were produced on the back of the animals (combined injury groups). Same wounds were produced on rats with no irradiation (single wound group). Wound healing was observed at different points after injury.</p><p><b>RESULTS</b>After total body irradiation with the dose of 1, 2, 3, 4, 5, 6, 7 or 8 Gy, the wound healing was obviously retarded as the dosages increased. The wound area remained was larger in the large dosage groups than in the small dosage groups. Seven days after injury, there was 33.5% wound surface left unhealed in the single wound group, whereas in the combined injury groups, 35.4%, 38.1%, 41.6%, 48.8%, 53.9%, 63.7%, 69.2% and 73.9% of the wound surfaces remained unhealed, respectively. Statistical analysis showed marked correlations between the various times after total body irradiation and various dosages to the percentage of unhealed wound surface. Nine dose-effect relation formulae were deduced according to the statistical results.</p><p><b>CONCLUSIONS</b>In soft tissue trauma combined with radiation injury, the delay of wound healing is related to the dose of radiation inflicted. It is also related to the time between injury and time of observation.</p>
Subject(s)
Animals , Female , Male , Rats , Dose-Response Relationship, Radiation , Rats, Wistar , Time Factors , Whole-Body Irradiation , Wound Healing , Radiation EffectsABSTRACT
Objective To observe the changes of glucocorticoi d receptor (GR) in hepatic cytoplasm in rats after scalding-induced pathologic al stress and its regulation. Methods The receptor binding capa city (R0) and the apparent dissociation constant (Kd) of GR in hepatic cytopla sm of normal, low-degree and heavy-degree scalded rats were measured with rad io-ligand binding assay, with ［3H］ dexamethasone as ligand. The changes of R0 and Kd of GR were regulated by injections of anti-rat TNFα, IL-1β a ntibodies, α-melanocyte-stimulating hormone (α-MSH), and KPV peptide( Ac- D-Lys-L-Pro-D-Val) respectively in vivo. Results The R 0 of GR in hepatic cytoplasm in rats 12 h after heavy-degree scalding ［Mass action robust: （205.52±30.14） fmol/mg; Scatchard: （208.45±30.78） fmol/mg ］were significantly lower than that of control group ［Mass action robust:（307 .86±24.22） fmol/mg;Scatchard:（306.71±27.96） fmol/mg］(P<0.01), but no s ignificant difference was found in the R0 of GR between the control and the ra ts 12 h after low-degree scalding ［Mass action robust: （285.19±16.62） fmol/ mg ; Scatchard: （296.64±16.06） fmol/mg］. The injection of anti-rat TNFα, IL-1β antibodies, α-MSH and KVP all prevented the decline of R0 of GR in h epatic cytoplasm in rats with severe scalding. Conclusion The injections of anti-rat TNFα, IL-1β antibodies, α-MSH or KPV can attenuate the reduction of GR in rat hepatic cytoplasm caused by severe scalding-induced pathological stress to some extent.
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Objective: To investigate the correlation between the expression of vascular endothelial growth factor(VEGF) and angiogenesis in tumor. Methods: VEGF 165 sense and antisense gene recombinants were introduced into human gastric cancer cells, respectively. Then the growth of transfected cells in nude mice and the microvascular density and histological change were examined. Results: The growth rate of tumor in nude mice inoculated with sense VEGF cells was markedly higher than that in nude mice inoculated with antisense-VEGF cells. In histological examination, the microvascular density in tumor caused by sense-VEGF cells was greatly higher than that in tumor caused by antisense VEGF cells. Conclusion: As starting angiogenesis, VEGF might promote the growth of tumor, and the inhibition of VEGF production might prevent solid tumor from growing.
ABSTRACT
Traumatic stress in the normal individual results in activation of the sympatho-adrenal system causing a rise in noradrenaline and adrenaline, acute phase response in liver ,and activation of the hypothalamic-pituitary-adrenocortical(HPA)system resulting in elevated levels of cortisol. Studies in animals and in humans with posttraumatic stress disorder indicate that successful adaptation to stress is a prerequisite for the survival of all organisms living in an enviroment in which noxious stimuli are constantly present.