Lung injury and toxic oxygen compounds
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Abstracts 149 surface were divided into 3 groups, those with bum only, those with bum followed by excision of the burned tissue 5 hours after injury and those with burn plus excision and given lysine vasopressin immedi- ately after burning. All three groups ofanimals showed a reduction in cardiac output to about 30 per cent of normal 4 hours after burning. Excision of the burned tissue resulted in an earlier recovery of the subnormal cardiac output and a greater blood flow to the hepatic artery and reduced flows to the proximal GI tract and skin and unchanged flows to the heart, kidneys and other organs 24 hours after burning. The mean blood loss during and after excision of burned tissue was only one third of that observed in the animals which did not receive lysine vasopressin. Vemersson E., Ahlgren I., Aronsen K. F. et al. (1983) Lysine vasopressin in excisional treatment of bums in pigs. ilcta. Chir. Scund. 149, 15. Animal model of immunosuppression Cell mediated immunity has been studied in burned mice using a system involving sensitivity to dinitro- fluorobenzene. Cell mediated immunity was depressed over a 2 week period following burning. Excision of burned tissue immediately after injury prevented immunosuppression, while transfer of burned tissue as a subcutaneous transplant to unburned mice induced severe immunodepression. Cell mediated immunity was restored by the intravenous infusion of peritoneal macrophages from unburned mice but not by infusion of lymphocytes or macrophages taken from burned mice. Hansbrough J. F., Peterson V., Kortz E. et al. (1983) Postbum immunosuppression in an animal model- monocyte dysfunction induced by burned tissue. Surgery93,415. Lung injury and toxic oxygen compounds Deep bums of rat skin caused depletion of the haemo- lytic activity of complement components and conver- sion of C,. Soon after burning C,, related chemotactic activity appeared in the serum at the time of neutro- penia. Increased lung permeability developed pro- gressively during the first 6 hours after injury and paralleled the changes in complement levels. Protec- tion from lung injury following remote skin burns could be induced by depleting the animals of comple- ment or neutrophils or by systemic treatment of the animals with a combination ofcatalase and superoxide dismutase; the latter implicating toxic oxygen products produced by activated blood neutrophils as a cause of acute lung injury. Till G. O., Beauchamp C., Menapace D. et al. (1983) Oxygen radical dependent lung damage following thermal injury of rat skin. J. Trauma. 23, 269.
Transcript of Lung injury and toxic oxygen compounds
Abstracts 149
surface were divided into 3 groups, those with bum only, those with bum followed by excision of the burned tissue 5 hours after injury and those with burn plus excision and given lysine vasopressin immedi- ately after burning. All three groups ofanimals showed a reduction in cardiac output to about 30 per cent of normal 4 hours after burning. Excision of the burned tissue resulted in an earlier recovery of the subnormal cardiac output and a greater blood flow to the hepatic artery and reduced flows to the proximal GI tract and skin and unchanged flows to the heart, kidneys and other organs 24 hours after burning. The mean blood loss during and after excision of burned tissue was only one third of that observed in the animals which did not receive lysine vasopressin.
Vemersson E., Ahlgren I., Aronsen K. F. et al. (1983) Lysine vasopressin in excisional treatment of bums in pigs. ilcta. Chir. Scund. 149, 15.
Animal model of immunosuppression
Cell mediated immunity has been studied in burned mice using a system involving sensitivity to dinitro- fluorobenzene. Cell mediated immunity was depressed over a 2 week period following burning. Excision of burned tissue immediately after injury prevented immunosuppression, while transfer of burned tissue as a subcutaneous transplant to unburned mice induced
severe immunodepression. Cell mediated immunity was restored by the intravenous infusion of peritoneal macrophages from unburned mice but not by infusion of lymphocytes or macrophages taken from burned mice.
Hansbrough J. F., Peterson V., Kortz E. et al. (1983) Postbum immunosuppression in an animal model- monocyte dysfunction induced by burned tissue. Surgery93,415.
Lung injury and toxic oxygen compounds
Deep bums of rat skin caused depletion of the haemo- lytic activity of complement components and conver- sion of C,. Soon after burning C,, related chemotactic activity appeared in the serum at the time of neutro- penia. Increased lung permeability developed pro- gressively during the first 6 hours after injury and paralleled the changes in complement levels. Protec- tion from lung injury following remote skin burns could be induced by depleting the animals of comple- ment or neutrophils or by systemic treatment of the animals with a combination ofcatalase and superoxide dismutase; the latter implicating toxic oxygen products produced by activated blood neutrophils as a cause of acute lung injury.
Till G. O., Beauchamp C., Menapace D. et al. (1983) Oxygen radical dependent lung damage following thermal injury of rat skin. J. Trauma. 23, 269.
