Phagocytic cell dysfunction
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448 Burns 119851 Vol. 1l/No. 8 direct observation using vital microscopy. Tissue sur- vival was measured by direct observation of the extent of necrosis. Significant oedema formed in the ears heated at temperatures above 48 “C but never in the contralateral unburned ears. Ear tissue blood flow was reduced to near zero at times after injury which decreased as the scalding temperature increased. Ear tissue survival was complete at temperatures up to 51 “C, at 52 “C about 50 per cent of the ear became necrotic, at 53°C most of the ear tissue was destroyed and the entire ear became necrotic at a temperature of 54 “C and above. Neither prompt cooling of the ear after scalding nor pre-scald administration of cimetidine, ketanserin, indomethacin or methyl prednisolone were able to prevent the necro- sis of the scalded ears. Blomeren I. and Baatre U. (1984) Postburn blood flow, edima and survives of thk hairy mouse ear after scald injury at different temperatures. Stand. J. Plust. Reconstr. Surg. 18, 269. Scalds and tissue survival (Part II) Histochemical and morphological studies showed the degree of damage inflicted on hairy mouse ears by immersion in water at 51 “C and 53 “C for 20 s. At the lower temperature there was scattered epidermal cell damage, intracellular oedema and mitochodrial des- truction; however, most microvessels were patent. At 53 “C these changes were much more marked leading to complete epidermal destruction and lysis by 2 h after burning. Many microvessels were occluded by cellular aggregates or debris after endothelial cell destruction. Histochemically, succinic dehydrogenase activity was markedly different following injury at the two tempera- tures. There was only partial dysfunction in epidermal cells 2 h after scalding at 51 “C whereas there was an almost total absence of enzyme activity from 5 min post injury after a 53°C scald. Ear necrosis invariably followed injury at this latter temperature. Blomgren I., Johansson B. J. and Lilja J. (1984) A morphological and histochemical study of the scalded hairy mouse ear. Stand. J. Plast. Reconstr. Surg. 18, 217. Phagocytic cell dysfunction Functional defects were measured in circulating neut- rophils and pulmonary alveolar macrophages taken from rats with burns covering between 16 and 20 per cent of the body surface area. Both types of cell were studied by flow cytometry following stimulation with PMA, using various cyanine dyes and determination of the change in fluorescence intensity. In addition the rate of generation of superoxide was measured in the alveolar macrophages using superoxide dismutase and cytochrome C. The results showed that both cells types had a pro- found inhibition of cell function 4 h after the burn with a oartial return towards control values later. Addi- Duque R. E., Phan S. H., Hudson J. L. et al. (1985) Functional defects in phagocytic cells following thermal injury: application of flow cytometric analysis. Am. J. Puthol. 118, 116. Responses to endotoxin plus burns Sheep with lung and soft tissue lymph fistulae received either E. coli endotoxin alone or endotoxin 3-5 days after either a 25 per cent or a 50 per cent body surface area burn. All the sheep receiving toxin alone survived whereas 5 of 13 with 25 per cent burns plus endotoxin and 5 of 7 with 50 per cent burns plus endotoxin died. The causes of death in the animals were either an early severe hypoxia or a later increased pulmonary dysfunc- tion. Absolute levels of thromboxane A, were not increased in the post-burn animals, nor was there a clear release of thromboxane A, from burned tissue to explain the increased response. Prostacyclin levels were less elevated in the burned animals in response to endotoxin thereby altering the thromboxane Az to PGI, ratio in favour of thromboxane. Whether the thromboxane A, caused the lung injury is uncertain. The endotoxin did not alter either the lymph flow or its protein content. Wong C., Wenger H. and Demling R. H. (1985) Effect of a body burn on the lung response to endotox- in. J. Trauma 25, 53. Synergism between antibacterial agents A mixture of silver sulphadiazine (6 nmoUm1) and sodium piperacillin (7.5 nmol/ml) inhibited the in vitro growth of Ps. neruginosa, whereas the in vitro MICs of the compounds separately were 5OnmoVml for silver sulphadiazine and 250 nmol/ml for sodium piperacillin. In burned mice infected with either silver sulphadiazine resistant or sensitive strains, the mortality in groups receiving combinations of piperacillin and silver sulpha- diazine was O-IO per cent compared with a much higher mortality rate when the antibacterial agents were used separately. Modak S. and Fox C. L. (1985) Synergistic action of silver sulfadiazine and sodium piperacillin on resistant Pseudomonas aeruginosa in vitro and in experimental burn wound infections. J. Trauma 25, 21. Effects of smoke inhalation Smoke at a temperature of less than 39 “C was inhaled into the lungs of sheep. As also observed in man the sheep developed diffuse pulmonary mucosal sloughing, pulmonary oedema and a decrease in systemic oxygen tension. The pulmonary oedema was due to an increase in microvascular permeability, with a contribution from neutrophil degranulation. There was an increase in lung lymph flow, lymph to plasma protein concentra- tion ratio and transvaxular protein flux while the pul- tionally the plasma of burned rats taken 4 h after injury monary vascular pressures remained constant. _ was inhibitorv to normal rat neutroohils. Fluorescent Herndon D. N., Traber D. L., Niehaus G. D. et al. , compounds suggestive of in vivo l‘ipid peroxidation (1984) The patho-physiology of smoke inhalation in- were maximally detectable at this time. jury in a sheep model. J. Trauma 24, 1044.
Transcript of Phagocytic cell dysfunction
448 Burns 119851 Vol. 1 l/No. 8
direct observation using vital microscopy. Tissue sur- vival was measured by direct observation of the extent of necrosis.
Significant oedema formed in the ears heated at temperatures above 48 “C but never in the contralateral unburned ears. Ear tissue blood flow was reduced to near zero at times after injury which decreased as the scalding temperature increased. Ear tissue survival was complete at temperatures up to 51 “C, at 52 “C about 50 per cent of the ear became necrotic, at 53°C most of the ear tissue was destroyed and the entire ear became necrotic at a temperature of 54 “C and above. Neither prompt cooling of the ear after scalding nor pre-scald administration of cimetidine, ketanserin, indomethacin or methyl prednisolone were able to prevent the necro- sis of the scalded ears.
Blomeren I. and Baatre U. (1984) Postburn blood flow, edima and survives of thk hairy mouse ear after scald injury at different temperatures. Stand. J. Plust. Reconstr. Surg. 18, 269.
Scalds and tissue survival (Part II) Histochemical and morphological studies showed the degree of damage inflicted on hairy mouse ears by immersion in water at 51 “C and 53 “C for 20 s. At the lower temperature there was scattered epidermal cell damage, intracellular oedema and mitochodrial des- truction; however, most microvessels were patent. At 53 “C these changes were much more marked leading to complete epidermal destruction and lysis by 2 h after burning. Many microvessels were occluded by cellular aggregates or debris after endothelial cell destruction.
Histochemically, succinic dehydrogenase activity was markedly different following injury at the two tempera- tures. There was only partial dysfunction in epidermal cells 2 h after scalding at 51 “C whereas there was an almost total absence of enzyme activity from 5 min post injury after a 53°C scald. Ear necrosis invariably followed injury at this latter temperature.
Blomgren I., Johansson B. J. and Lilja J. (1984) A morphological and histochemical study of the scalded hairy mouse ear. Stand. J. Plast. Reconstr. Surg. 18, 217.
Phagocytic cell dysfunction Functional defects were measured in circulating neut- rophils and pulmonary alveolar macrophages taken from rats with burns covering between 16 and 20 per cent of the body surface area. Both types of cell were studied by flow cytometry following stimulation with PMA, using various cyanine dyes and determination of the change in fluorescence intensity. In addition the rate of generation of superoxide was measured in the alveolar macrophages using superoxide dismutase and cytochrome C.
The results showed that both cells types had a pro- found inhibition of cell function 4 h after the burn with a oartial return towards control values later. Addi-
Duque R. E., Phan S. H., Hudson J. L. et al. (1985) Functional defects in phagocytic cells following thermal injury: application of flow cytometric analysis. Am. J. Puthol. 118, 116.
Responses to endotoxin plus burns Sheep with lung and soft tissue lymph fistulae received either E. coli endotoxin alone or endotoxin 3-5 days after either a 25 per cent or a 50 per cent body surface area burn. All the sheep receiving toxin alone survived whereas 5 of 13 with 25 per cent burns plus endotoxin and 5 of 7 with 50 per cent burns plus endotoxin died. The causes of death in the animals were either an early severe hypoxia or a later increased pulmonary dysfunc- tion. Absolute levels of thromboxane A, were not increased in the post-burn animals, nor was there a clear release of thromboxane A, from burned tissue to explain the increased response. Prostacyclin levels were less elevated in the burned animals in response to endotoxin thereby altering the thromboxane Az to PGI, ratio in favour of thromboxane. Whether the thromboxane A, caused the lung injury is uncertain. The endotoxin did not alter either the lymph flow or its protein content.
Wong C., Wenger H. and Demling R. H. (1985) Effect of a body burn on the lung response to endotox- in. J. Trauma 25, 53.
Synergism between antibacterial agents A mixture of silver sulphadiazine (6 nmoUm1) and sodium piperacillin (7.5 nmol/ml) inhibited the in vitro growth of Ps. neruginosa, whereas the in vitro MICs of the compounds separately were 5OnmoVml for silver sulphadiazine and 250 nmol/ml for sodium piperacillin. In burned mice infected with either silver sulphadiazine resistant or sensitive strains, the mortality in groups receiving combinations of piperacillin and silver sulpha- diazine was O-IO per cent compared with a much higher mortality rate when the antibacterial agents were used separately.
Modak S. and Fox C. L. (1985) Synergistic action of silver sulfadiazine and sodium piperacillin on resistant Pseudomonas aeruginosa in vitro and in experimental burn wound infections. J. Trauma 25, 21.
Effects of smoke inhalation Smoke at a temperature of less than 39 “C was inhaled into the lungs of sheep. As also observed in man the sheep developed diffuse pulmonary mucosal sloughing, pulmonary oedema and a decrease in systemic oxygen tension. The pulmonary oedema was due to an increase in microvascular permeability, with a contribution from neutrophil degranulation. There was an increase in lung lymph flow, lymph to plasma protein concentra- tion ratio and transvaxular protein flux while the pul-
tionally the plasma of burned rats taken 4 h after injury monary vascular pressures remained constant. _ was inhibitorv to normal rat neutroohils. Fluorescent Herndon D. N., Traber D. L., Niehaus G. D. et al. , compounds suggestive of in vivo l‘ipid peroxidation (1984) The patho-physiology of smoke inhalation in- were maximally detectable at this time. jury in a sheep model. J. Trauma 24, 1044.
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