Endotoxin and thromboxane A2 production
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532 Burns (1986) Vol. 12/No. 7 late maintained body weight, induced a better nitrogen balance, caused significant increases in the weights of the carcass, liver and gastrocnemius muscle and higher levels of serum albumin, transferrin and C3. Trocki 0.. Mochizuki H., Dominioni L. et al. (1986) Intact protein versus free amino acids in the nutritional support of thermally injured animals. J. Parenter. Entr. Nutr. 10, (2). 139-145. Early and late oedema formation The rates of tissue oedema formation and lymph Row were measured in burned sheep. Both early (within 8 h of injury) and late (5 days post-injury) oedema forma- tion was markedly increased by 2-3 mmHg increases in microvascular hydrostatic pressure. The early oedema formation was attributed to over zealous fluid resuscita- tion. The late oedema formation, in response to a slight microvascular pressure increase, is presumably a reflec- tion of incomplete healing of pores within the vascular endothelium. Inhibition of the local release of prostacy- clin did not alter the rate of early or late oedema formation. Ryan P., Katz A., Lalonde C. et al. (1986) Effect of microvascular hydrostatic pressure and local prostanoid production on early and late postburn edema forma- tion. J. Burn Care Rehahil. 7, (l), 15-23. Endotoxin and thromboxane A2 production In sheep with deep burns covering 25 per cent of the body surface area E. coli endotoxin was injected either beneath the eschar or intravenously. Subeschar inoculation produced a marked increase in burn tissue content of thromboxane A2-as reflected by increases in burn lymph and pulmonary artery thromboxane B2 levels. Pulmonary artery pressure in- creased, Paoz decreased and lung lymph flow only showed a moderate increase with no evidence of in- creased lung permeability. Thromboxane A2 produc- tion and the lung response were prevented by the subeschar inoculation of ibuprofen. Intravenous endotoxin produced a significant increase in lung thromboxane A2 and a two-phase lung injury, the first phase being similar to that seen with the subeschar inoculation, followed by an increase in lung protein permeability. Burn tissue endotoxin can stimulate local thromboxane A2 production leading to distant lung dysfunction without the need for circulating endotoxin. The source of the thromboxane A2 is the burn, while with endotoxin the source is the lung. Demling R. H., Wenger H., Lalonde C. C. et al. (1986) Endotoxin induced prostanoid production by the burn wound can cause distant lung dysfunction. Surgery 99, (4). 421-431.
Transcript of Endotoxin and thromboxane A2 production
532 Burns (1986) Vol. 12/No. 7
late maintained body weight, induced a better nitrogen balance, caused significant increases in the weights of the carcass, liver and gastrocnemius muscle and higher levels of serum albumin, transferrin and C3.
Trocki 0.. Mochizuki H., Dominioni L. et al. (1986) Intact protein versus free amino acids in the nutritional support of thermally injured animals. J. Parenter. Entr. Nutr. 10, (2). 139-145.
Early and late oedema formation The rates of tissue oedema formation and lymph Row were measured in burned sheep. Both early (within 8 h of injury) and late (5 days post-injury) oedema forma- tion was markedly increased by 2-3 mmHg increases in microvascular hydrostatic pressure. The early oedema formation was attributed to over zealous fluid resuscita- tion. The late oedema formation, in response to a slight microvascular pressure increase, is presumably a reflec- tion of incomplete healing of pores within the vascular endothelium. Inhibition of the local release of prostacy- clin did not alter the rate of early or late oedema formation.
Ryan P., Katz A., Lalonde C. et al. (1986) Effect of microvascular hydrostatic pressure and local prostanoid production on early and late postburn edema forma- tion. J. Burn Care Rehahil. 7, (l), 15-23.
Endotoxin and thromboxane A2 production In sheep with deep burns covering 25 per cent of the body surface area E. coli endotoxin was injected either beneath the eschar or intravenously.
Subeschar inoculation produced a marked increase in burn tissue content of thromboxane A2-as reflected by increases in burn lymph and pulmonary artery thromboxane B2 levels. Pulmonary artery pressure in- creased, Paoz decreased and lung lymph flow only showed a moderate increase with no evidence of in- creased lung permeability. Thromboxane A2 produc- tion and the lung response were prevented by the subeschar inoculation of ibuprofen. Intravenous endotoxin produced a significant increase in lung thromboxane A2 and a two-phase lung injury, the first phase being similar to that seen with the subeschar inoculation, followed by an increase in lung protein permeability. Burn tissue endotoxin can stimulate local thromboxane A2 production leading to distant lung dysfunction without the need for circulating endotoxin. The source of the thromboxane A2 is the burn, while with endotoxin the source is the lung.
Demling R. H., Wenger H., Lalonde C. C. et al. (1986) Endotoxin induced prostanoid production by the burn wound can cause distant lung dysfunction. Surgery 99, (4). 421-431.
