74 Burns (1990) Vol. 16/No. 1

activity. Inhibition of xanthine oxidase activity by allopurinol prevents endotoxin-induced mucosal injury and reduces the incidence of bacterial translocation from 83 per cent to 30 per cent.

Deitch E. A., Ma W. J., Li M. et al. (1989) Endotoxin-induced bacterial translocation: a study of mechanisms. Surgpry 106, (2), 292-300.

Oxygen free radicals, Factor VIII antigen and tissue damage Rats with deep burns were used to explore whether oxygen free radicals from xanthine oxidase contributed to the release of Factor VIII antigen in organ endothelial cells distant from a bum. Compared with sham burned animals there was an increase in Factor VIII antigen in blood but a decrease in lung and kidney tissue contents. These changes appeared to be the result of xanthine oxidase metabolites since they did not occur in rats pretreated with allopurinol (a specific xanthine oxidase inhibitor) or dimethylthiourea (a permeable oxygen free radical scavenger).

Gross0 M. A., Viders D. E., Brown J. M. et al. (1989) Local skin burn causes systemic (lung and kidney) endothelial cell injury reflected by increased circulating and decreased tissue Factor VIII related antigen. Surgery 106, (2), 3lO-317.

Bile content of IgA in burned rats The bile content of IgA in rats with 20-30 per cent TBSA bums was found to be decreased by 90 per cent by 18-21 h after injury. In contrast, the bile volume, the concentration of bile protein and the free secretory component had not changed. Although blood flow to the liver 18 h after burning was not changed, there was a significant reduction in the total IgA concentration in plasma; both mIgA and pIgA were decreased. Decreased local hepatic synthesis and or transport of pIgA across the hepatocyte may have caused the reduced bile content of IgA.

Hormatz P. R., Carter E. A., Sullivan D. et al. (1989) Effect of thermal injury in the rat on transfer of IgA protein into bile. Ann. surg. 210,(2), 203-207.

Bacterial translocation in genetically distinct mice The rate of bacterial translocation from the gastrointestinal tract was assessed in three genetically distinct strains of mice with 25 per cent TBSA bums. Translocation to the mesenteric lymph nodes occurred in Balb/c mice but not in CD-l or C57/bl mice. This translocation occurred with bum-induced gut mucosal injury, which was only present in the Balb/c mice.

Part of the gut mucosal injury appears to be due to xanthine oxidase-generated oxygen free radicals since inhibition of xanthine oxidase activity with allopurinol, or inactivation of the enzyme by a molybdenum-free tungsten diet prevented the mucosal injury and reduced the extent of bacterial translocation.

Ma L., Ma J. W., Deitch E. A. et al. (1989) Genetic susceptibility to mucosal damage leads to bacterial translocation in a murine bum model. 1. Trauma 29, (9), 1245-1251.

Keratinocyte growth on collagen sheet Control or low calcium supplemented media were used to culture rat keratinocytes on a collagen sheet. The rate of proliferation of these cells was assessed by the rate of incorporation of [‘HI thymidine into DNA and showed that cells grown in the supplemented media had an enhanced rate of proliferation. Full skin thickness defects on rats were covered with this keratinocyte collagen sheet culture and then biopsied 45 and 60 days later. The re-epithelialized wounds showed Barr bodies, thereby confirming the presence of the original keratinocytes.

Morykwas M. J., Stevenson T. B., Marcel0 C. L. et al. (1989) In vitro and in vivo testing of a collagen sheet to support keratinocyte growth for use as a bum wound covering. J. Truuma 29, (8), 1163-1167.

Tissue permeability and isoproterenol The role of bradykinin in altered capillary permeability was assessed in canine hind paw skin following a continuous femoral artery infusion. Two hours of infusion produced marked increases in skin lymph flow, skin lymph to plasma total protein concentra- tion and femoral artery blood flow. At the end of this infusion five dogs received isoproterenol which increases heart rate and reversed the increase in lymph to plasma total protein concentra- tions. When bradykinin was infused for 8 h there was less albumin in the tissues of dogs given isoproterenol.

Mullins R. J., Malias M. A. and Hudgens R. W. (1989) Isoproterenol inhibits the increase in microvascular membrane permeability produced by bradykinin. J. Trauma 29, (8). 1053- 1064.

Postburn complement-mediated haemodynamic changes Complement depleted or control rats received either a scald or sham scald covering 50 per cent TBSA. Measurements were then made of cardiac output (CO), mean arterial pressure (MAP), heart rate, systemic vascular resistance (SVR), stroke volume, cardiac power, haematocrit and complement activity. In rats with normal complement levels the bum produced a marked early depression in CO and MAP and a rise in SVR. The haemodynamics returned to normal by 12 h and became hyperdynamic by 24 h. Serum haemolytic complement activity fell immediately and progres- sively after the bum, indicating significant complement activation.

Complement depletion attenuated the early decline in CO, limited the rise in SVR, improved the heart rate, stroke volume and the late cardiac function.

Schirmer W. J., Schirmer J. M., Naff G. B. et al. (1989) Complement-mediated hemodynamic depression in the early postbum period. 1, Trauma 29, (7), 932-939.

Granulocyte stimulation and survival A large number of mice with burns covering 15 per cent TBSA were used to test whether granulopoietic growth factor (G-CSF), used in combination with gentamicin to treat Ps. aerug&u- infected bums, could improve the survival rates of the animals. The five groups of animals were: (1) burn only ; (2) burn + infec- tion; (3) burn +.infection + G-CSF; (4) bum + infection + gen- tamicin; (5) burn + infection + gentamicin + G-CSF. All treatment groups showed improved survival compared with the bum -t infection group which all died by day 9 postbum. Group 5 showed improved survival compared with groups 3 and 4.

Silver G. M., Gamelli R. L. and O’Reilly M. (1989) The beneficial effect of granulocyte colony stimulating factor (G-CSF) in combination with gentamicin on survival after pseudomonas bum wound infection. Surgoy 106, (2), 452-456.

LABORATORY STUDIES

Factors suppressing fibroblast proliferation Macrophage regulation of Abroblast proliferation was investi- gated. Unstimulated macrophages produce growth factors that increase proliferation. Activation of macrophages by hypoxia alone had little effect on macrophage regulation of fibroplasia. Lipopolysaccharide (LPS)-activated macrophages suppressed fibroplasia and the combination of hypoxia and LPS augmented the suppression.

Conditioned supematants from LPS-activated macrophages contained mr Tumour Necrosis Factor alpha, which by itself can suppress fibroblast proliferation in relatively high concentrations.

Bankey P., Fiegel V., Singh R. et al. (1989) Hypoxia and endotoxin induce macrophage-mediated suppression of fibroblast proliferation. J. Trauma 29, (7), 972-980.