154 Burns (1990) Vol. 16/No. 2

from haemoglobin. Standard bum resuscitation does not restore adequate I& for tissue oxygen demands. The 30 per cent increase in PO, achieved by increasing & does not lead to a further release of oxidants.

Dernling R. H., Lalonde C., Fogt F. et al. (1989) EiTect of increasing oxygen delivery postbum on oxygen consumption and oxidant-induced lipid peroxidation in the adult sheep. Crit. Cure Med. 17, (lo), 1025-1030.

Oedema, histamine, complement and xanthine oxidaae Histamine, xanthine oxidase and oxygen radicals have a major role in the formation of bum oedema. Histamine and its metabolites stimulate the catalytic activity of xanthine ox&se, but not xanthine dehydrogenase, in the plasma and pulmonary artery endothelial cells of rats. Following burns there are parallel rises in the levels of histamine and xanthine ox&se. Burn oedema is reduced by treatment with a mast cell stabilizer (Gomolyn), by complement depletion and by cimetidine; it is not affected by neutrophil depletion.

Friedl H. P., Till G. O., Trentz 0. et al. (1989) Roles of histamine, complement and xanthine oxidase in thermal injury of skin Am. J Pa&d. 135, (I), 203-218.

Benefits of early enteral feeding Guinea-pigs with bums covering 30 per cent of the body surface area were resuscitated with equal volumes of either Ringer’s lactate solution or a liquid diet containing 20 per cent protein, 12 per cent lipid and 68 per cent carbohydrate by continuous infusion through a tube gastrostomy. The cardiac outputs in both groups were the same at 24 h postinjury and not less than those in unburned control animals. However, at 24 h postinjury the total jejunal blood flow was increased by 56 per cent and the caecal blood flow by 99 per cent in the diet group compared with the Ringer’s lactate group; which may have a beneficial effect on mucosal barrier function. The bums caused little change in the blood flow to tissues other than the intestine. Early feeding of the burned guinea-pigs suppressed the excessive cortisol response.

Inoue S., Lukes S., Alexander J. W. et al. (1989) Increased gut blood flow with early enteral feeding in burned guinea pigs.]. Bum Cure &!&if. 10, (4), 300-308.

Drug modification of arachidonic acid metabolites The effectiveness of three drugs (Venopirin, aspirin and Cataclot) which modify the arachidonate cascade reactions leading to thromboxane A, production were tested in burned rabbits.

In burned animals not treated with the drugs platelet reductions and renal dysfunction occurred within 8 h of injury; the renal abnormalities could not be prevented by adequate infusion therapy. However, giving Venopirin suppressed the reduction in platelet numbers and improved renal function. In contrast, giving aspirin or Catailot did not change-the reduced platelet numbers although they did improve renal fundion.

In animals not receiving any of these three drugs there were elevations in thromboxane B, and in the ratio of thromboxane B, to 6ketoprostaglandin F1+b. In contrast, the administration of these three drugs prevented these elevations.

Ono I., Ohura T., Azami K. et al. (1989) The effects of drugs on the arachidonate cascade in experimentally burned rabbits. J. Bum Care Rehabil. 10, (4), 314-320.

Postanaesthesia increased oxygen consumption Oxygen delivery (Do,) and oxygen consumption (Qo,) were studied in six sheep receiving only halothane anaesthesia and 14

sheep with full skin thickness burns covering 15 per cent of the body surface area and receiving the same anaesthesia for excision and grafting operations either 3 h or 5 days after injury.

In.the controls 3 h of anaesthesia reduced Do, by 22 per cent and Vo, by 30 per cent from awake values, primarily because of a decrease in cardiac output because oxygen extraction from haemoglobin also decreased. No base deficit developed. On regaining consciousness the Do, and Vo, transiently increased to 9 per cent above normal.

In the burned animals wound excision and complete graft cover 3 h after injury reduced the Do, by 24 per cent and the Vo, by 32 per cent. A base de&it of -3 mmol/l developed during the operation and Vo, increased to 25 per cent above normal when consciousness returned. In the bumed animals with wound excision and complete graft cover 5 days after injury the 00, decreased by 35 per cent, the Vo, decreased by 42 per cent and a base deficit of - 5 mmol/l developed Postoperatively an oxygen debt developed because Vo, increased by 32 per cent during 1-2 h after the return of consciousness. This oxygen debt was not caused by bacteraemia, or hypothermia, or the presence of an open wound, or shivering. The anaesthesia-induced oxygen debt developed because of the greatly increased tissue oxygen needs.

Demling R. H. and Lalonde C. (1989) Oxygen consumption is increased in the postanesthesia period after bum excision. J. Bum care R&&l. 10, (5), 381-387.

Altered RFS system activity following scalds The phagocytic activity of the reticuloendothelial system @ES) was measured in scalded rats using 99”‘Tc colloidal sulphur. Splemc phagocytic activity was reduced by the scald with most of the colloid being removed by lung tissue. Liver uptake of the colloid was virtually unchanged. The changes were observed within hours of injury and remained essentially unchanged for 7 days after injury. This failure of phagocytic activity may prevent the removal of bacterial and fungal cells from the blood.

Trop M., S&i&in E. J., Jung W. K. et al. (1989) Effect of acute bum trauma on phagocytic activity of the reticuloendothelial system in rats. J. Burn Care Rehabi~. 10, (S), 388-393.

Myelopoiesis in burned rats The leukocytosis stimulated by deep bums covering between 10 and 30 per cent of the body surface of rats consisted of an influx of morphologically mature appearing polymorphonuclear neutro- phils. Premature bone marrow release of immature cells did not contribute significantly. Bone marrow granulocyte activity examined by in vitro clonal cell cultures over a period of 5 weeks showed that marrow progenitor cell numbers were significantly increased for 2-4 weeks after injury.

Gruber D. F. and Farese A. M. (1989) Bone marrow myelopoie- sis in rats following loo/o, 2O%, or 30% thermal injury. J. Bum Care Rehabil. 10, (5), 410417.

Depressed host cellular defence mechanisms As part of the host defence mechanisms against bacterial and fungal infection resides with polymorphonuclear leucocytes (PMNLs), the effect of thermal injury on these cells was deter- mined in rats. Deep burns covering 20 per cent of the body surface produced a marked increase in the numbers of PMNLs in blood for up to 6 weeks aft er injury but the cells were individually less active. The cells were electrophysiologically less responsive (an altered state of membrane depolarization) and they produced less H,O, (a depressed oxidative capability). Both these aspects of PMNL cell function reduced their ability to combat infection.

Gruber D. F. and D’Alesandro M. M. (1989) Alteration of rat polyrnorphonuclear leukocyte function after thermal injury. J. Bum Care R&&l. 10, (5), 394401.