Abstracts

significantly subnormal for I4 to 28 days after burning; the MLC responses were significantly depressed at 48 hours after burning but then quickly returned to normal. As the proliferative capacity of T cells to soluble antigens is contained within the inducer cell subpopulation and both inducer and suppressor sub- population cells respond to MLC, the observed increase in MLC responses, coupled with a sustained depression of SKSD and mumps responses, suggests activation of a population of suppressor cells. A direct assay of the suppressor cell function confirmed these results.

Keane R. M., Munster A. M., Birmingham W. et al. (1982) Suppressor cell activity after major injury. Indirect and direct functional assays. J. Truuma 22, 770.

Neutrophil chemotactic responses Serial measurements of neutrophil chemotaxis were made in 34 patients with a mean bum size of 33 per cent (range IO-75 per cent)of the body surface area to determine whether the commonly observed impaired chemotaxis is primarily related to an acquired cellular defect or to humoral factors. Twenty-eight of the 34 patients showed an impaired chemotactic response which could not be attributed to cell directed inhibi- tors or inactivators. The chemotactic defect could not be reversed by normal human serum suggesting that the defect was not related to the absence of normal circulating humoral substances. Silver sulphadiazine had no suppressive effect on neutrophil chemotaxis. Impaired neutrophil chemotaxis following burning injury appears to be due to an acquired cellular defect.

Deitch E. A. and McDonald J. C. (1982) Influence of serum on impaired neutrophil chemotaxis after thermal injury. J. Sicrx Rcs. 33, 25 I.

Virus induced fever Four patients out of 73 admissions with bums covering more than 40 per cent of the body surface had pro- longed fevers (temperatures between 38.3” and 40.0 “C for periods of between one week and one month) occuring at least one month after burning. The patients had lymphocytosis without atypical lympho- cytes and were subsequently shown to have cytomega- lovirus infections with titres rising to I in 1024. The cause of unexplained fevers should always be con- sidered before prescribing potentially toxic and very expensive antibiotics for presumed bacterial causes of fever.

Deepe G. S., MacMillan B. G. and Linneman G. C. (I 982) Unexplained fever in bum patients due to cyto- megalovirus infection. J. Amer. Med. Assoc. 248,2299.

LABORATORY STUDIES Gastrointestinal tract activity Gastric emptying time, small intestinal motility and colonic transit time were measured in rats with bums covering about I5 per cent of the body surface area. Compared with the findings in normal control rats the bum injury caused a marked inhibition of gastro- intestinal motility. This inhibition was significantly

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improved by a continuous saline infusion, whereas saline infusion alone had no effect on the gastro- intestinal propulsive motility of normal rats.

Chen C. F., Chapman B. J., Munday K. A. et al. (1982) The effects of thermal injury on gastrointestinal motor activity in the rat. Burns 9, 142.

Cholinesterase in healing tissue The regeneration of cholinesterase positive structures was studied during the healing of full thickness skin loss bums in guinea-pigs. Acetylcholinesterase ac- tivity disappeared from the burned tissue within I4 days of injury and then reappeared after the third week. Cholinergic fibres innervating arterioles became visible on the 2lst day and thereafter gradually increased in number and staining intensity at the edges of the bum. In the centre of the healing bum the cholinergic fibres disappeared during the fourth week after burning either because of an absence of target organs or because of the formation of dense collagenous scar tissue.

Kishimoto S., Maruo M.. Yasuno H. et al. (1982) The regeneration of cholinesterase positive structures in the process of bum wound healing in the skin of the guinea-pig. Bllrns. 9, I2 I.

Healing and catecholaminergic nerve fibres The changes in catecholaminergic nerve tibres was studied during the healing of full thickness skin loss burns in guinea-pigs. Fluorescence histochemistry showed sympathetic denervation within 48 hours of burning and regenerating sympathetic fibres by 7 days after burning. Regenerating fibres surrounded regener- ating blood vessels at the edges of the bum and gradually increased in number and density until about 2 weeks after burning. Thereafter the density of the fibres decreased. As the wound contracted there was degeneration of both blood vessels and nerve libres in the central area of the wound.

Kishimoto S., Maruo M., Ohse C. et al. (1982) The regeneration of the sympathetic catecholaminergic nerve fibres in the process of bum wound healing in guinea-pigs. J. Invest. Dermatol. 79, 141.

Causes of anaemia The anaemia of thermal injury appears to be due at least in part to inhibition of erythropoiesis. In vitro studies showed that serum from burned patients inhi- bited red cell but not white cell colony growth and that this effect was related to the presence of a substance in the serum rather than to the absence of a factor required for colony formation. The inhibitory effect was also not due to topical medications nor to episodes of bacterial sepsis at the time the serum was obtained. Serial studies showed that inhibition was often not pre- sent in the immediate postbum period but developed gradually reaching a maximal intensity 20 to 30 days after burning and then gradually returned towards normal as the bum healed.

Wallner S. F., Vautrin R. M. Buerk C. et al (1982) The anaemia of thermal injury: studies of erythropoiesis rn r,i/ro. J. Truumu. 22, 774.