- Email: [email protected]
Animal model for hypermetabolism
Abstracts
Incidence of autoantibodies Indirect immunofluorescence tests for autoantibodies were made on the sera from 51 patients with burns covering between 0.5 and 80 per cent of the body surface. Anti-smooth muscle antibodies were found in 36-6 per cent of the patients within 24 h of burning, and antimitochondrial antibodies were found in 31'8 per cent by the same time. Antinuclear antibodies were only rarely found. The frequency with which smooth muscle antibodies were observed increased with the increasing severity of the burn, in contrast to the lack of any relationship with antimitochondrial antibodies. No correlation was found between the appearance of the anti-smooth muscle, or the antimitochondrial antibodies and subsequent changes in the clinical condition of the patients. Dobke M., Danowska A. and Kondrat W. (1978) Antinuclear (ANA), antimitochondrial (AMA) and anti-smooth muscles (SMA) autoantibodies following thermal trauma. Burns 5 195.
A N I M A L STUDIES Animal model for hypermetabolism Growing guinea-pigs and mature rats are good models of the human metabolic response to thermal injury, showing a dose-response relationship between burn size and metabolic rate; an elevation in metabolic rate related to the stage of convalescence and hypermetabolism that may be altered but not abated by external heating. A 50 per cent body surface burn must be produced before reliable elevations in metabolic rate are observed. The mature rat is the better model and is suitable for evaluation of the mediators and modulators of the hypermetabolic response to thermal injury. Herndon D. N., Wilmore D. W. and Mason A. D. (1978) Development and analysis of a small animal model simulating the human postburn hypermetabolic response, J. Surg. Res. 25, 394.
Glucose kinetics There are persistent alterations in glucose metabolism in the rat during the first week after a burn covering 20 per cent of the body surface. The basal rate of endogenous glucose production is elevated, and it is not suppressed to a normal level by the infusion of glucose. Hormone estimations suggest that the increased glucagon levels cause the elevated rate of gluconeogenesis both before and during glucose infusion. Basal glucose uptake was also elevated after burning and there was a normal increment in the glucose metabolic clearance rate during an infusion of glucose. The increase in the glucose metabolic clearance rate, relative to the increase in the insulin concentration, was equal in the burned and non-burned control rats. This indicated a normal responsiveness
355
to insulin after burning. As there 'was no impairment in the capacity to take up exogenous glucose there seems no necessity to treat the hyperglyeaemia resulting from glucose infusions by treating the presumed insulin resistance with the administration of exogenous insulin. Allsop J. R., Wolfe R. R. and Burke J. F. (1978) Glucose kinetics and responsiveness to insulin in rats injured by burns. Surg. Gyneeol. Obstet. 147, 565.
Nicotinic acid and vascular permeability Nicotinic acid has been suggested to decrease plasma volume loss after burns. However, conflicting data have appeared recently, with reports of laboratory measurements of major derangements in cardiovascular function after extensive full-thickness skin loss burns. Investigations were carried out on the microvascular effect of nicotinic acid on water and albumin leakage after small partial-thickness skin loss burns in the rat. No effect of nicotinic acid on albumin leakage was observed at 30 min, 3 h and 6 h. A minimal but significant (P<0"05) decrease in water content of burned tissue was observed 30 min post burn. The studies confirm in rats the previous work with sheep and dogs, showing that nicotinic acid has slight, if any, effect on fluid and protein loss after burns. Brouhard B. H., Carvajal H. F. and Miller T. H. (1978) Effect of nicotinic acid on vascular permeability after thermal trauma in the rat. J. Trauma 18, 774.
Gastric mucosal lesions and pH Two hours after rats were subjected to full-thickness skin loss burns covering 30 per cent of the body surface, 93 per cent of the animals had gastric mucosal erosions. At 5 h this increased to 100 per cent, but at 24 and 72 h the lesions were fewer and less severe. Histological study suggested that lesions noted at 24 and 72 h represented erosions formed earlier. No mucosal abnormalities were noted in control rats. A causal relationship between mucosal ischaemia and the development of erosions is suggested by the presence of arteriovenous shunts at 2 and 5 h only. Significant increases in H + back diffusion and protein leakage into the gastric lumen at 2 and 5 h also implicated changed mucosal permeability in the aetiology of erosions. The return of H + back diffusion to control values at 24 and 72 h, when lesions were still present, appears to contradict the theory that permeability changes are secondary to erosion formation. Kitajima M., Wolfe R. R., Trelstad R. L. et al. (1978) Gastric mucosal lesions after burn injury: relationship to H + back diffusion and the microcirculation. J. Trauma 18, 644.
Incidence of autoantibodies Indirect immunofluorescence tests for autoantibodies were made on the sera from 51 patients with burns covering between 0.5 and 80 per cent of the body surface. Anti-smooth muscle antibodies were found in 36-6 per cent of the patients within 24 h of burning, and antimitochondrial antibodies were found in 31'8 per cent by the same time. Antinuclear antibodies were only rarely found. The frequency with which smooth muscle antibodies were observed increased with the increasing severity of the burn, in contrast to the lack of any relationship with antimitochondrial antibodies. No correlation was found between the appearance of the anti-smooth muscle, or the antimitochondrial antibodies and subsequent changes in the clinical condition of the patients. Dobke M., Danowska A. and Kondrat W. (1978) Antinuclear (ANA), antimitochondrial (AMA) and anti-smooth muscles (SMA) autoantibodies following thermal trauma. Burns 5 195.
A N I M A L STUDIES Animal model for hypermetabolism Growing guinea-pigs and mature rats are good models of the human metabolic response to thermal injury, showing a dose-response relationship between burn size and metabolic rate; an elevation in metabolic rate related to the stage of convalescence and hypermetabolism that may be altered but not abated by external heating. A 50 per cent body surface burn must be produced before reliable elevations in metabolic rate are observed. The mature rat is the better model and is suitable for evaluation of the mediators and modulators of the hypermetabolic response to thermal injury. Herndon D. N., Wilmore D. W. and Mason A. D. (1978) Development and analysis of a small animal model simulating the human postburn hypermetabolic response, J. Surg. Res. 25, 394.
Glucose kinetics There are persistent alterations in glucose metabolism in the rat during the first week after a burn covering 20 per cent of the body surface. The basal rate of endogenous glucose production is elevated, and it is not suppressed to a normal level by the infusion of glucose. Hormone estimations suggest that the increased glucagon levels cause the elevated rate of gluconeogenesis both before and during glucose infusion. Basal glucose uptake was also elevated after burning and there was a normal increment in the glucose metabolic clearance rate during an infusion of glucose. The increase in the glucose metabolic clearance rate, relative to the increase in the insulin concentration, was equal in the burned and non-burned control rats. This indicated a normal responsiveness
355
to insulin after burning. As there 'was no impairment in the capacity to take up exogenous glucose there seems no necessity to treat the hyperglyeaemia resulting from glucose infusions by treating the presumed insulin resistance with the administration of exogenous insulin. Allsop J. R., Wolfe R. R. and Burke J. F. (1978) Glucose kinetics and responsiveness to insulin in rats injured by burns. Surg. Gyneeol. Obstet. 147, 565.
Nicotinic acid and vascular permeability Nicotinic acid has been suggested to decrease plasma volume loss after burns. However, conflicting data have appeared recently, with reports of laboratory measurements of major derangements in cardiovascular function after extensive full-thickness skin loss burns. Investigations were carried out on the microvascular effect of nicotinic acid on water and albumin leakage after small partial-thickness skin loss burns in the rat. No effect of nicotinic acid on albumin leakage was observed at 30 min, 3 h and 6 h. A minimal but significant (P<0"05) decrease in water content of burned tissue was observed 30 min post burn. The studies confirm in rats the previous work with sheep and dogs, showing that nicotinic acid has slight, if any, effect on fluid and protein loss after burns. Brouhard B. H., Carvajal H. F. and Miller T. H. (1978) Effect of nicotinic acid on vascular permeability after thermal trauma in the rat. J. Trauma 18, 774.
Gastric mucosal lesions and pH Two hours after rats were subjected to full-thickness skin loss burns covering 30 per cent of the body surface, 93 per cent of the animals had gastric mucosal erosions. At 5 h this increased to 100 per cent, but at 24 and 72 h the lesions were fewer and less severe. Histological study suggested that lesions noted at 24 and 72 h represented erosions formed earlier. No mucosal abnormalities were noted in control rats. A causal relationship between mucosal ischaemia and the development of erosions is suggested by the presence of arteriovenous shunts at 2 and 5 h only. Significant increases in H + back diffusion and protein leakage into the gastric lumen at 2 and 5 h also implicated changed mucosal permeability in the aetiology of erosions. The return of H + back diffusion to control values at 24 and 72 h, when lesions were still present, appears to contradict the theory that permeability changes are secondary to erosion formation. Kitajima M., Wolfe R. R., Trelstad R. L. et al. (1978) Gastric mucosal lesions after burn injury: relationship to H + back diffusion and the microcirculation. J. Trauma 18, 644.