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PubMed1988

Attenuation of burn-induced changes in hemodynamics and glucose metabolism by the PAF antagonist SRI 63-675.

The importance of platelet-activating factor (PAF) in producing hypotension, hemoconcentration and alterations in carbohydrate metabolism following thermal injury was investigated in chronically catheterized rats. Animals were fasted overnight, anesthetized with pentobarbital, and then injected with saline or the PAF antagonist SRI 63-675 prior to a 25% body surface area scald injury. Burned animals showed a sustained 20-30% fall in mean arterial pressure that was attenuated by the PAF antagonist. Burn also produced a prolonged increase in hematocrit. Animals pretreated with SRI 63-675 showed a similar degree of polycythemia after 1 h, but thereafter hematocrit fell and was not different from sham-burned animals. Burn increased the plasma glucose (45-52%) and lactate (5-6 fold) concentrations, and tended to produce an early increase and a later decrease in the rate of glucose appearance (Ra). These metabolic changes were associated with elevated plasma levels of glucagon and catecholamines. The PAF antagonist prevented the hyperglycemia, reduced the hyperlactacidemia, and prevented the late fall of glucose Ra. Treated animals still showed increased levels of glucagon, while catecholamine concentrations were reduced by 50%. Short-term survival (4 h) was markedly improved (86 vs. 43%). These results suggest that PAF produced following thermal injury is responsible, at least in part, for the early hemodynamic changes and hemoconcentration. However, the role of PAF as a mediator of burn-induced glucose dyshomeostasis appears secondary to its hemodynamic effects.

Animals↗
PubMed1992

Influence of a long-acting bradykinin antagonist, Hoe 140, on some acute inflammatory reactions in the rat.

We studied the influence of Hoe 140, a bradykinin antagonist, on inflammatory reactions induced in rats. Hoe 140 reduced paw oedema induced by bradykinin alone, bradykinin plus prostaglandin (PG) E1, carrageenan, urate crystals or urate crystals plus captopril. The inhibitory effect of Hoe 140 lasted for at least 4 h. Hoe 140 also reduced plasma exudation in sponges implanted in the back of the rat. However it did not modify paw oedema induced by zymosan or by heating the paw at 55 degrees C for 30 s. Carrageenan oedema developed to a small extent in kininogen-deficient rats while the swelling induced by heating the paw of kininogen-deficient rats was the same as that measured in normal animals. Hoe 140 had no effect on the slight swelling induced by carrageenan in kininogen-deficient rats. We conclude that the kinin system is involved in inflammatory reactions induced by carrageenan, urate crystals, sponge implantation but not by zymosan and scalding.

Alprostadil↗
PubMed1975

Burns to infants using walking aids.

Thirty-one burns and scalds to infants using walking aids are recorded. The mechanism of injury and resulting morbidity are described. The need for more rigerous precautions is discussed.

Accidents, Home↗
PubMed1984

Clinical experience with a new hydrogel wound dressing.

A new dressing is described which appears to improve wound healing after partial-thickness skin loss. The period between dressing changes is increased and patient discomfort decreased. It has been particularly useful in the treatment of scalds in children. There is no evidence of an increased infection rate. Alternative methods of sterilization may reduce the small number of minor hypersensitivity reactions.

Burns↗
PubMed1993

Paediatric trauma in the rural developing world: low cost measures to improve outcome.

We reviewed 181 injured children admitted to a rural African hospital from 1987 to 1990 to ascertain factors influencing survival and functional outcome. Burns were the most common (39 per cent), occurred in the youngest patients, and were due to domestic scalding in 54 per cent of cases. Of the patients, 65 per cent presented more than 24 h after injury and 81 per cent presented without any previous treatment. Major disability occurred in 14 per cent of survivors and was associated with Injury Severity Score (ISS), extremity injury, and delayed presentation. Mortality was associated with the ISS. The mean ISS was 6.3. An ISS of 20-25 was associated with 75 per cent mortality. Trauma caused 8 per cent of hospital deaths in the 5-19 years age group. To reduce the mortality and disability from paediatric trauma in the rural developing world, we recommend: (i) prevention strategies targeting domestic burns in younger children, (ii) increased attention to care of extremity injuries and burns, and (iii) increased use of non-medical health care providers in more remote areas.

Adolescent↗
PubMed1989

Burn injuries during the puerperium in Zaria, Nigeria.

Of the 35 women who sustained burn injuries during the puerperium in Zaria, 31 had practised ritual hot baths or "Wankan-jego" which caused severe scalds. Five of the women also developed peripartum cardiac failure. Two died. Three of the newborns also died partly as a result of the mothers' illness. Formal education and general economic development would help in eliminating this preventable source of maternal and infant morbidity and mortality.

Adolescent↗
PubMed1983

Neutral proteinase activity in skeletal muscle from thermally injured rats.

Male Sprague-Dawley rats that received 60% total body surface, full-thickness, scald burns on the dorsum and abdomen were used in this study. Neutral proteinase and Ca2+-activated neutral proteinase activities were measured in gastrocnemius and soleus muscles at 3 and 21 days after the thermal injury. Neutral proteinase activity decreased significantly in the soleus (50%) and gastrocnemius (46%) muscles on the third postburn day. Ca2+-activated neutral proteinase was unchanged at this time. Neutral proteinase and Ca2+-activated neutral proteinase activities were unaltered at 21 days postinjury. These results may reflect a protein-sparing effect on the third postburn day which could be an early intracellular change prior to an increase in selected enzyme proteins during the hypermetabolic phase after thermal injury.

Animals↗
PubMed1984

The immunomodulating effect of TP5 and indomethacin in burn-induced hypoimmunity.

Hypoimmunity after major trauma and thermal injury appears to predispose to septicemia. An increase of immune suppressive T cells and the inhibitory monocytes product PGE2 has been demonstrated postburn and are suggested as contributing to postburn hypoimmunity. TP5, the biologically active part of thymopoientin, has an immunomodulating effect on T cells. Indomethacin, an irreversible blocker of the prostaglandin synthesis has been suggested to reduce the inhibitory monocytes-mediated immunosuppression. In this study strains 2 and 13 guinea pigs received 20-30% TBSA scald burn and were subsequently injected with either TP5 or indomethacin or a combination of both on the 3 following days postburn. The ability of splenocytes to produce a secondary immune response to SRBC was measured in the in vitro AFC assay. The animals who had received TP5 and indomethacin showed significant improvement in their ability to mount an immune response in the AFC assay.

Animals↗
PubMed1987

Analysis of altered capillary pressure and permeability after thermal injury.

In order to investigate the effects of thermal injury on microvascular hemodynamics and permeability, hindpaw arterial (PA), venous (PV), and capillary (PC) pressures, blood (QB) and lymph (QL) flows, and lymph (CL) and plasma (CP) total protein concentrations were measured before and for 3 hr after a 10-sec 100 degrees C scald burn in 11 dogs. Prior to injury in eight experiments (Group I--permeability analysis) venous pressure was elevated by outflow restriction until the minimal CL/CP was obtained. In three experiments (Group II--hemodynamic analysis) outflow was not restricted. Lymph and plasma protein fractions ranging in size from 37 to 120 A were measured using gradient gel electrophoresis and capillary equivalent pore sizes were calculated. In the early postburn period, PC increased from 24 +/- 2 (mean +/- SE) to 47 +/- 5 mm Hg (P less than 0.05) and precapillary resistance (RA) decreased from 6.6 +/- 0.2 to 2.5 +/- 0.2 mm Hg/ml/min/100 g (P less than 0.05) while postcapillary resistance (RV) remained unchanged. Pre- to postcapillary resistance (RA/RV) fell by 74%. The reflection coefficient for total proteins (calculated as sigma = 1 - CL/CP) decreased from 0.87 +/- 0.01 to 0.45 +/- 0.02 (P less than 0.01). Permeability of the postburn capillary endothelium was described by using two populations of equivalent pores. Preburn pore radii were 50 and 300 A with 13% of the capillary filtrate passing through the large pores. Pore radii increased after injury to 70 and 400 A with 49% of the filtrate passing through the large pores. The postburn total tissue filtration coefficient (Kf) increased to 2.4 times the control. Over the first 3 hr postburn, 53% of the increase in capillary filtration was attributable to increased capillary pressure and 47% to increased permeability. We conclude that the early rapid edema formation following thermal injury is the result of marked increases in both capillary filtration pressure and filtration through large nonsieving pores.

Animals↗
PubMed1987

Flow redistribution in a hyperdynamic small animal burn: comparison to patterns in sepsis.

Visceral hypoperfusion with local accumulation of lactate in the ischemic tissues has been reported in a septic rat model despite a hyperdynamic systemic circulation. This visceral ischemia is felt to contribute to the multiple system organ failure (MSOF) syndrome associated with sepsis. The purpose of this study was to determine whether a similar redistribution of blood flow existed in rats after a severe thermal injury as it too is associated with MSOF. Twenty-four hours after animals were subjected to either a resuscitated 50% scald burn (BURN) or sham treatment (SHAM), thermodilution cardiac output (CO), effective hepatic blood flow (EHBF) by galactose clearance at low concentrations, effective renal plasma flow (ERPF) by para-aminohippurate clearance, and blood, liver, and skeletal muscle pyruvate (P), and lactate (L) concentrations were determined. CO increased 52% in BURN (46.5 +/- 2.8 ml/min/100 g, n = 21) versus SHAM (30.7 +/- 1.0 ml/min/100 g, n = 22; P less than 0.001) while EHBF increased only 18% (BURN: 6.81 +/- 0.36 ml/min/100 g, n = 8 vs SHAM: 5.77 +/- 0.29 ml/min/100 g, n = 8; P less than 0.025) and ERPF showed an insignificant 24% increase (BURN: 2.98 +/- 0.32 ml/min/100 g, n = 6 vs SHAM: 2.40 +/- 0.40 ml/min/100 g, n = 6; P less than 0.10), demonstrating a redistribution of flow. There was no local accumulation of lactate in blood, liver, or skeletal muscle and no derangement in P/L ratios. This study when compared to previous observations in sepsis suggests that (1) the flow redistribution of sepsis has features differentiating it from solely a "stress response".(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effect of indomethacin on burn-induced immunosuppression.

Recent interest in the role of prostaglandin inhibitors as immunomodulators following major injury prompted us to study the effect of indomethacin on burn-induced immunosuppression in rats as measured by the delayed-type hypersensitivity (DTH) skin test response, ability to contain an intradermal bacterial challenge (10(8) Staphylococcus aureus 502A injected intradermally), and overall survival from spontaneous burn wound sepsis. Fifty male Sprague-Dawley rats sensitized to keyhole limpet hemocyanin (KLH) were subjected to a 30% full-thickness scald burn. Group 1 (n = 24) received indomethacin at 0.5 mg/kg intraperitoneally once daily with the first dose given immediately following the burn. Group 2 (n = 24) received vehicle only. Prostaglandin E2 measured by radioimmunoassay on day 17 was 2553 +/- 832 pcg/ml serum (+/- SEM) in the vehicle group and 1042 +/- 231 pcg/ml in the indomethacin group (P = 0.058, unpaired t test). Burn injury induced a decrease in the DTH response to KLH and an increase in the Staph lesion size (P less than 0.05) which was not corrected by indomethacin treatment. All animals developed spontaneous burn wound sepsis by day 14. Survival after 17 days in the indomethacin group was 100% compared to that of the vehicle group, 79%, P less than 0.05 (Fisher exact test). We conclude that despite unmeasurable corrections of the burn-induced suppression of the DTH response and local nonspecific bacterial defenses, low-dose indomethacin improves survival following burn sepsis.

Abscess↗
PubMed1989

Burn injury alters intestinal glutamine transport.

Several studies have established that intestinal glutamine (GLN) metabolism is altered during catabolic states. It remains unclear whether these alterations are due to a defect in metabolism or in transport of the amino acid. The present study examines the kinetics of GLN transport across basolateral membrane vesicles (BLMV) of enterocytes obtained from control rats and rats subjected to 20% full-thickness scald burn, 48 hr previously. BLMV were prepared from freshly isolated enterocytes using differential centrifugation with separation on a Percoll density gradient. BLMV were enriched (10- to 12-fold) with Na+-K+-ATPase while markers for brush border membranes were impoverished. Previous studies from our laboratory indicated that, in this preparation, GLN transport is into an osmotically sensitive space, dependent on GLN concentration, linear up to 30 sec, and both temperature and Na+ dependent. Our results indicate that in thermal injury, initial rates of GLN uptake were depressed (y = 3.67 + 0.435X for burned rats vs y = 18.7 + 0.907X for controls, P less than 0.01). Kinetic analysis of GLN uptake showed a marked decrease in transport Vmax (81.8 +/- 15 nmole/mg protein/15 sec for burned rats vs 185 +/- 17 nmole/mg protein/15 sec for controls, P less than 0.001). Transport Km also decreased from 0.25 +/- 0.004 mM for controls to 0.08 +/- 0.03 mM glutamine for burned rats (P less than 0.001). Kinetic studies performed at GLN levels greater than 0.6 mM showed that GLN uptake proceeded by a nonsaturable process in both the control and burned rats. No significant alteration in this nonsaturable component was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Hepatocellular membrane function during chronic burn injury.

Hepatocellular membrane dysfunction, as indicated by depolarization of the membrane potential, occurs after acute injury and early bacteremia. To determine whether hepatocellular membrane dysfunction occurs in the setting of ongoing thermal injury and infection, Wistar rats were divided into four groups: (1) sham-burned, freely fed controls (FF); (2) rats sustaining approximately 30% total body surface area dorsal full-thickness scald burn (Burn); (3) rats sustaining burns as in group 2 followed by immediate inoculation of 1 x 10(8) CFU Pseudomonas aeruginosa (Burn/Inf); and (4) sham-burned rats pair-fed to the food intake of the Burn/Inf group (PF). On the third and seventh days postburn, body and liver weights were determined. In vivo hepatocellular transmembrane potentials were measured and hepatic ATP, RNA, DNA, and protein contents were assayed. By Day 7, despite greater weight loss in the Burn/Inf group than due to starvation alone (P less than 0.01 Burn/Inf vs FF and PF), hepatic mass was conserved. This was associated with hyperpolarization of the hepatic transmembrane potential (-46.6 +/- 1.5 vs -32.1 +/- 0.6 mV, Burn/Inf vs FF, P less than 0.01) and increases in RNA (141 +/- 9 vs 91 +/- 4 mg/liver, Burn/Inf vs FF, P less than 0.01) and DNA (37 +/- 5 vs 22 +/- 2 mg/liver, Burn/Inf vs FF, P less than 0.05) contents, with no change in ATP or hepatic protein contents. There was a significant hypercorticosteronemia observed in the Burn/Inf group (43 +/- 9 vs 2.8 +/- 0.7 micrograms/dl, Burn/Inf vs FF, P less than 0.01). This hepatic membrane hyperpolarization and augmented RNA content were not secondary to burn or starvation alone as the response in these groups was significantly less than that of the Burn/Inf group. It is suggested that this hepatic membrane hyperpolarization is one mechanism by which hepatic function is maintained during ongoing burn infection in the rat.

Adenosine Triphosphate↗
PubMed1991

Marked increase of plasma hyaluronan after major thermal injury and infusion therapy.

Hyaluronan (HYA) is an important structural element in skin and is presumably participating in regulation of the interstitial fluid volume. HYA is transported via the lymphatics from the tissues to the blood, where its concentration is normally very low. Fluid flux through the interstitium is markedly increased after thermal injury. The present study was performed to determine whether major thermal injury would affect plasma levels of HYA. In halothane-anesthetized sheep subjected to 40% BSA full-thickness scald burns, plasma HYA concentration increased from 116 +/- 19 (mean +/- SEM) to 172 +/- 18 ng/ml within 1 hr after injury (P less than 0.05). After 3 hr of fluid therapy plasma HYA concentration was further elevated to 10 times baseline (1417 +/- 322 ng/ml) (P less than 0.01). To clarify whether this rise represented an increased "washout" of interstitial HYA, attributable either to the burn injury or the subsequent fluid therapy, awake sheep were subjected to overhydration. Following a 3-hr infusion of lactated Ringer's 2.5 liter/hr, plasma HYA concentration increased to 2-3 times baseline. Lung lymph flow and its concentration of HYA increased, leading to an increase in the lymphatic flux of HYA to 10-20 times baseline. In peripheral lymph HYA flux increased 2-3 times baseline. Infusion of lactated Ringer's markedly increased lymphatic removal of HYA. However, plasma concentrations of HYA were 3 times higher after thermal injury than following fluid challenge alone, suggesting that thermal injury per se may also increase input of HYA into the systemic circulation.

Animals↗
PubMed1991

Thermal skin injury: effect of fluid therapy on the transcapillary colloid osmotic gradient.

The effects of fluid therapy on interstitial colloid osmotic and hydrostatic pressures in thermally injured skin were investigated in anesthetized rats subjected to full-thickness scald burns to 40% of the body surface area and resuscitation for 3 hr by either lactated Ringer's or plasma. Interstitial fluid hydrostatic pressure (Pif) was reduced from -2 mm Hg to -20 to -40 mm Hg after injury, which will profoundly increase transcapillary filtration. Following the onset of fluid therapy, Pif increased to slightly positive values. In control, colloid osmotic pressure in plasma (COPp) was 20.6 +/- 0.4 mm Hg and in interstitial fluid (COPif) 13.7 +/- 0.3 mm Hg (means +/- SEM). The transcapillary oncotic pressure gradient (COPgrad = COPp-COPif) was 6.9 +/- 0.4 mm Hg. Following nonresuscitated thermal injury, COPp declined to 18-19 mm Hg (P less than 0.05) and COPif was reduced to 10.4 +/- 0.5 mm Hg (P less than 0.05). Fluid therapy by lactated Ringer's markedly reduced COPp (12.3 +/- 0.3 mm Hg; P less than 0.05), and COPgrad was almost abolished (2.6 +/- 0.7 mm Hg; P less than 0.05). In contrast, plasma infusion maintained COPp, whereas COPgrad increased significantly (11.1 +/- 1.2 mm Hg; P less than 0.05). Noncolloid saline solutions have been preferred for the initial fluid therapy for burns. The present study provides evidence that this will reduce both COPp and COPgrad, a situation in which edema formation will be favored.

Animals↗
PubMed1992

Effect of cyclosporine on adrenocortical response to injury and infection.

The effects of cyclosporine administration on the adrenocortical response to the severe stress of burn wound sepsis were studied in Wistar rats. Animals were treated with cyclosporine (10 mg/kg/day) or saline by gavage for 10 days, then subjected to 30% scald burns with wound inoculation with Pseudomonas. Animals were sacrificed on Postburn Days (PBDs) 1, 4, and 7 for determination of serum corticosterone and ACTH levels and adrenal weights and histology. Adrenal glands from animals sacrificed on PBD 7 were also analyzed for DNA, RNA, and protein content. Cyclosporine treatment without injury had no significant effect on body weight gain, adrenal mass, or baseline ACTH or corticosterone levels. During sepsis, cyclosporine-treated animals demonstrated a significantly diminished adrenocortical response compared to those given only saline. Serum corticosterone levels in the cyclosporine group were 45, 53, and 62% lower on PBDs 1, 4, and 7, respectively, than in saline-treated controls (P < 0.01 on each day). ACTH levels were 43 and 36% lower in cyclosporine-treated animals on PBDs 4 and 7, respectively, compared to the saline-treated group (P < 0.05 on each day). Adrenal hyperplasia occurred in both groups by PBD 7, but increases in adrenal mass and in histologic changes associated with hyperplasia (lipid depletion, vascular dilation) were less pronounced in cyclosporine-treated animals compared to those receiving saline, while adrenal composition remained similar between the two groups. Thus, cyclosporine administration is associated with an attenuated adrenocortical response to the stress of sepsis due to diminished circulating levels of ACTH.

Adrenal Cortex↗
PubMed1992

The effect of albumin or crystalloid resuscitation on bacterial translocation and endotoxin absorption following experimental burn injury.

Burn injury induces immune suppression and increases susceptibility to infection. Hypoalbuminemia is an early and consistent finding following thermal injury and is independently associated with gastrointestinal dysfunction and increased rates of infectious morbidity. This study assessed the effects of albumin resuscitation on burn-induced immunosuppression, bacterial translocation, and absorption of gut endotoxin. Male Sprague-Dawley rats, presensitized to keyhole limpet hemocyanin (KLH), underwent a 20% dorsal scald burn injury, followed by laparotomy and IVC catheterization for fluid resuscitation. Animals were randomized to one of three resuscitative regimens: Ringer's lactate 3 ml/kg/% burn, Ringer's lactate 9 ml/kg/% burn, or 5% human albumin 3 ml/kg/% burn. Delayed hypersensitivity (DTH) responses to KLH were depressed 24 hr following injury (preburn 8.9 +/- 0.2 mm, post-burn 3.1 +/- 0.3 mm, P less than 0.001) and were significantly lower in animals in whom gram-negative bacterial translocation had occurred (2.3 +/- 0.4 vs 3.6 +/- 0.2 mm, P less than 0.005). Serum albumin levels were lower and rates of gram-negative bacterial translocation higher for those animals receiving low volume crystalloid resuscitation; animals resuscitated with albumin or high volume crystalloid experienced similar degrees of postinjury hypoalbuminemia and bacterial translocation. Uptake of radiolabeled endotoxin was maximal in animals resuscitated with albumin. Bacterial translocation is believed to be responsible for a significant number of late nosocomial infections following trauma. These data suggest that the adequacy of early resuscitation rather than the type of resuscitative solution is the more important factor in minimizing translocation.

Animals↗
PubMed1987

Increases in plasma beta-endorphin and tail flick latency in the rat following burn injury.

In children with burn injuries we found, in earlier studies, an inverse association of plasma beta-endorphin immunoactivity (iB-EP) and pain levels. To further explore the effects of burn trauma on the peripheral release of beta-endorphin and the occurrence of centrally mediated stress analgesia, plasma iB-EP levels and tail flick latency (TFL) were measured in rats subjected (while anesthetized) to scald injury. In comparison to sham burn (dip in tepid water), burn injury increased plasma iB-EP and TFL; both the duration and magnitude of these effects were directly proportional to the extent of burns. In rats receiving no treatment, TFLs were unchanged throughout the time of the burn experiments. At 2 days post-burn TFLs were invariably back to pre-burn levels. Administration of the long-acting opioid antagonist naltrexone prior to burn injury prevented the rise in TFL. Thus the trauma of burns appeared to bring about a stress-induced analgesia (SIA). The marked increase in iB-EP during this SIA and its antagonism by naltrexone suggest that it was opioid and hormonal in character.

Analgesia↗