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Effects of Panax notoginseng saponins on myocardial Gsalpha mRNA expression and ATPase activity after severe scald in rats.

The aim of this study was to investigate the changes of myocardial Gsalpha mRNA expression and ATPase and the effects of Panax notoginseng saponins (PNS) on that after burns in rats. Wistar rats were exposed to a 95 degrees C water bath for 10s to produce 30% TBSA skin-full-thickness scalds. Myocardial Gsalpha mRNA level, cAMP content and adenyl cyclase (AC) activities were determined with dot blotting hybridization, radioimmunoassay and indirect method, respectively. The ATPase activities in plasma membrane of cardiomyocytes and erythrocytes were measured colorimetrically. At 3, 6, 9 hours after scalds, the myocardial Gsalpha mRNA expression decreased significantly (P<0.01). PNS (100, 200 mg kg(-1), i.p.) markedly increased these levels (P<0.01). The elevation was correlated significantly with PNS dose (r=0.95, P<0.05). At 3, 6, 9, 12, 24, 48 hour after the scalds, the myocardial cAMP content and AC basal activity was reduced significantly. PNS (100, 200 mg kg(-1), i.p.) increased cAMP content and enhanced AC activity markedly in comparison with the 3rd hour postburn group. The activities of (Ca(2+)-Mg(2+))-ATPase and (Na(+)-K(+))-ATPase in plasma membrane of myocardial cells and red blood cells in scald group were significantly lower than those in the normal control group (P<0.01). PNS (100 mg kg(-1), i.p.) improved these indexes significantly after scalds (P<0.01 or 0.05). These data suggested that the effects of PNS on myocardium in burned rats involved its action to increase myocardial Gsalpha mRNA expression and AC activity, cAMP content as well as ATPase activities.

Adenosine Triphosphatases↗

Conjugated triene oxidation products of alpha-farnesene induce symptoms of superficial scald on stored apples.

The sesquiterpene alpha-farnesene (1) and its conjugated triene oxidation products accumulate in the skin of apples after harvest and are implicated as the causal agents of superficial scald. Conjugated triene oxidation products and analogues were synthesized and applied to the surface of Granny Smith apples either as vapors or in squalane. Farnesyl hydroperoxide (2a), trienol (2b), endoperoxide (3a), dehydronerolidol (5), and cumyl hydroperoxide (4) all produced the symptoms of superficial scald when applied at nanomolar doses. Scald-inducing activity was dependent on the mode of application. Farnesyl hydroperoxide (2a) was the most active conjugated triene when applied directly to the apple skin. Trienol (2b) also induced scald symptoms and partially reversed the inhibition of scald caused by diphenylamine.

Food Handling↗

Ultrasound assessment of scald scars in Asian children receiving pressure garment therapy.

BACKGROUND/PURPOSE: Scar formation after scald injury in children is managed commonly by application of pressure garment. The duration of the treatment depends on clinical assessment. The objective of the study was to evaluate the efficacy of the pressure garment therapy and to correlate the clinical assessment scar thickness with ultrasound measurement. METHODS: Prospective study of children with hypertrophic scars receiving pressure garment therapy was carried out between 1993 and 1998. The scars were mapped with paper cutting. Representative scar sites were scored clinically according to Vancouver General Hospital Burn Assessment Scale (pigmentation, vascularity, pliability, height, pain, itchiness). Blind to the clinical results, 2 radiologists measured the scar thickness of the same sites with ultrasonography (5 to 10 MHz transducer, General Electric LOGIQ 500). The correlation between the clinical scores and ultrasound measurement of scar thickness were analysed using analysis of variance (ANOVA). RESULTS: The median age of 58 children with scald injury (M:F = 36:22) was 2.8 years (0.5 to 15.8 years). The mean percentage of scald was 8.8% (24% had scald area >10%). In addition, there were 5 children with burn from naked flame and 9 children with keloid secondary to surgical incisions. With pressure garment therapy, the scar thickness reached a plateau 1 (1/2) years after the injury and began to decline gradually thereafter. The clinical estimation of scar thickness correlated well with the ultrasound measurement (ANOVA, P =.003, Adjusted R square = 0.99). The accuracy rate of clinical thickness estimation was 67%. Overestimation and underestimation accounted for 15% and 18%, respectively. There also was good correlation between total clinical score and the ultrasound measurement (ANOVA, P <.001). CONCLUSIONS: In children with scald injury, the pressure garment needs to be continued for a minimum of 1 year. Ultrasound measurement correlates well with overall score of the Vancouver General Hospital Burn Assessment Scale but not individual components of the scoring system except wound height.

Adolescent↗

Conservative treatment of scald burns is superior to early excision.

Early excision of deep burns has been advocated; however, it is difficult to clinically determine the depth of scald burns during the early postburn period. This prospective, randomized study was designed to determine whether early excision was superior to conservative treatment of scald injuries. Patients with scald injuries (which were not caused by grease) of clinically indeterminant depth were randomized to early (n = 12) or late (n = 12) excision; all patients with obvious superficial and full-thickness injuries were excluded. In the early excision group, all deep wounds were tangentially excised and grafted within 72 hours of admission, whereas in the late treatment group wounds were excised and grafted after 2 weeks had passed since injury. Area excised, postburn day of excision, percent graft take, operating-room time, blood replacement, incidence of infection, and length of hospital stay were compared. No patient experienced a significant wound infection or systemic sepsis. A significantly smaller area of excision was necessary for those patients who were treated with delayed surgery, and concomitant decreases in operating-room time and blood loss were observed. Notably, only one half of the patients who were randomized to the delayed excision group ultimately required surgical intervention to achieve wound closure. Graft take was comparable for both groups, as was length of hospital stay. Early clinical evaluation of scald injuries appears to be equivocal, and later evaluations reveal a less severe injury. Financial gains can be made when surgical excision of scald injuries is delayed until 2 weeks after injury because of a related reduction in hospital expenditures.

Bandages↗

Lymph isolated from a regional scald injury produces a negative inotropic effect in dogs.

Large surface-area burns in patients have been associated with a severe impairment in cardiac performance, as evidenced by a decline in cardiac output. The mechanisms responsible for this profound myocardial dysfunction are largely unknown. We investigated the effects of lymph isolated from the scalded hind limb of dogs on regional myocardial blood flow, coronary vascular reactivity, and contractile performance. Dogs were instrumented with ultrasonic dimension crystals in the myocardium supplied by the left anterior descending (LAD) and by the left circumflex (LCx) coronary arteries. After cannulating a hind limb lymphatic, lymph was infused directly into the LAD before and after a 10-second 100 degrees C hind limb scald. Scalding alone did not alter myocardial contractile performance in the LAD or LCx regions, coronary artery blood flow, or systemic hemodynamics. Interestingly, postburn lymph infused into the LAD resulted in a 38% decline in LAD zone segment shortening (p < 0.01 vs baseline) that lasted throughout the 5-hour observation period. In contrast, segment shortening in the (control) LCx region was unaffected by postburn lymph injections into the LAD. Regional myocardial blood flow (radiolabeled microspheres) in the LAD and LCx regions was unchanged after scald injury or intracoronary injection of postburn lymph. In addition, LAD coronary artery vascular reactivity to acetylcholine and nitroglycerin was also unaffected by the regional thermal injury or by injection of lymph into the LAD. These data suggest that a regional scald injury results in the production and release of a potent myocardial depressant factor(s) that produces a direct negative inotropic effect on the canine myocardium.

Animals↗

The effect of education and safety devices on scald burn prevention.

A prospective study was designed to evaluate the effects of education on the incidence of pediatric scald burns. Demographic data from our Trauma Registry identified the Zip code area of greatest risk. Eighty of 121 families with children in a large rental property were chosen randomly for the education program. Twenty of these families also had an anti-scald device installed in the bathtub faucet; all had two or more children under age 5 years. Families were surveyed before and after intervention. Safety knowledge improved post-education as judged by correct survey responses. Although 90% of the families had water heaters set at "warm" (< or = 120 degrees F), the actual temperature at the tap was above 130 degrees F in 71%. The anti-scald devices did work, but at 9 months all but one had been removed because of sediment buildup, which prevented water flow. In the year of the study, the number of scald burns from the target Zip code area decreased from 15 to 12. This was a pilot project for programs that can test public response to general safety education. An anti-scald device in conjunction with education works well in theory, but a better device needs to be engineered. In view of discrepancies between water heater settings and tap water temperature, housing authorities could play a vital role in implementing safety measures.

Accident Prevention↗

Evaluation of a pediatric scald burn clinical pathway.

Scald burns make up more than 75% of the pediatric burns patients who are admitted to our burns unit. A pediatric scald burn pathway was implemented at our center in November 1999, the aim of which was to improve consistency in the management of the acute phase of injury. This study assessed the effectiveness of the first 18 months of this scald burn pathway. Aspects of the management of pediatric scald burn patients were reviewed. This included all the patients admitted over a 6-month period 1 year before the implementation of the pathway and the first 6 months and between 12 and 18 months after the implementation of the pathway. Data collected included patient demographics, total body surface area burned, and key management guidelines, including nasogastric feeding, intravenous cannulation, analgesia prescription, multidisciplinary referrals, and family education Thirty-seven patients were enrolled in the first 6 months of the pathway's use. Between 12 and 18 months, a further 38 patients were enrolled. The patients within the three groups were similar in age and burn size. A comparison among the groups with respect to compliance with the treatment guidelines is presented graphically. In conclusion, the management of pediatric scald burns in the acute phase is more consistent since the implementation of the clinical pathway.

Acute Disease↗

Developing a focused scald-prevention program.

Scalds account for a high percentage of burn injuries in young children. The purpose of this project was to use a formative evaluation process to design a pilot scald-prevention program for a high-risk population. The burn registry and U.S. Census were used to define a high-risk population. A total of 53 children younger than age 6 were admitted to a local burn center with scalds during a 4-year period. Cooking or food accounted for 84% of these injuries. A total of 21% of the patients resided in one zip code, representing an incidence rate of 23 per 100,000, which was statistically significant. Focus group meetings were conducted with parents in this zip code. They were queried about scald injury knowledge, prevention practices, and attitudes toward interventions. A prevention program was designed based on the findings. Workshops are conducted with high-risk groups in the zip code. Attendees consent to a home visit where prevention practices are assessed and taught. A pre/post test and home risk assessment survey is used to measure change. The Burn Registry, U.S. Census, and focus groups were complimentary formative evaluation measures that assisted in developing a targeted scald prevention project.

Accident Prevention↗

Permeability of thermally damaged skin: I. Immediate influences of 60 degrees C scalding on hairless mouse skin.

Freshly sacrificed hairless mice were burned dorsally by direct contact with 60 degrees C water for periods ranging from 15 seconds to 8 min. Wounds ranging in degree from superficial epidermis damage to injury penetrating well into subcutaneous musculature were inflicted. Burned skin sections and reference abdominal skin sections were excised, placed in diffusion cells and investigated with regards to their permeabilities to water, methanol, ethanol, n-butanol and n-octanol. The data were couched in terms of ratios of permeability coefficients of burned skin to normal skin (scalding coefficients) for the same animal. Scalding increased permeability of skin to all compounds studied but the effects leveled out by 60 seconds. Protracted scalding was without great effect despite progressively increased depth of damage to the tissue as noted in histological sections. The degree of lost barrier competency attributable to 60 degrees C scalding was not marked for any compound but was definitely different for different alkanols. An approximately 3-fold permeability increase was noted with n-butanol, the most affected compound. The data demonstrate that near instantaneous alterations in permeability of skin accompany scalding, that decreased barrier competency does not correlate with the severity of a burn as measured in depth of the burn, and that thermal alteration of permeabilities is dependent on the physicochemical characteristics of the permeants.

Abdomen↗

Release of substance-P-like immunoreactivity in dog paw lymph after scalding injury.

The level of substance-P-like immunoreactivity (SPLI) in dog paw lymph was determined before and after scalding injury of the paw. At basal conditions, no SPLI could be detected in the paw lymph. Scalding induced an immediate increase of the SPLI-levels. Within 5-10 min after the scalding injury the levels increased up to 28 fmol ml-1 and then gradually decreased within 30-90 min after the injury. It is suggested that scalding injury results in release of substance P from sensory nerve endings, and that this release may contribute to the inflammatory response to scalding injury and, possibly, also wound healing.

Animals↗

Methysergide reduces nonnutritive blood flow in normal and scalded skin.

Methysergide is a serotonin antagonist and has been demonstrated to reduce wound blood flow and edema formation. We have determined the effect of methysergide on protein kinetics in normal and scalded skin of anesthetized rabbits. L-[ring-(13)C(6)]- or L-[ring-(2)H(5)]phenylalanine was used to reflect skin protein kinetics by use of an ear model, and L-[1-(13)C]leucine was used to reflect whole body protein kinetics. The results were that infusion of methysergide (2-3 mg. kg(-1). h(-1)) reduced the blood flow rate in normal skin by 50% without changing skin or whole body protein kinetics. After scald injury on the ear, administration of methysergide for 48 h reduced the weight of scalded ears (43 +/- 4 vs. 30 +/- 5 g, P < 0.01) and ear blood flow rate (42.6 +/- 4.9 vs. 5.8 +/- 1.0 ml. 100 g(-1). min(-1), P < 0.0001) and did not change wound protein kinetics. Methysergide reduced arteriovenous shunting and maintained inward phenylalanine transport from the blood to the skin pool. Using the microsphere technique, we found that the infusion of methysergide decreased blood perfusion by 33-36% in both normal and scalded ear skin. We conclude that methysergide administration reduces nonnutritive, as opposed to nutritive, blood flow in normal and scalded skin.

Animal Nutritional Physiological Phenomena↗

Analysis of regional hemodynamic regulation in response to scald injury.

Ultrasonic probes were placed around dog femoral arteries to record blood flow. Hind paw scalding with boiling water (5 s) caused a marked increase in ipsilateral femoral blood flow that persisted for the 2-h observation period. Contralateral femoral blood flow and systemic and pulmonary vascular resistances were unchanged. Compared to scald only animals, methysergide pretreatment diminished and shortened the femoral vasodilator response to scald (109 +/- 14 vs 243 +/- 27 ml/min at 5 min; 59 +/- 14 vs 191 +/- 31 ml/min at 2 h). Pretreatment with ritanserin, BW A1433U83, atropine, ICI 118551, diphenhydramine, ranitidine, meclofenamate, L-nitro-arginine methyl ester, 3-amino-1,2,4-triazine, and U 37883A had no effect on the increased femoral blood flow response to scald, suggesting this vasodilator response is not dependent upon activation of serotonergic2, adenosineA1, muscarinic, beta 2-adrenergic, histaminergic1 or histaminergic2 receptors, on cyclooxygenase products, endothelium-derived relaxing factor derived from nitric oxide (NO) synthase III, NO derived from NO synthase II, or KATP channels, respectively. Methysergide given after burn immediately reduced the augmented femoral blood flow to preburn levels, suggesting the vasodilator response to scald is mediated through continual activation of local serotonergic1-like receptors, which may be target site(s) for therapeutic interventions to influence burn-induced hemodynamic alterations.

Adamantane↗

Antinociceptive effect of the combination of pentazocine with morphine in the tail-immersion and scald-pain tests in rats.

We investigated the antinociceptive effect of pentazocine hydrochloride (pentazocine) in combination with morphine hydrochloride (morphine) using two antinociceptive tests; i.e., the tail-immersion and scald-pain tests, in rats. In the tail-immersion test, the rat's tail was immersed in warm water at 47 degrees C, and the latency to a nociceptive response was measured. In the scald-pain test, the right hind foot was scalded by immersion into hot water at 57 degrees C. Two hours later, additional thermal stimulus was applied to the same foot, and the latency to a nociceptive response was measured. Subcutaneous treatment with either pentazocine (6, 12, 24 mg/kg) or morphine (1.5, 3, 6 mg/kg) alone dose-dependently showed antinociceptive effects in both tests. The ED50 values (95% confidence limit) of pentazocine and morphine were 13.0 (5.4-31.5) and 2.4 (1.6-3.7) mg/kg in the tail-immersion test and 11.0 (4.5-26.6) and 3.8 (1.8-7.2) mg/kg in the scald-pain test, respectively. Simultaneous treatment with pentazocine at the similar dose augmented the morphine (1.5 mg/kg)-induced antinociception, but did not diminish the morphine (6 mg/kg)-induced antinociception in both tests. These results suggest that the simultaneous administration of pentazocine at the antinociceptive dose and morphine exerts additional antinociceptive activity against thermal and scald-induced inflammatory pain.

Analgesics, Opioid↗

Effects of clonidine on myocardial beta-adrenergic receptor-adenyl cyclase-cAMP system after scalds in rats.

AIM: To study the role of clonidine (Clo) on the myocardial beta-adrenergic receptor (beta-AR)-adenyl cyclase (AC)-cAMP system after the scalds in rats. METHODS: A 30% skin-full-thickness scald was produced by immersing rats in 95 degrees C water for 9 s. Clo 0.1-3.0 mg.kg-1 was injected i.p. to rats at 30 min before scalds, yohimbine (Yoh) 0.05 mg.kg-1 or prazosin (Pra) 0.03 mg.kg-1 to rats at 30 min before i.p. Clo. beta-AR density and affinity, AC activity, phosphoric diester hydrolases (PDH) activity, and cAMP content were determined with radioreceptor assay, indirect method, enzymeradiochemical assay, and radioimmunoassay, respectively. RESULTS: Clo inhibited the decrease of the myocardial beta-AR density, the attenuation of AC activity, and the reduction of cAMP content at 12 h after the scalds. Yoh partially reversed the effects of Clo on the three parameters. But Pra did not. CONCLUSION: Clo reversed the changes of the myocardial beta-AR-AC-cAMP system resulted from the scalds in rats.

Adenylyl Cyclases↗

[The dynamic change in the expression of interleukin 18 mRNA in the tissue of scalded rats after delayed resuscitation].

OBJECTIVE: To explore the dynamic change in the expression of interleukin 18 (IL-18) mRNA in the tissue of scalded rats after delayed resuscitation. METHODS: Wistar rats inflicted by 30% TBSA III degree scalding were employed as the model. Fifty-four rats were randomly divided into normal control (C), scalding and delayed resuscitation group (SD) and preventive group of selective decontamination of digestive tract (SDD) group. The RT-PCR was applied to determine the tissue contents of IL-18 mRNA in intestine, lungs, liver and kidneys at 2, 8, 16 and 24 PBHs. RESULTS: Plasma level of LPS increased significantly and reached summit level at 8 and 24 PBHs after delayed resuscitation after scalding (P < 0.01), but decreased obviously (P < 0.05) after the preventive application of SDD. Furthermore, the expression of tissue IL-18 mRNA in lungs, liver and kidneys since 2 PBHs increased evidently when compared to that before scalding and reached peak value at 8 PBH (P < 0.01) and lasted up to 24 PBHs. The expression of IL-18 mRNA could be inhibited to varying degrees by preventive application of SDD (P < 0.05-0.01). It was indicated by correlative analysis that plasma level of LPS was positively correlated to the expression of tissue IL-18 mRNA in intestine, lungs and liver (r = 0.298, 0.290 and 0.365 respectively with P < 0.05-0.01). CONCLUSION: The expression of tissue IL-18 mRNA in intestine, lungs, liver and kidneys increased significantly during early postburn stage and progressively enhanced thereafter. And the expression of tissue IL-18 mRNA in a variety of body tissue was significantly affected by post-traumatic endotoxemia.

Animals↗

[Study on the mechanism of hepatocytic insulin signal transduction defects in severely scalded rats].

OBJECTIVE: To investigate the mechanism of hepatocytic insulin signal transduction defects in severely scalded rats, so as to clarify the molecular basis of postburn insulin resistance. METHODS: Wistar rats inflicted by 30% III degree scalding on the back were employed as the model. The rat hepatocytic insulin receptor was partially purified by wheat-germ agglutinin (WGA)-sepharose 4B affinity chromatography. The change of receptor tyrosine protein kinase (TPK) activity, the receptor beta-subunit autophosphorylation and the hepatocytic insulin receptor binding behavior of scalded rats during early stage of scalding were observed by means of insulin receptor binding test, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography of phosphorylation of insulin receptor and phosphorylation of exogenous substrate. RESULTS: There exhibited no evident changes of hepatocytic insulin receptor maximal binding capacity and affinity at 3 postburn days (PBDs) in scalded rats. The autophosphorylation capacity of the receptor beta-subunit decreased significantly. And the receptor TPK activity decreased obviously and its reaction to insulin stimulation decreased markedly. CONCLUSION: The defects of the insulin receptor signal transduction in hepatocyte leading to the post-receptor defects of insulin biological effects might be molecular mechanism of postburn insulin resistance.

Animals↗

[Study on the intra- and extra-hepatocyte distribution of sodium ions in scalded rats during early postburn stage].

OBJECTIVE: To investigate the characteristics of the intra- and extra-hepatocyte sodium ions distribution in scalded rats during early postburn stage,with the aim of improving burn shock resuscitation regime and the resuscitation effects. METHODS: Adult Sprague-Dawley rats were randomly divided into sham scalding (C, n = 12) and scalding (S, n = 7) groups. The rats in S group were subjected to 40% TBSA III degree scalding on the back and were catheterized via jugular vein for fluid resuscitation. The rats in C group were catheterized via jugular vein without fluid infusion and were sham scalded by warm water in temperature of 37 degrees. The changes in the intra- and extra-hepatocyte sodium ion contents were determined in vivo by (23)Na-magnetic resonance spectrum technology, while the existing state of the intra- and extra-hepatocyte sodium ion was determined by detecting (23)Na-magnetic resonance horizontal delaying time (T(2)). RESULTS: The extra-hepatocyte sodium content in S group at 24 postburn hours (PBHs) was 17% less than that in C group. In addition, the T(2f) (fast T(2)) in S group remained stable but maintained a higher ratio during the observation time. This suggested that the sodium binding sites in extra-hepatocyte matrix increased relatively and that intra-hepatocyte sodium content increased by 57%. But the T(2) and the fast and slow parts of the T(2) kept stable, which implied that intra-hepatocyte catabolizing products were increased. This led to an increase in the sodium ion binding sites within intra-hepatocyte matrix in proportion to the sodium ion content. CONCLUSION: During early postburn stage, the extra-hepatocyte sodium in a remote organ such as the liver exhibited relative deficiency due to its ingress into hepatocyte cytoplasm and to the increase of sodium combining sites.

Animals↗

[The isolation and purification of 19S regulator compound and the change of its protein level in rat skeletal muscle after severe scalding].

OBJECTIVE: To explore the role of 19S regulator compound protein in the degradation of skeletal muscle protein in scalded rats. METHODS: Wistar rats were scalded and they were randomly divided into normal and 1, 2, 3, 5, and 7 postburn day (PBD) groups with 8 rats in each group. The 19S regulator compound of skeletal muscle in scalded rats was isolated and purified with chromatography. Rabbit-anti-rat antibody IgG of 19S regulator compound was prepared conventionally. The antibody was injected to rats in injection group (I) in which 19S antibody in dose of 3 mg/kg BW was injected for two times via tail vein with 6-hour interval. The rats in I group were decapitated on 1, 2 and 3 post-injection days, respectively. The scalded rats in control group (C) were treated in the same way, except that the antibody was replaced by normal saline. The change in content of 19S regulator compound was determined by western-blot. Meanwhile, the releasing rate of tyrosine from the skeletal muscle of scalded rats was also detected by fluorescent photography. RESULTS: 19S regulator compound with high purity was obtained. The content of 19S regulator compound in rat skeletal muscle was increased significantly after 2 PBD. But the protein degradation rate was also obviously increased on 2 PBD. The antibody of 19S compound might inhibit the enhancement of protein degradation. CONCLUSION: Burn injury might up-regulate the protein level of skeletal muscle 19S regulator compound, which therefore activated the protein degradation by 26S protease compound. This might be an important factor leading to postburn negative nitrogen balance.

Adenosine Triphosphatases↗