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[Experimental study on the relationship between neuropeptide substance P and wound healing in scalded rats].

OBJECTIVE: To explore the relationship between neuropeptide substance P (SP) and wound healing in scalded rats. METHODS: (1) Scalded rats with different degrees of scald injury were employed as the experimental model and were sacrificed at 24 post scald hour (PSH), and on 3, 7 and 14 post scald days (PSD). The SP content in the wound was detected with radioimmunoassay method. (2) The murine granulation tissue fibroblasts (GTF) were cultured with different culture media, and divided into control, SP and Spantide (SP receptor antagonism) groups. The effects of SP and Spantide on the cellular activity and apoptotic rate of murine GTF were assessed in vitro. RESULTS: There was significant difference of the SP content among the superficial (145 +/- 78) ng/g, partial (94 +/- 48 ng/g) and full thickness (53 +/- 27 ng/g) scald wounds at 24 PSH (P < 0.01), while the SP content in partial thickness burn wound on 3 and 7 PSD obviously increased; and that in deep partial thickness burn wound obviously increased on 7 and 14 PSD. But the SP content remained unchanged in full thickness scald wound. (2) SP could promote the activity of GTF and inhibit its apoptosis (The GTF activity in control, SP groups were 0.21 +/- 0.05, 0.36 +/- 0.07, respectively, P < 0.01). Spantide could inhibit the interaction between SP and GTF. CONCLUSION: SP can promote GTF proliferation, and the SP content in wound is closely associated with the depth of the injury and wound healing capacity.

Animals↗

[Study on the proliferation of epidermal cells of wound edge in deep partial thickness scald injury in rat].

OBJECTIVE: To investigate the rule and possible mechanism of epidermal proliferation in wound edge of deep partial thickness scald injury in rat. METHODS: Twenty-four Sprague-Dawley rats inflicted with deep partial thickness scald were randomized into pre-scalding, 3 post-scalding day (PSD), 7PSD and 14PSD groups, with 6 rats in each group. Skin specimens from the wound edge were harvested for the observation of the histological characteristics of the epidermis. Cell cycles of epidermal cells were analyzed with flow cytometry. The expressions of cyclin D1, cyclin B1, cdk4 and the histone H1 kinase activity of MPF in epidermal cells were determined by Western blotting. RESULTS: Augmentation of nuclei and nucleoli was found in the epidermal cells from the wound edge in 3PSD group, while increased number of epidermal cells with obviously augmented nuclei and nucleoli were found in 14PSD group. The percentage of the cells in S phase increased in 14 PSD group. The percentage of epidermal cells in G2/M phase began to increase in 3PSD group, and that in 7PSD (4.5 +/- 0.6) and 14PSD (5.4 +/- 1.0) groups were obviously higher than that in pre-scalding group (2.9 +/- 1.1, P < 0.05). The expression of cyclin D1 increased significantly in 3PSD group. The expression of cdk4 decreased in 3PSD group, but began to increase in 14PSD group. There was no difference in the expression of cyclin B1 among groups. The MPF activity was significantly increased in 14PSD group. CONCLUSION: There was enhanced DNA synthesis and mitosis in epidermal cells of rats with deep partial scald during early post-scald stage, and active proliferation of epidermal cells was observed on 14PSD. The expression of cyclinD1/cdk4 complex and the activity of MPF increased since 14PSD, indicating that there was a special regulative pattern during wound healing.

Animals↗

[Influence of sea water immersion on inflammation and healing of the wounds in scalded rats].

OBJECTIVE: To investigate the influence of sea water immersion on inflammation and healing of the wounds in scalded rats. METHODS: One hundred and forty-four male Wistar rats with 10% TBSA superficial partial-thickness scald were randomly divided into A (n=72, with scald) and B (n=72, with seawater immersion for 4hrs immediately after scald) groups. The serum contents of K+, Na+, Cl- were determined at 0 post-scald hour (PSH), 6PSH, 12PSH and 24 PSH with electrocyte analysis apparatus, and the changes in serum interleukin-6 (IL-6) and tumor necrosis factor (TNF-alpha) levels were determined at 0 PSH, 6PSH and 12 PSH with enzyme-linked immunosorbent assay (ELISA). The histopathological changes in the rats of the two groups were observed, and wound healing time was respectively calculated. RESULTS: The serum contents of K+, Na+, Cl- in B group were obviously higher than those in A group. And the serum content of TNF-alpha and IL-6 in B group at 6 PSH [(140 +/- 22) ng/L, (160 +/- 41) ng/L] were significantly higher than those before scald [(29 +/- 15) ng/L, (62 +/- 17)] ng/L and in A group [(120 +/- 12) ng/L, (124 +/- 22) ng/L, ( P < 0.05)]. Compared with A group, re-epithelization of the wound differentiation in all layers of epidermis were delayed in B group, with more severe wound swelling, exudation, and topical inflammatory response. The wound healing time in B group was (16.3 +/- 1.6) d, which was obviously longer than that in A group [(14.1 +/- 1.8) d, P < 0.05)]. CONCLUSION: Sea water immersion combined with scald injury can aggravate the inflammatory response of the wound and delay the wound healing process.

Animals↗

[The influence of apoptosis of lymphocytes of Peyer's patches on the pathogenesis of gut barrier damage in severely scalded mice].

OBJECTIVE: To investigate the changes in cellular apoptosis of Peyer's patches in severely scalded mice, and to explore its role in the pathogenesis of gut barrier damage. METHODS: Forty BALB/c mice were randomly divided into normal control, 12 post-scald hour (12PSH), 24PSH and 72PSH groups, with 10 in each group. The mice in all PSH groups were inflicted with 20% TBSA full-thickness scald on the back. The mice in all the groups were sacrificed at different time points, and Peyer's patches were harvested from all the mice for HE staining, DNA gel electrophoresis, and flow cytometry ( FCM) examination with FITC conjugated Annexin-v and propidium iodide( PI) staining of cells. RESULTS: HE staining revealed that there were relatively abundant apoptotic cells scattering in Peyer's patches of scalded mice . DNA electrophoresis of Peyer's patches revealed typical " ladder" pattern at all indicated time points in scalded mice. Apoptotic percentage of detached Peyer's patches cells in control and scalded group were (4. 9+/-2. 1)% , (26.7+/-3. 1)% , (21.6 +/-4.0)% ,(12. 8 +/-2.0)% , respectively, and the percentage reached the peak at 12 PSH. CONCLUSION: Apoptosis is a principle modality of cell death of small intestinal Peyer's patches lymphocytes in severely scalded mice, and it might contribute to immunity barrier failure of intestinal wall after severe thermal injury.

Animals↗

[Influence of scald on the cytoskeleton of colonic smooth muscle cells of the rats].

OBJECTIVE: To investigate the changes in the morphology and cytoskeleton (CSL) content of the CSL in the colonic smooth muscle cells (SMCs) of rats in early postscald stage, so as to elucidate the mechanism of dysfunction of gastrointestinal motility. METHODS: Seventy Wistar rats were randomly divided into normal control (n = 10, without scald) , and scald ( n = 60, with 10 cm x 7 cm wound inflicted on the back) groups. The colonic smooth muscle tissue of 10 normal rats and scalded rats were harvested at 1, 3, 6, 12, 24 and 48 postscald hours( PSH) and divided into two parts: one for histologic examination, and the other for the detection of CSL changes in the colonic smooth muscle tissue by flowcytometry method. RESULTS: The electron microscope examination showed that the arrangement of cytoskeleton of SMC of the scalded rats during 1 to 3 PSH was disordered, and sparse, and the condensed area was uneven, with fragmentation. But the morphology and distribution of CSL gradually restored to normal state during 6 to 12 PSH, and it approached that of normal group at 48 PSH. The CSL content in the colonic smooth muscle tissue of scalded rats was obviously increased at 1 PSH (610+/-23) , decreased thereafter, evidently lower than that in control group at 3 PSH (92+/-17) , and then it started to increase at 12 PSH, exceeding the normal value at 24 PSH, and continued to rise until 48 PSH. There was significant difference in CSL content in the colonic smooth muscle tissue of the rats between scald and control group ( P < 0.05 or 0. 01). CONCLUSION: Changes in the morphology and CSL content in the colonic smooth muscle tissue can be observed at early stage after a scald, which imply the kinetic balance between damage and repair in the body. In addition, changes in CSL content in the colonic smooth muscle tissue may be important factors in producing colonic dysfunction, damage of intestinal wall structure, and dynamic abnormalities of the colonic smooth muscle.

Actins↗

Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat.

Following severe burns, patients frequently develop a profound resistance to nondepolarizing neuromuscular blockers. Several mechanisms have been proposed to account for this, including upregulation of nicotinic acetylcholine receptors. We investigated the effects of a 30% body surface area (BSA) scald on neuromuscular transmission in slow-twitch soleus (SOL) and fast-twitch extensor digitorum longus (EDL) of rats. Rats were sacrificed 72 h after the injury, a time at which sepsis is unlikely and body weight gain and core temperature have returned to normal. Further groups of rats were sham operated and either pair fed to the scalded rats or freely fed to assess the influence of food restriction. When compared with muscle from pair-fed control rats, scald resulted in an almost 50% increase in miniature endplate potential (mEPP) frequency in both SOL and EDL. However, scald did not increase mean mEPP amplitude in SOL, although it did cause a 10% increase in EDL. Scald injury did produce a significant increase in the size of the evoked endplate potential in SOL (33%) and EDL (37%). These data indicate that a significant increase in the quantal content of evoked transmitter released in SOL (38%) and EDL (30%) occurred by 72 h after scald. Such an increase may contribute to the resistance to nondepolarizing neuromuscular blockers documented in patients following thermal injury.

Acetylcholine↗

The effects of catalase, indomethacin and FPL 55712 on vascular permeability in the hamster cheek pouch following scald injury.

The effects of scald injury and scald injury with pretreatment on plasma and water content were studied in the superfused hamster cheek pouch. Catalase (30,000 Units/kg), indomethacin (2.5 mg/kg) and FPL 55712 (2 mg/kg) were administered prior to 10 second scald with 100 degrees C normal saline. Plasma content was measured with 125 I serum albumin and water content was calculated by loss on drying. Significant (P less than 0.05) decreases in plasma content compared to scald alone were observed following pretreatment with catalase (29%) indomethacin (31%) or FPL 55712 (52%). Water content in scalded pouches was significantly reduced by catalase (29%) and FPL 55712 (42%). Pretreatment when combined also resulted in significant reduction of plasma content but not water content. Results suggest that free-radicals, prostaglandins and leukotrienes are involved in vascular response by scald injury.

Animals↗

Effects of scalding injury on the components of rabbit paw lymph.

A technique for lymph collection has been described. Rabbit paw lymph was collected by this technique before and after scalding injury (75 degrees C for 20 s). The lymph concentrations of zinc, copper, iron, cobalt and lipid peroxide were measured. After scalding, the lymph flow increased rapidly and reached a maximum at 1 h, and then decreased gradually. The lymph concentrations of copper, iron and cobalt increased about two-fold in the first 30 min and the elevated levels persisted until 4 h. However, the increase of zinc was less than that of the other three metals. Total protein concentrations also increased twofold in lymph and the elevated level persisted for 4 h. Using gel filtration, the elution pattern of lymph after scalding was almost the same as that before scalding. Lipid peroxide in lymph increased about three-fold following scalding. However, the plasma concentrations of total protein and lipid peroxide did not change significantly following scalding.

Animals↗

Role of Rho kinase and actin filament in the increased vascular permeability of skin venules in rats after scalding.

OBJECTIVE: To investigate the role of the Small GTPase Rho and endothelial cytoskeleton in the increased vascular permeability of rat skin after scalding. METHODS: Rats were subjected to scalding local ventral skin and a venule was isolated from scalded skin and cannulated by micropipette. The venular permeability was measured with a fluorescence ratio technique and expressed with the permeability coefficient to albumin (P(a)). The venular F-actin filaments were observed by staining with rhodamine phalloidin and laser confocal scanning microscopy. A specific Rho kinase inhibitor Y-27632 was added into vessel bathing solution or preincubated with vessels to evaluate the role of Rho kinase in regulating of vascular barrier function. RESULTS: Scalding increased P(a) value of skin venule about threefold compared to normal skin venules (P<0.01) and was maintained for 120 min. Inhibition of Rho kinase with Y-27632 (30 micromol/l in low-concentration group; 60 micromol/l in high-concentration group) significantly attenuated the hyperpermeability responses to scalding in a dose dependent fashion. A prominent peripheral actin rim (PAR) existed at the outer area of endothelial cells and apparently delineated the cell-to-cell borders. In the control group, the PARs were arranged smoothly and fairly continuously. However, occasionally PARs did show focal interruption with focal fluorescein isothiocyanate (FITC)-albumin leakage. In the burned group, PARs were less organized and accompanied by a large amount of FITC-albumin leakage. Inhibition of Rho kinase with Y-27632 dramatically reduced P(a) value with recovery of actin filament arrangement in venule after scalding. CONCLUSION: Burn leads to dermal venular permeability increase with endothelial cytoskeleton depolymerization and disruption. Rho signal transduction pathway is involved in these responses.

Actins↗

Downregulation of glucocorticoid receptors of liver cytosols and the role of the inflammatory cytokines in pathological stress in scalded rats.

Preliminary experiments indicated that target cells were resistant to glucocorticoid (GC) after pathological stress. This study was designed to investigate the alterations in plasma corticosterone level and GC receptor (GR) of liver cytosols, to assess the relative inflammatory cytokines contribution to GC resistant, and to observe the action of alpha-melanocyte-stimulating hormone (alpha-MSH) on the potential implications of glucocorticord regulatory effects in burned rats. Male Wistar rats (weight range, 180-200g) received a 35% total body surface area immersion scald and were randomly divided to receive either tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL-1beta), polyclonal antibody (pAb), alpha-MSH, Ac-D-Lys-L-Pro-D-Val (KPV peptide), or saline (control). The binding capacity (Rt) of the steroid-binding sites was measured by radioligand binding assay, using [3H]dexamethasone as the ligand. We examined plasma levels of IL-1beta, TNFalpha, IL-10, and corticosterone following scald challenge in rats. The Rt of GR (208.45+/-30.78fmol/mg of protein) in hepatic cytosol in rats, 12h later the scald was significantly lower than that (306.71+/-27.96fmol/mg of protein) of the control group (P<0.01). The injections of anti-rat TNFalpha (257.80+/-12.82fmol/mg of protein), IL-1beta antibody (254.46+/-21.21fmol/mg of protein), alpha-melanocyte-stimulating hormone (278.32+/-7.76fmol/mg of protein) and KPV peptide (263.46+/-17.46fmol/mg of protein) might prevent the Rt of GR from decreasing in hepatic cytosols of rats with scald, respectively (all of P<0.05) in vivo. Scald-induced robust increases in plasma IL-1beta (214.08+/-27.25pg/ml), TNFalpha (111.18+/-23.97pg/ml), IL-10 (177.50+/-15.79pg/ml) and corticosterone (2680+/-443.23ng/ml) levels after 12h. The administration of TNFalpha, IL-1beta pAb, alpha-MSH and KPV might attenuate these increases. These studies suggest that pro-inflammatory cytokines are involved in downregulation of GRs and thus alpha-MSH and KPV might increase the level of GR in rats with immersion scald.

Animals↗

Presence of Campylobacter inthe respiratory tract of broiler carcasses before and after commercial scalding.

Campylobacter could be detected in the thoraco-abdominal cavity of broiler carcasses even if they were carefully eviscerated by hand with no evidence of intestinal rupture or leakage. If Campylobacter is present in the air sacs, which are unavoidably torn during evisceration, it could contaminate the thoraco-abdominal cavity of the eviscerated carcass. This study was done to determine if Campylobacter contamination is present in the respiratory tract of broilers prior to evisceration. Whole carcass rinses and respiratory tract washes were done on broiler carcasses collected at a commercial processing plant just before and just after scalding. Samples were cultured for presence and numbers of Campylobacter, Escherichia coli, coliforms, and total aerobic bacteria. Campylobacter isolates were subtyped by sequencing the short variable region of the flaA gene. The same subtypes of Campylobacter were detected in whole carcass rinse samples as in respiratory tract wash samples from individual broilers. Furthermore, the same numbers and subtypes of Campylobacter were recovered from respiratory tracts of carcasses collected before scalding and those collected after scalding. However, respiratory tracts of carcasses after scalding had higher numbers of E. coli, coliforms, and total aerobic bacteria than those tested before scalding. Although some bacterial counts were higher in the respiratory tracts of carcasses after scalding, Campylobacter counts were not. It appears that Campylobacter is present in the respiratory tracts of broilers as they enter processing, and contamination may be due to airborne bacteria during production or transport.

Animals↗

Acute respiratory failure that complicates the resuscitation of pediatric patients with scald injuries.

Respiratory failure that requires endotracheal intubation is an uncommon but potentially fatal complication of scald burns in children. Because scalds are rarely associated with a direct pulmonary injury, the pathophysiology of respiratory failure is unclear. A possible mechanism may be upper airway edema, diminished pulmonary compliance secondary to fluid resuscitation, or both. To identify an at-risk population for intubation after a scald injury, the hospital courses of 174 consecutive patients under the age of 14 years who were admitted after a scald injury to a single burn center during a 6-year period were examined. Seven of these patients (4%) required endotracheal intubation. No patient older than 2.8 years or who had a scald injury that covered less than 19% of the total body surface area required intubation. Patients who required intubation were younger (mean age, 1.4 vs. 2.8 years, P<.001), had a larger mean burn size (29.9% vs. 12.3% total body surface area, P<.001), and required more fluid resuscitation (7.66 vs. 4.07 cc/kg per percentage of total body surface area burned, P<.001) than patients who did not require intubation. Examination of the adequacy of resuscitation revealed that the intubated patients had an average hourly urine output of 0.84 cc/kg during the first 24 hours, suggesting that resuscitation was not excessive. Multivariate analysis demonstrated that both larger burn size (P = .041) and younger age (P = .049) were independent predictors of the need for intubation. Young patients with large body surface area burns that required large volumes of resuscitation comprise an at-risk group for respiratory failure after a scald injury. Increased vigilance is merited during the resuscitation of these patients.

Adolescent↗

Epidemiology of scalds in vulnerable groups in New South Wales, Australia, 1998/1999 to 2002/2003.

In this study, the recently introduced International Classification of Disease, 10th revision, code for hot tap water scalds was used to examine the epidemiology of these cases and other scalds injuries in children younger than 5 years of age and adults aged 65 years and older. Although the trunk was the most common area in which scalds occurred, young children were more likely to sustain head and neck scalds (15%, 95% confidence interval 10.8-18.3) because of hot tap water than older people (2%, 95% confidence interval 0.2-4.4). Hospital separation rates for hot water scalds decreased significantly during the study period in both boys (chi(2) = 15.6, df = 1, P < .001) and girls (chi(2) = 5.6, df = 1, P < .001) who were younger than 5 years of age, which might be attributable to the introduction of new standards regulating the provision of hot tap water to various buildings. The severity of scalds cases did not seem to be correlated with the length of hospital stay, which remained unchanged in both age groups.

Accidents, Home↗

Efflux of cyclic AMP, prostaglandin E2 and F2 alpha and thromboxane B2 in leg lymph of rabbits after scalding injury.

Leg lymph was collected from pentobarbital anaesthetized rabbits before and after scalding injury of the paw (75 degrees C for 20 s), and the contents of cyclic AMP (cAMP), prostaglandin E2 (PGE2) and PGF2 alpha and thromboxane B2 (TXB2) in lymph were determined. After injury lymph flow increased about four times. The maximal rate of flow was found between 30 and 60 min after scalding. The efflux of cAMP and immunoreactive iPGE2, iPGF2 alpha and iTXB2 also increased. The maximum values were detected at approximately 0-30, 30-60, 30-60 and 180-240 min, respectively, after the injury. The output of cAMP, iPGE2 and iPGF2 alpha and iTXB2 in lymph of the contralateral non-scalded paw remained low throughout the experiments. When rabbits were injected with indomethacin (2.5 mg/kg) or diclofenac sodium (2.5 mg/kg) immediately after the scalding injury, the efflux of cAMP, iPGE2 and iPGF2 alpha were low. Lymph flow was markedly reduced after treatment with diclofenac sodium; treatment with indomethacin did not significantly affect lymph flow. The results suggest a prostaglandin-dependent formation of cAMP following scalding injury which may be related to the initial responses to scalding.

Animals↗

Effects of methysergide administration on edema formation at the site of scald.

Femoral blood flow (Qa), hind paw lymph flow (Qlym), and lymph-to-plasma protein concentration ratio (Clym/Cp) were monitored before and 4 h after 1) 5-s 100 degrees C paw scald, 2) methysergide (1 mg/kg iv) 20 min before scald, 3) methysergide 30 min after scald, and 4) methysergide only. Before experimentation, hind paw venous pressure was elevated and maintained until steady-state Qa, Qlym, and minimal Clym/Cp levels were reached. The reflection coefficient (sigma d) was determined as 1 - minimal Clym/Cp; the filtration coefficient (Kf) was calculated. Methysergide alone caused no changes. Increases in Qa, Qlym, Clym/Cp, and Kf were identified in all scald groups. Compared with scald only animals, pre- and postscald methysergide blunted the increases in Qa, Qlym, Kf, and paw weight gain without an effect on sigma d. These data demonstrate that methysergide reduces edema formation at the site of scald, perhaps by modulating the burn-induced vasodilator response and/or by limiting the burn-induced increase in microvascular surface area.

Animals↗

Changes of biological functions of dipeptide transporter (PepT1) and hormonal regulation in severe scald rats.

AIM: To determine the regulatory effects of recombinant human growth hormone (rhGH) on dipeptide transport (PepT1) in normal and severe scald rats. METHODS: Male Sprague-Dawley rats with 30% total body surface area (TBSA) III degree scald were employed as the model. In this study rhGH was used at the dose of 2 IU/kg(-1)d(-1). An everted sleeve of intestine 4 cm long obtained from mid-jejunum was securely incubated in Kreb's solution with radioactive dipeptide (3H-glycylsarcosine, 3H-Gly-Sar, 10 microCi/ml) at 37 degrees C for 15 min to measure the effects of uptake and transport of PepT1 of small intestinal epithelial cells in normal and severe scald rats. RESULTS: Abundant blood supply to intestine and mesentery was observed in normal and scald rats administered rhGH, while less supply of blood to intestine and mesentery was observed in rats without rhGH. Compared with controls, the transport of dipeptide in normal rats with injection of rhGH was not significantly increased (P=0.1926), while the uptake was significantly increased (P=0.0253). The effects of transport and uptake of PepT1 in scald rats with injection of rhGH were significantly increased (P=0.0082, 0.0391). CONCLUSION: Blood supply to intestine and mesentery of rats was increased following injection of rhGH. The effects of uptake and transport of dipeptide transporters in small intestinal epithelial cells of rats with severe scald were markedly up-regulated by rhGH.

Animals↗

Survival and death of Salmonella typhimurium and Campylobacter jejuni in processing water and on chicken skin during poultry scalding and chilling.

Salmonella Typhimurium and Campylobacter jejuni were inoculated in scalding water, in chilled water, and on chicken skins to examine the effects of scalding temperature (50, 55, and 60 degrees C) and the chlorine level in chilled water (0, 10, 30, and 50 ppm), associated with the ages of scalding water (0 and 10 h) and chilled water (0 and 8 h), on bacterial survival or death. After scalding at 50 and 60 degrees C, the reductions of C. jejuni were 1.5 and 6.2 log CFU/ml in water and <1 and >2 log CFU/cm2 on chicken skins; the reductions of Salmonella Typhimurium were <0.5 and >5.5 log CFU/ml in water and <0.5 and >2 log CFU/cm2 on skins, respectively. The age of scalding water did not significantly (P > 0.05) affect bacterial heat sensitivity. However, the increase in the age of chilled water significantly (P < 0.05) reduced the chlorine effect. In 0-h chilled water. C. jejuni and Salmonella Typhimurium were reduced by 3.3 and 0.7 log CFU/ml, respectively, after treatment with 10 ppm of chlorine and became nondetectable with 30 and 50 ppm of chlorine. In 8-h chilled water, the reduction of C. jejuni and Salmonella Typhimurium was <0.5 log CFU/ml with 10 ppm of chlorine and ranged from 4 to 5.5 log CFU/ml with 50 ppm of chlorine. Chlorination of chilled water did not effectively reduce the bacteria attached on chicken skins. The D-values of Salmonella Typhimurium and C. jejuni were calculated for the prediction of their survival or death in the poultry scalding and chilling.

Animals↗

[The effect of hyperoxic solution on acute myocardial hypoxia in scalded rabbits].

OBJECTIVE: To investigate the effects of hyperoxic solution on acute myocardial hypoxia in scalded rabbits. METHODS: Rabbits inflicted with 30% TBSA III degree scald injury and/or acute myocardial ischemia were employed as the model. Animals were randomly divided into 4 groups, i.e. scalded rabbits treated with hyperoxic solution (A), scalded rabbits treated with normal saline (B), scalded rabbits without any treatment (C(b)) and normal healthy rabbits (C(h)). The cardiac function, blood rheology, blood gas analysis and the ratio of infarction to ischemic areas were dynamically monitored. RESULTS: (1) The cardiac function of the rabbits in B group was evidently worse than that in C(h) group (P < 0.01) and A group (P < 0.05). (2) The whole blood viscosity in A, C(b) and especially B groups was obviously increased compared with that in C(h) group (P < 0.05). While the viscosity in A group was much lower than that in B group (P < 0.01), it was similar to that in C(b) group (P > 0.05). (3) The PO(2) in A group was significantly higher than that in B and C (C(b), C(h)) groups (P < 0.01). (4) The ratio of infarction to ischemic areas in A group was remarkably lower than that in B group (P < 0.01). CONCLUSION: The hyperoxic solution may exert beneficial effects on acute myocardial ischemia in scalded rabbits. The mechanism might be related to the immediate correction of hypoxia in vital organs with simultaneous lowering of blood viscosity and the establishment of myocardial collateral circulation after the infusion of hyperoxic solution.

Animals↗