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Biomedical subjects

Z Y Sheng

Publications and source records attributed to Z Y Sheng.

At least 19 recordsLinked to original sources

Pathomorphological and quantitative bacteriological findings in various forms of primary surgery on gunshot wounds of extremities.

It is well-known that 'wound excision' is essential in the primary treatment of wounds in war, particularly thorough debridement of the devitalized tissues around the path of a penetrating projectile. Nowadays, the gunshot wounds in peacetime have become prevalent. Instead of the traditional method of 'wound excision' (excision), we used the method of 'incision and drainage' (incision) in the primary surgery of these gunshot wounds of extremities. To determine the treatment effectiveness of these different surgical methods (incision and excision), two groups of dogs were shot in the proximal part of one hind leg with an American M-16 rifle. One group was treated by the method of 'excision'; in the other group 'incision' were performed. No difference in infection rate was noted between the two groups. Similarly, no difference in bacterial count was found between the two groups during the observation period. Also, there was no difference in healing time; the wounds in both groups had healed by 19.2-21.4 days. Microscopic examination revealed a little normal muscle tissue in the necrotic zone of the incision group which might augment the repair process. These results suggest that there are no differences in the effectiveness in preventing infection between the two methods. 'Incision' might be superior to 'excision' for the management of the gunshot wounds of extremities in peacetime, as it involves a simple operation and there are advantages for tissue healing.

Animals↗

Effect of recombinant bactericidal/permeability-increasing protein on endotoxin translocation and lipopolysaccharide-binding protein/CD14 expression in rats after thermal injury.

OBJECTIVE: To investigate the potential mechanisms underlying the in vivo effect of recombinant bactericidal/permeability-increasing protein (rBPI21) on endogenous bacteria or endotoxin translocation and lipopolysaccharide-binding protein/CD14 expression secondary to thermal injury. DESIGN: Prospective, randomized, controlled animal study. SETTING: College hospital animal research laboratory. SUBJECTS: Thirty-six male Wistar rats weighing 250-300 g. INTERVENTIONS: The rats were anesthetized, and a 35% total body surface area full-thickness burn was created. Animals were randomized to receive treatment with either rBPI21 or the control protein (albumin). rBPI21 (2 mg/kg body wt, BPI group) or a protein control preparation (burn group) in the same dose was administered in an intravenous bolus at 30 mins and 4 hrs after thermal injury. All animals were killed at 12 and 24 hrs postburn (six to ten rats for each interval). In addition, eight rats were taken as normal controls. MEASUREMENT AND MAIN RESULTS: Our data showed that treatment with rBPI21 was effective in preventing endotoxin translocation secondary to severe burns. Meanwhile, tissue lipopolysaccharide-binding protein, CD14, and tumor necrosis factor-alpha mRNA expression in various organs were inhibited markedly by rBPI21 secondary to acute insults (p <.05-.01). Furthermore, significant reduction in serum aminoleucine transferase concentrations and elevation in intestinal diamine oxidase activities in the rBPI21-treated group were found compared with controls (p <.05-.01). CONCLUSIONS: These findings indicate that endotoxin accumulated in local sites after thermal injury can markedly up-regulate lipopolysaccharide-binding protein/CD14 and tumor necrosis factor-alpha mRNA expression in various organs. Meanwhile, up-regulation of lipopolysaccharide-binding protein/CD14 expression would be the major molecular mechanism of increasing sensitivity to endogenous endotoxin response after burns. Early treatment with rBPI21may be effective in attenuating multiple organ damage resulting from gut-origin endotoxin translocation. This might be associated with the down-regulation effects of tissue lipopolysaccharide-binding protein and CD14 gene expression by the use of rBPI21.

Acute-Phase Proteins↗

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats.

AIM: To explore the kinetic changes in plasma D(-)-lactate and lipopolysaccharide (LPS) levels, and investigate whether D(-)-lactate could be used as a marker of intestinal injury in rats following gut ischemia/reperfusion, burn, and acute necrotizing pancreatitis (ANP). METHODS: Three models were developed in rats: (1)gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; (2)severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and (3)ANP induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct. Plasma levels of D(-)-lactate in systemic circulation and LPS in portal circulation were measured by enzymatic-spectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken for histological analysis. RESULTS: One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D(-)-lactate and LPS levels, and there was a significant correlation between the plasma D(-)-lactate and LPS (r = 0.719, P<0.05). The plasma concentrations of D(-)-lactate and LPS increased significantly at 6h postburn, and there was also a remarkable correlation between them (r=0.877 P<0.01). D(-)-lactate and LPS levels elevated significantly at 2h after ANP, with a similar significant correlation between the two levels (r = 0.798, P < 0.01). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were observed in all groups. CONCLUSION: The changes of plasma D(-)-lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D(-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.

Animals↗

[The current condition and research progress of normal wound repair and "un-controlled" wound repair].

OBJECTIVE: To describe the concept of "un-controlled wound repair" and review its current progress in basic research and clinical treatment. METHODS: The literature review and comprehensive analysis methods were used in this study. RESULTS: The results showed that the normal wound repair and "un-controlled" wound repair had made big progress in cellular, molecular and genetic levels in recent years and these progresses had enhanced the treatment progress in clinic. CONCLUSION: All data indicate that the wound repair is made a big progress both in basic and clinic fields. New high techniques, such as clone, biochip and stem cell and their use will promote the deep study of "un-controlled" wound repair.

Cicatrix, Hypertrophic↗

[Effects of basic fibroblast growth factor on the healing of cutaneous chronic wounds].

OBJECTIVE: To observe the effects of basic fibroblast growth factor(bFGF) on the healing of cutaneous chronic wounds. METHODS: Twenty-eight cases with thirty-three wounds from trauma, diabetes, pressure and radiation injuries were locally treated with bFGF in a dosage of 150 U/cm2 wounds. The healing time of wounds was used to evaluate the treatment results. RESULTS: The healing time in all of chronic wounds were accelerated. All wounds from trauma, diabetes and pressure were healed within 4 weeks and another 2 wounds from radiation injuries were healed over 4 weeks. The healing rate within 4 weeks was 93.9%. CONCLUSION: The results indicate that bFGF can be used as a promoter to accelerate the healing of chronic wounds in clinic.

Adolescent↗

Influence of selective decontamination of the digestive tract on cell-mediated immune function and bacteria/endotoxin translocation in thermally injured rats.

OBJECTIVE: To determine the influence of pretreatment with selective decontamination of the digestive tract (SDD) on systemic immunosuppression, and the relationship between bacteria/endotoxin translocation and abnormalities of immune function in thermally injured rats. DESIGN, MATERIALS, AND METHODS: Animals were subjected to a 40% full-thickness scald injury, and divided into SDD-treated and control groups. The treatment group received SDD (polymyxin E, tobramycin, and 5-flucytosine) by gavage twice daily for 3 days before the experiment and continued for 5 days after thermal injury. The control group was given the same amount of water. The parameters reflecting cell-mediated immunity, including splenocyte proliferation in response to mitogens, interleukin 2 (IL-2) production, and lymphocyte subpopulation, were measured before injury and 1 and 5 days after burn, respectively. MEASUREMENTS AND MAIN RESULTS: Thermal injury resulted in marked reduction in splenocyte proliferative response to T-cell mitogens, IL-2 production, and T-helper/suppressor cells (CD4/CD8) ratio. Prophylactic treatment with SDD significantly decreased the incidences of bacterial translocation and endotoxemia, prevented suppressive mitogenic response and inadequate IL-2 production (p < 0.05-0.01) but did not affect the abnormal ratio of CD4 to CD8 T lymphocytes in blood (p > 0.05). CONCLUSIONS: These results suggest that bacteria/endotoxin translocation from the gut appears to be involved in cell-mediated immune dysfunction as a consequence of thermal injury. Pretreatment with SDD might attenuate postburn immunosuppression by preventing translocation events.

Animals↗

Elevated serum neopterin level: its relation to endotoxaemia and sepsis in patients with major burns.

The present study was conducted to determine the relationship between levels of neopterin and endotoxin in the circulation, and whether the neopterin level was related to the development of severe sepsis after extensive burns. This prospective study included 35 patients with burn size greater than 30% (30-98%), and 22 healthy volunteers who served as a comparison group. Neopterin levels increased in most patients on day 3 post-burn, but they were not significantly correlated with the extent of the burn surface (P > 0 center dot 05). A high serum neopterin level was found in patients with sepsis (n = 15), and a marked elevation persisted throughout the observation period. The difference between septic and non-septic patients (n = 20) became significant on 14 and 28 days post-burn. Although the presence of early endotoxaemia did not influence the alterations in serum neopterin, patients with endotoxaemia had much higher neopterin values than those who showed no endotoxaemia from the second week onward (P < 0 center dot 05-0 center dot 01). In addition, circulating endotoxin and neopterin levels were positively correlated in patients who developed endotoxaemia on day 14 (r = 0 center dot 368, P < 0 center dot 05) and day 21 (r = 0 center dot 439, P < 0 center dot 01) after major burns. These results suggest that thermal injury can lead to an elevation of serum neopterin independent of the burn surface area. The initial increase in the neopterin level may be a part of the acute-phase response to tissue injury itself, whereas the endotoxin release in the circulation may be responsible for the continuous induction of neopterin during the late stage. In addition, the presence of a constant high neopterin level is associated with a critical event in the development of severe burn sepsis.

Adolescent↗

Reduction of circulating prostaglandin E2 level by antiserum against core lipopolysaccharide in a rabbit model of multiple organ failure.

OBJECTIVE: To determine the potential role of prostaglandin E2 (PGE2) in the development of multiple organ dysfunction or failure (MOF), the possible effects of antiserum directed against Re chemotype lipopolysaccharide (LPS, from Re mutant of Escherichia coli F515) on circulating PGE2 level and survival rate, and whether there is an elevation in the plasma LPS concentration that could account for the induction of arachidonic acid metabolite in a rabbit model of MOF caused by acute hypovolemic insult. DESIGN, MATERIALS, AND METHODS: An animal model of MOF in rabbits, engendered by feeding live Escherichia coli O111:B4 before hemorrhagic shock (35-40 mm Hg for 60 min), was used in the present study. Re-LPS antiserum was given intravenously in the treatment group at the onset of hemorrhage and 4 hours after resuscitation. The animals that received equal volumes of normal rabbit serum and antiserum served as the control group. MEASUREMENTS AND MAIN RESULTS: The circulating PGE2 level was not increased at the end of shock (p > 0.05), but it was found to be significantly elevated 24 hours after hemorrhage and resuscitation in both groups. However, Re-LPS antiserum administration markedly decreased peak PGE2 level (p < 0.05) and attenuated multiple organ damage caused by acute insult. Concomitantly, there were also lower LPS concentrations in the treatment group as compared with the control group (p < 0.05-0.01). The survival rate was significantly increased in antiserum-treated rabbits 96 hours postinjury (treatment vs. control: 58.0% vs. 11.1%, p < 0.01). CONCLUSIONS: The results suggest that an excessive generation and release of PGE2 may be involved in the pathogenesis of immunosuppression and MOF following hemorrhage and resuscitation. Re-LPS antiserum has an inhibitory effect on overproduction of circulating PGE2 and the ability to improve survival with MOF. Gut-derived endotoxemia, bacterial translocation, or both, could account, at least in part, for the PGE2 formation and release in animals response to acute hypovolemic insult.

Animals↗

[An experimental study on injury of intestinal immuno-barrier in rat after scald].

A dynamic observation on injury of intestinal immuno-barrier in scalded rat was performed to investigate the relationship between the injury of intestinal immuno-barrier and bacterial translocation. After 40% TBSA third degree scald, a decrease of IgA in intestinal content and the number of CD3+ and CD4+ T lymphocyte, and reduction of IgA coat rate of intestinal bacteria were observed. At the same time, an increase in the incidence of bacterial translocation was detected. The results indicated that intestinal immuno-barrier was damaged and its protective function was weakened after an extensive thermal injury, and it suggested that the injury of intestinal immuno-barrier might play an important role on the development of postburn bacterial translocation and postburn sepsis.

Animals↗

The potential etiologic role of tumor necrosis factor in mediating multiple organ dysfunction in rats following intestinal ischemia-reperfusion injury.

Endogenous inflammatory cytokines may function as mediators in the development of remote organ damage in response to local ischemic insult. This study was designed to (a) explore the potential role of tumor necrosis factor (TNF) formation in the pathogenesis of systemic tissue injury, (b) determine the relationship between induction of TNF and gut-derived endotoxemia and/or bacterial translocation, and (c) evaluate the protective effect of anti-TNF monoclonal antibody (MoAb) for vital organs following intestinal ischemia-reperfusion in rats. Animals were subjected to superior mesenteric artery occlusion (SMAO) for 45 min. Systemic plasma TNF levels increased rapidly after the onset of reperfusion, reaching a peak value 2 h later (P < 0.01). TNF elevation was found to be associated with gut origin endotoxemia, where the maximal TNF levels occurred approximately 2 h after the initial appearance of endotoxin in portal vein. Prophylactic treatment with anti-TNF MoAb markedly blunted the elevation in plasma TNF levels and afforded protection from the development of hypotension, vital organs dysfunction, and metabolic acidosis. Significant improvement in 48-h survival rate was observed by administration of anti-TNF MoAb prior to inducing ischemia (P = 0.007). These findings suggest that intestinal ischemia-reperfusion could result in TNF production, which may play a key role in mediating subsequent septic response and systemic tissue injury. It seems likely that passage of endotoxin and bacteria from the gut can be responsible for the TNF formation

Amine Oxidase (Copper-Containing)↗

Role of gut-derived endotoxaemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract.

This study was performed to investigate: (1) the role of gut-derived endotoxin/bacterial translocation in the pathogenesis of sepsis, and (2) the possible effects of selective decontamination of the digestive tract (SDD) on mortality in rats following 40 per cent full-thickness scald injury. In the SDD-treated group, Enterobacteriaceae and yeasts were eradicated from the caecal mucosa, while the mucosal flora consisting of mainly anaerobes was well preserved, within 3 days. The incidence of bacterial translocation to the mesenteric lymph nodes (MLN) and viscerae was significantly lowered on postburn days 1, 3 and 5 (P < 0.05-0.01). Meanwhile, pretreatment with SDD resulted in reductions of the faecal endotoxin levels in different segments of intestinal tract to less than 0.5 per cent (0.04-0.45 per cent) of the untreated control; there was also a significant attenuation of the elevation of endotoxin concentrations in both portal and systemic blood. Intestinal diamine oxidase (DAO) activity returned to baseline on day 5 in rats receiving SDD but not in controls. The 5-day survival rate in the SDD-treated group was elevated by 26.7 per cent as compared with controls (P < 0.05). These data suggested that endotoxin/bacterial translocation took place early and commonly, which in turn contributed to postburn sepsis and mortality. SDD was effective in preventing gut origin endotoxaemia and bacterial translocation, and improving the survival rate in rats following severe thermal injuries.

Amine Oxidase (Copper-Containing)↗

The association of circulating endotoxaemia with the development of multiple organ failure in burned patients.

In this study, we examined the relationship of plasma endotoxin levels to the development of multiple organ failure (MOF), and the outcome in patients with thermal injury. A prospective cohort study of 17 patients admitted with burns covering more than 70 per cent of body surface area was undertaken. Circulating endotoxin concentrations were measured by modified limulus amoebocyte lysate assay in serial samples of plasma. Seven out of 17 burned patients developed MOF according to multiple criteria. The plasma endotoxin concentrations of patients with MOF were 0.512-1.127 EU/ml, which were significantly higher than that of 10 patients without MOF (0.216-0.553 EU/ml), on 3, 14, 21 and 28 days postburn (p < 0.05-0.01). A significantly higher incidence of positive endotoxin tests (> or = 0.120 EU/ml) was found in patients who developed MOF as compared to those patients who did not develop MOF during the observation period (p < 0.05). As the mean endotoxin levels increased, the incidence of MOF and death rate also increased, and persistent endotoxemia carried a poor prognosis. The present investigation provides further evidence that endotoxemia in severely burned patients commonly occurs. Circulating endotoxin has also been found to be strongly associated with the development of MOF and mortality following major burn injury.

Adult↗

Gut-derived endotoxemia and multiple system organ failure following gunshot wounds combined with hemorrhagic shock: an experimental study in the dog.

The purpose of this study was to explore the causative effects of high-velocity bullet injury (5.56 mm, 930 m/sec) combined with hemorrhagic shock on gut-derived endotoxemia and multiple system organ dysfunction or failure. The concentration of endotoxin in both portal and systemic blood was markedly increased after gunshot wounds together with hemorrhagic shock (p < 0.05-0.01). The portal/systemic lipopolysaccharide ratio persistently decreased in the combined wound (CW) group at 24 to 72 hours after injury, and it was much lower in the CW group than that in the single gunshot wound (SW) group. Also, a significant increase of fecal endotoxin content was found in the CW group as compared to the SW group (118.30 +/- 75.36 vs. 8.89 +/- 3.32 micrograms/g, p < 0.01), which was paralleled with the population of gram-negative bacilli in the intestinal tract. The incidence of multiple system organ failure, multiorgan dysfunction (including single organ failure) in the CW group were 30.8% (4 of 13) and 38.5% (5 of 13), respectively. These results suggested that severe trauma could lead to gut origin endotoxemia and bacterial translocation, which might play an important role in the pathogenesis of sepsis and multiple system organ failure following gunshot wounds.

Animals↗

Inhibitory effects of low-dose polymyxin B on hemorrhage-induced endotoxin/bacterial translocation and cytokine formation in rats.

The current experiments were performed to determine the effects of a subtherapeutic dose of polymyxin B sulfate on gut origin endotoxemia/bacterial translocation, and tumor necrosis factor (TNF) and interleukin-1 (IL-1) release following hemorrhagic shock (30 mm Hg, 90 min) in rats. The results showed that significant portal and systemic endotoxemia took place in the control group (portal, 0.269 to 0.845 endotoxin units (EU)/mL; systemic, 0.164 to 0.655 EU/mL), but not in the treatment group (except 0.5 hour in portal blood: 0.207 +/- 0.094 EU/mL). Concomitantly, the incidence of bacterial translocation to the mesenteric lymph nodes and viscera were reduced significantly at 0.5, 2, 6, and 24 hours postresuscitation in animals receiving polymyxin B (p < 0.05 to 0.01), whereas there were no differences with respect to number of translocating bacteria between the two groups (p > 0.05). Marked elevation of plasma TNF levels and IL-1 activities of peritoneal macrophages were also found in untreated controls at 0.5 to 2 hours (p < 0.05) and 6 to 24 hours (p < 0.05 to 0.01), respectively, but prevented by administration of low-dose polymyxin B. The 48-hour survival rate was improved from 41.7% in the control group to 75.0% in the treatment ones (p > 0.05). These data suggest that pretreatment with a subtherapeutic dose of polymyxin B is effective to inhibit hemorrhage-induced endotoxin/bacterial translocation from the gut and excessive TNF and IL-1 production.

Animals↗

The concept and diagnosis of multiple systems organ failure.

There are still controversies concerning the concept and diagnosis of multiple systems organ failure (MSOF), since the term does not precisely define its true nature, and its differential diagnosis with other irrelevant clinical conditions, such as senile dysfunction of organs, agonal state, etc, remains unclarified. Our studies on both human burn patients and rat model by means of electron spin resonance (ESR) showed that there was an excessive generation of free oxygen radicals resulting in lipid peroxidation of cell membrane of various tissues. The intestine seemed to be particularly sensitive to hypoperfusion-reperfusion injury, as diamine oxidase activity of the ileum was lowered and translocation of bacteria occurred, indicating failure of intestinal mucosal barrier function. Concomitant determinations of plasma endotoxin (LPS) and tumor necrosis factor alpha (TNFa) levels showed significant elevation, especially in patients who finally developed MSOF. The data suggested that intestinally derived bacteria and/or LPS exacerbate the systemic responses initiated by ischemia reperfusion injury and the presence of large amounts of devitalized tissue. Early diagnosis is important in order to improve the prognosis. However, current criteria of diagnosis for MSOF do not conduce to an early diagnosis, as they only describe the end stage manifestations, while our therapeutic strategy should be directed against different levels of initiators, systemic mediators, and effectors of injury. Therefore, it is important to emphasize the role of septic responses in the development of the syndrome. We propose that the name of the syndrome be changed to "sepsis with organ dysfunction" or "mediator injury of organs".

Animals↗

[Delayed fluid resuscitation induced bacterial translocation after lethal thermal injury: role of oxygen free radical injury of intestinal mucosa].

The Present investigation was undertaken to examine the effect of delayed fluid resuscitation (DFR), after lethal thermal injury on oxygen free radical (OFR) injury of intestinal mucosa and its relationship to bacterial translocation. Four groups of gnotobiotic rats with 5 strains of bacteria were studied: sham injury group (control) (n = 6): early fluid resuscitation (EFR) group (n = 24) receiving resuscitation (Parkland) immediately after scald (40% TBSA, third degree); DFR group (n = 24) receiving resuscitation 6 hours after scald; treatment group (n = 12), rats with DFR receiving VitE and VitC treatment before resuscitation 12, 24, 48 and 72 hours after injury, animals (n = 6, at each point) were sacrificed. Plasma endotoxin level, mucosal SOD, GSHPx, MDA and diamine oxidase (DAO) of ileum were determined, and cultures of the mesenteric lymph nodes (MLN), liver, spleen, heart, lung, kidney and blood were done. The level of mucosal MDA and plasma endotoxin and the incidence of bacteria translocation (IBT) to tissues were significantly higher and mucosal SOD, GSHPx, DAO activity significantly lower in DFR group as compared with that in EFR group at most of the time points. In DFR group, mucosal MDA content was negatively correlated with mucosal DAO activity, which correlated positively with plasma endotoxin level and IBT. After treatment with VitE and VitC, mucosal MDA content was decreased, plasma endotoxin level and IBT were significantly decreased, and mucosal DAO activity was significantly increased. Our data indicated that DFR in cases of burn shock can result in OFR injury of intestinal mucosa, disrupting mucosal barrier and promoting translocation of intestinal bacteria and endotoxin.

Amine Oxidase (Copper-Containing)↗

[Influential factors of water evaporation from burn wound].

To determine various influential factors of water evaporation from burn wound, we scalded 120 rats and divided them randomly into 12 groups. The rate of evaporation was studied under different temperatures and moistures. The experimental results showed that high temperature and low moisture were beneficial to the treatment of burn wound. Escharectomy, skin grafting and film forming agents could reduce evaporation. Azone could change the permeability of the skin and accelerate water evaporation.

Animals↗