Endothelial glycocalyx as a potential theriapeutic target in organ injuries / 中华医学杂志(英文版)

OBJECTIVE@#The endothelial glycocalyx (eGC) is a dynamic and multicomponent layer of macromolecules found at the surface of vascular endothelium, which is largely underappreciated. It has recently been recognized that eGC is a major regulator of endothelial function and may have therapeutic value in organ injuries. This study aimed to explore the role of the eGC in various pathologic and physiologic conditions, by reviewing the basic research findings pertaining to the detection of the eGC and its clinical significance. We also explored different pharmacologic agents used to protect and rebuild the eGC.@*DATA SOURCES@#An in-depth search was performed in the PubMed database, focusing on research published after 2003 with keywords including eGC, permeability, glycocalyx and injuries, and glycocalyx protection.@*STUDY SELECTION@#Several authoritative reviews and original studies were identified and reviewed to summarize the characteristics of the eGC under physiologic and pathologic conditions as well as the detection and protection of the eGC.@*RESULTS@#The eGC degradation is closely associated with pathophysiologic changes such as vascular permeability, edema formation, mechanotransduction, and clotting cascade, together with neutrophil and platelet adhesion in diverse injury and disease states including inflammation (sepsis and trauma), ischemia-reperfusion injury, shock, hypervolemia, hypertension, hyperglycemia, and high Na as well as diabetes and atherosclerosis. Therapeutic strategies for protecting and rebuilding the eGC should be explored through experimental test and clinical verifications.@*CONCLUSIONS@#Disturbance of the eGC usually occurs at early stages of various clinical pathophysiologies which can be partly prevented and reversed by protecting and restoring the eGC. The eGC seems to be a promising diagnostic biomarker and therapeutic target in clinical settings.

Effects of dezocine-remifentanil intravenous anaesthesia on perioperative signs, serum TNF-alpha and IL-6 in liver cancer patients undergoing radiofrequency ablation

Objective: To analyse the impact of dezocine-remifentanil intravenous anaesthesia on perioperative signs, serum tumour necrosis factor-alpha [TNF-alpha], and interleukin-6 [IL-6] in liver cancer patients undergoing radiofrequency ablation [RFA]

Study Design: An experimental study

Place And Duration Of Study: Renmin Hospital of Wuhan University, Wuhan, China, from January 2017 to February 2018

Methodology: Eighty patients with small hepatocellular carcinoma [SHCC] were selected as the research object. They were divided into Group A and Group B with the random number table method, with 40 cases in each group. Group A were given dezocine-remifentanil intravenous anaesthesia and Group B were given midazolam-remifentanil intravenous anaesthesia. Patients' situations in the surgery were compared between the two groups. Changes in heart rate [HR], mean arterial pressure [MAP] and blood oxygen saturation [SpO₂] were recorded before the surgery [T₀], at 5 minutes after the RFA [T₁] and at the end of the RFA [T₂]. Levels of tumour necrosis factor-alpha; [TNF-alpha;] and interleukin-6 [IL-6] on the 1² day after the RFA were compared between the two groups

Results: The wake-up time in Group A was shorter than Group B [p<0.001], and the VAS pain score in Group A was lower than Group B [p<0.001]. At T₁, the MAP in Group A was higher than Group B [p<0.001]. There was no significant difference in MAP between the two groups at T₀ and T₂ [p=0.881, 0.696, respectively]. At T₁ and T₂, the HR in Group A was lower than Group B [all p<0.001]. There was no significant difference in HR between the two groups at T₀ [p=0.684]. There was no significant difference in SpO₂ between the two groups at T₀, T₁ and T₂ [p=0.654, 0.884 and 0.798, respectively]. On the 1st day after the RFA, the level of TNF-alpha;, IL-6 in Group A were lower than those of Group B [all p<0.001]. There was no significant difference in the incidence of intraoperative complications between the two groups [p=0.644]

Conclusion: Compared with midazolam-remifentanil intravenous anaesthesia, the dezocine-remifentanil method has a better analgesic effect, shorter wake-up time, and can effectively regulate the expression of inflammatory cytokines TNF-alpha; and IL-6. However, the effect of remifentanil on the respiratory function is dose-dependent. Therefore, respiratory cycle monitoring and management should be strengthened during the surgery

A randomized trial of Chinese medicine Lirukang Granule combined with psychological intervention for cyclomastopathy and menoxenia / 中国结合医学杂志

<p><b>OBJECTIVE</b>To observe the influence of therapy with Chinese medicine Lirukang Granule (, LRKG) combined with psychological intervention on anxiety states and sex hormones in patients with cyclomastopathy and menoxenia.</p><p><b>METHODS</b>A total of 470 subjects were randomly assigned to three groups by the net-central randomization system, the treatment group (161 patients, treated with LRKG and psychological intervention), the Chinese medicine group (157 patients, treated with LRKG), and the psychological intervention group (152 patients, treated with psychological intervention). The dose of LRKG was 12 g three times per day; psychological intervention included establishing relations, cognitive intervention and psychological persuasion, 30-40 min per session, once a week. The therapy duration for all groups was three months. The efficacy was compared and anxiety state/State-Trait Anxiety Invertory (STAI) scoring was measured before and after treatment. The serum estradiol (E2), progesterone (P), prolactin (PRL) and follicle stimulating hormone (FSH) levels of 60 patients selected randomly from each group during the luteal phase were measured before and after treatment, and a group of 20 healthy women were evaluated for comparison. A follow-up was arranged for one year after treatment.</p><p><b>RESULTS</b>Thirty subjects were lost to follow-up. (1) Comparison of efficacy: the markedly effective rate and the total effective rate of the treatment group were 86.67% (131/150) and 98.00% (147/150), respectively; of the Chinese medicine group, 64.58% (93/144) and 90.27% (130/144), respectively; and of the psychological intervention group, 0% (0/146) and 3.42% (5/146), respectively. The markedly effective rate and the total effective rate in the treatment group were significantly higher than those in the Chinese medicine and psychological intervention groups (P < 0.05). (2) Comparison of STAI scoring: STAI scoring was decreased dramatically in the treatment group after treatment compared with that of the Chinese medicine group (P < 0.01), but there was no significant difference compared with the psychological intervention group. (3) Comparison of levels of sex hormones: E2, P, PRL and FSH of the three patient groups were disordered before treatment, and significantly different from healthy women (P < 0.01). After treatment, the levels of P and FSH of the treatment group were significantly increased (P < 0.01), E2 and PRL were significantly reduced, which were also significantly decreased compared with the psychological intervention groups (P < 0.01). (4) FOLLOW-UP: the markedly effective rate and the total effective rate of the treatment group remained higher than those of the other two groups after one year of treatment (P < 0.05). (5) Adverse reactions: no obvious adverse reactions were found among the three groups.</p><p><b>CONCLUSIONS</b>Therapy with Chinese medicine combined with psychological intervention was effective for short-term and long-term treatment of cyclomastopathy and menoxenia. The mechanism might be related to the regulation of sex hormones.</p>

Ligustrazine attenuates acute lung injury induced by blunt chest trauma

To investigate the effects of ligustrazine on acute lung injury induced by blunt chest trauma. This study was performed in the Animal Center of Renmin Hospital of Wuhan University, Wuhan, China between September 2009 and September 2010. Male Sprague-Dawley rats were randomly allocated into 4 groups: sham control group [group C, n=60], ligustrazine treatment group [group C+L, n=60], blunt chest trauma model group [group T, n=60], and the trauma plus ligustrazine treatment group [group T+L, n=60]. The lung contusion was induced as previously described. Animals of the T+L group were intraperitoneally injected with ligustrazine. Acute lung injury was evaluated by histopathology of the lung, and apoptosis was determined by terminal dUTP nick-labeling. Pulmonary edema was estimated using Evans blue dye extravasation and wet/dry ratios of lung tissue. The expression of caspase-3, Bcl-2, and Bax in the lung, as well as blood plasma tumor necrosis factor [TNF] -a were also measured. The ligustrazine treatment significantly attenuated lung injury induced by blunt chest trauma, as shown by decreased apoptosis index, and pulmonary edema [p=0.04]. The blood plasma TNF-alpha level after blunt chest trauma significantly deceased after the administration of ligustrazine [p=0.03] In addition, the ligustrazine treatment significantly alleviated the expression of caspase-3 [p=0.03], and increased the ratio of Bcl-2toBax [p<0.03]. Ligustrazine effectively protects lung injury induced by blunt chest trauma, and the protective effects seem to be mediated by attenuation of cell apoptosis via an increased ratio of Bcl-2/Bax and decreased caspase-3 activity

Effects of penehyclidine hydrochloride on apoptosis of lung tissues in rats with traumatic acute lung injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of penehyclidine hydrochloride on apoptosis of lung tissue cells and its mechanism in acute lung injury following blunt chest trauma in rats.</p><p><b>METHODS</b>Sprague Dawley (SD) rats (n equal to 54) weighing (250+/-5) g were divided equally and randomly into three groups: normal control group (C group, n equal to 18), trauma model group (T group, n equal to 18) and penehyclidine hydrochloride treatment group (P group, n equal to 18). Each group was further divided into three subgroups according to the time points of 3, 12 and 24 hours after experiment (at each time point, n equal to 6 for each subgroup). Rats of P group were intraperitoneally injected with penehyclidine hydrochloride for 2 mg/kg immediately after blunt chest trauma and rats in its 24 hours subgroup were once again injected with penehyclidine hydrochloride in the same dose 12 hours after injury. Lung tissue samples were collected at every time point and cell apoptosis in lung tissues were measured by TUNEL. Apoptotic index (AI) was calculated, expressions of bax and bcl-2 were detected by immunohistochemical staining of SABC, and lung tissue sections were taken for light and electron microscopic observation.</p><p><b>RESULTS</b>As compared with C group, at every time point, AI and expressions of bax and bcl-2 in T group were higher (P less than 0.05), and the ratio of bcl-2/bax markedly decreased (P less than 0.05), especially in the 24 hours subgroup. The ratio in T group (0.468+/-0.007) was lower than that in C group (1.382+/-0.058, t equal to 12.5, P less than 0.01). Lung tissue injuries were significant under a light microscope, and the number of apoptotic cells increased obviously under a transmission electron microscope. As compared with T group at the same phase, AI and expression of bax decreased in P group (P less than 0.05 and P less than 0.01), while the expression of bcl-2 increased significantly (P less than 0.01), and the ratio of bcl-2/bax markedly increased (P less than 0.05), especially in the 24 hours subgroup. The ratio in P group (1.012+/-0.070) was much higher than that in T group (0.468+/-0.007, t equal to 8.3, P less than 0.01). The injury of lung tissues was relieved, and apoptosis of cells decreased obviously under a transmission electron microscopic observation.</p><p><b>CONCLUSIONS</b>Apoptosis and expressions of bax and bcl-2 in lung tissues might be involved in the pathogenesis of lung injury induced by blunt chest trauma. Penehyclidine hydrochloride can alleviate lung injuries by inhibiting apoptosis of lung tissue cells, during which effects of penehyclidine hydrochloride on regulating expressions of bax and bcl-2 may play an important role.</p>

Isoflurane induces expression of vascular endothelial growth factor through activating protein kinase C in myocardial cells / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>Vascular endothelial growth factor (VEGF) plays important roles in establishing collateral circulation of ischemic myocardium. This study aimed to investigate the effect of isoflurane on VEGF expression and the potential intracellular signal transduction pathway in cultured rat myocardial cells in order to further reveal the molecular mechanism of myocardial preservation of isoflurane.</p><p><b>METHODS</b>Primary myocardial cells of Sprague-Dawley rats were isolated and cultured. They were divided randomly into control group, isoflurane group, protein kinase C (PKC) inhibitor group and PKC inhibitor+isoflurane group where cells were respectively incubated without any treatment, treated by 0.5, 1.0 and 1.5 minimum alveolar concentration (MAC) of isoflurane for 6 hours, by PKC inhibitor calphostin C at a final concentration of 50 nmol/L and by 50 nmol/L calphostin C+1.0 MAC isoflurane for 6 hours. VEGF expression was detected by enzyme-linked immunosorbent assay (ELISA) and the expression levels of PKC isoforms were determined by Western immunoblotting method.</p><p><b>RESULTS</b>Isoflurane increased the VEGF expression in myocardial cells in a dose-dependent way. VEGF levels were significantly higher in 1.0 and 1.5 MAC isoflurane groups than in the control group (both P < 0.01). The effect of isoflurane on upregulating VEGF expression was blocked by PKC inhibitor calphostin C (P < 0.01), but calphostin C did not alter VEGF expression (P > 0.05). Isoflurane induced the activation and translocation of PKCε. Immunoblotting analysis revealed that the immunoreactivity of PKC ε increased significantly in the membrane fractions and deceased significantly in the kytoplasm fractions for cells treated with 1.0 MAC isoflurane as compared with the untreated cells, but not of PKC-α, PKC-δ and PKC-ζ (P less than 0.01).</p><p><b>CONCLUSION</b>Isoflurane induces myocardial cells to release VEGF through activating PKC-epsilon from the endochylema to the cytomembrane, suggesting a possible novel mechanism of isoflurane protecting myocardial cells.</p>

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1 / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (HO-1), a cytoprotective defense against oxidative injury.</p><p><b>METHODS</b>After being anesthetized with chloralhy- drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for 40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO-1 was injected intraperitoneally at 40 micromol/kg/day for two consecutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin IX, an inhibitor of HO-1 was injected intraperitoneally at 20 mg/kg 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO(2)) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-histochemical technique and for light microscopic examination.</p><p><b>RESULTS</b>The PaO(2) was significantly lower in all the experimental groups compared with sham group (90 mm Hg +/- 1 mm Hg). However, the values of PaO(2) in IPO (81 mm Hg +/- mm Hg) and HM+I/R (80 mm Hg+/- mm Hg) were higher than that in I/R (63 mm Hg +/- 9 mm Hg) and ZnPPIX+IPO (65 mm Hg +/- 8 mm Hg) groups (P less than 0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P less than 0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P less than 0.05, P less than 0.01). The lung wet/dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P less than 0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P less than 0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX.</p><p><b>CONCLUSION</b>Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.</p>

Protective effects of pretreatment with Radix Paeoniae Rubra on acute lung injury induced by intestinal ischemia/reperfusion in rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of pretreatment with Radix Paeoniae Rubra (RPR) on acute lung injury induced by intestinal ischemia/reperfusion in rats and its protective mechanism.</p><p><b>METHODS</b>Thirty-two Wistar rats were randomly divided into four groups: Sham-operation group, ischemia/reperfusion group (I/R group), RPR-pretreatment group and hemin group. The model of intestinal ischemia/reperfusion was established by clamping the superior mesenteric artery for 1 hour followed by 2-hour reperfusion. The effect of RPR on the expression of heme oxygenase-1 (HO-1) in lung tissues was detected by immunohistochemistry and morphometry computer image analysis. Arterial blood gas analysis, lung permeability index, malondialdehyde (MDA) and superoxide dismutase (SOD) contents in lungs were measured. The histological changes of lung tissue were observed under light microscope.</p><p><b>RESULTS</b>The expression of HO-1 in RPR-pretreatment group and hemin group was obviously higher than that in sham-operation group and I/R group (P < 0.01). The level of MDA and lung permeability index in RPR-pretreatment and hemin group were significantly lower than those in I/R group (P < 0.01 or P < 0.05), while the activity of SOD in RPR-pretreatment and hemin group was obviously higher than that in I/R group (P < 0.01). Under light microscope, the pathologic changes induced by I/R were significantly attenuated by RPR.</p><p><b>CONCLUSION</b>Intestinal ischemia/reperfusion may result in acute lung injury and pretreatment with RPR injection can attenuate the injury. The protective effect of RPR on the acute lung injury is related to its property of inducing HO-1 expression and inhibiting lipid peroxidation.</p>

Effect of Radix Paeoniae Rubra on the expression of HO-1 and iNOS in rats with endotoxin-induced acute lung injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of Radix Paeoniae Rubra (RPR) on the expression of heme oxygenase (HO-1) and induced nitric oxide synthase (iNOS) in endotoxin-induced acute lung injury in rats and its protective mechanism.</p><p><b>METHODS</b>Forty Wistar rats were divided randomly into 5 groups with 8 rats in each group: saline control group (NS group), lipopolysaccharide group (LPS group), RPR-treatment group, RPR-prevention group and Hemin group. The effect of RPR on protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid, malondialdehyde (MDA) content in the lung and the activity of serum NO were observed. Arterial blood was drawn for blood-gas analysis. The expression of HO-1 and iNOS in lung tissues was detected by immunohistochemistry and morphometry computer image analysis. The histological changes of the lung were observed under light microscope.</p><p><b>RESULTS</b>Compared with that in NS group, the expression of HO-1 and iNOS was markedly increased in LPS group (P<0.01). In RPR-treatment, RPR-prevention, and Hemin groups, the expression of iNOS was significantly lower, while the expression of HO-1 was higher than that in LPS group (P<0.05). The protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid, the content of MDA and the activity of serum NO in LPS group were significantly higher than those in NS group (P<0.01). There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in the LPS group (P<0.01); these parameters of lung injury however, were significantly lower in RPR-treatment, RPR-prevention, and Hemin groups than LPS group (P<0.05 or P<0.01). The pathologic changes of lung tissues were substantially attenuated in RPR-treatment, RPR-prevention, and Hemin groups than LPS group.</p><p><b>CONCLUSIONS</b>The high expression of HO-1 reflects an important protective function of the body during lipopolysaccharide-induced acute lung injury. The protective effect of RPR on lipopolysaccharide-induced acute lung injury is related to the inhibition of iNOS expression and the induction of HO-1 expression.</p>

Effect of Shenfu Injection (ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells and its mechanism during ischemia-reperfusion in rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms.</p><p><b>METHODS</b>Ischemia-reperfusion model was established in rats. Twenty-four rats were divided into 3 groups with 8 rats in each, eg, ischemia-reperfusion (I/R) group, SF-treated group, and control group. In both SF and I/R groups, the superior mesenteric artery was closed with forceps for 1 hour and then reperfused for 2 hours. Either SF (3 ml/kg, SF group) or normal saline (I/R and control groups) was injected intravenously and continuously for 5 ml/kg with a micropump before the superior mesenteric artery was closed. The superior mesenteric artery was not closed for animals in control group. The expression of casapse-3 and Fas, and the level of TNF-alpha and pathological changes of the ileal mucosal tissue were assayed.</p><p><b>RESULTS</b>(1) The number of apoptosis cells increased obviously in I/R group and was significantly higher than that in SF and control groups (P<0.05). (2) The expression of caspase-3, Fas, and TNF-alpha was significantly higher in I/R group than SF and control groups (P<0.01); however, there was not significant difference in the expression of capase-3 between control group and SF group. There was a positive correlation between the expression of caspase-3, Fas, and TNF-alpha, and the number of apoptosis cells. (3) Under light microscope, intestinal mucosal impairment was found milder in SF group than I/R group (P<0.05).</p><p><b>CONCLUSIONS</b>SF can depress the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-alpha, Fas, caspase-3, and accordingly alleviate the ischemia and reperfusion injury of intestinal mucosal epithelial cells.</p>

Protective effects of hypovolemic hypotension preconditioning on cardiopulmonary function after myocardium ischemia/reperfusion injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To identify the protective effects of hypovolemic hypotension preconditioning on cardiopulmonary function after myocardial ischemia/reperfusion injury and to explore the possible mechanism.</p><p><b>METHODS</b>Twenty-four male white rabbits were randomly assigned to two groups. In the control group, ischemia/reperfusion animals(Group I/R, n=10) were subjected to thirty-minute occlusion of left anterior descending coronary artery and two-hour reperfusion. Animals in hypovolemic hypotension preconditioning group (Group HHP, n=14) experienced brief systemic ischemia preconditioning through blood withdrawal to lower blood pressure to 40%-50% of the baseline before myocardial ischemia/reperfusion. Hemodynamic parameters were recorded. Blood sample was taken to measure superoxide dismutase (SOD), malondialdehyde (MDA) and nitrogen monoxide (NO) changes with blood gas analysis. Myocardium specimens were sampled to examine apoptosis-related gene interleukin-1 beta converting enzyme (ICE) mRNA.</p><p><b>RESULTS</b>Cardiac mechanical function and lung gas exchange remained stable in Group HHP with a significant increase in NO level; while in Group I/R without preconditioning, cardiopulmonary dysfunction was present after 2 h reperfusion associated with a significant reduction in NO formation and an increase in MDA (P<0.001). There was negative expression of ICE mRNA in the two groups.</p><p><b>CONCLUSIONS</b>Hypovolemic hypotension preconditioning significantly improves cardiopulmonary function and increases NO formation and the protective benefit associated with hypovolemic hypotension preconditioning of the heart may be regulated through NO mediated mechanism.</p>

The effect of Shen-Fu on gastrointestinal tract injury and its potential mechanism during cardio-pulmonary bypass in patients undergoing cardiac surgery / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of Shen-Fu (SF) injection on gastrointestinal tract injury and its potential mechanism.</p><p><b>METHODS</b>Thirty-eight patients undergoing elective open heart surgery were assigned to Group C (control group, n=18) and Group SF (n=20) randomly. In Group SF, the patients received intravenous injection of SF (0.5 ml/kg) at the beginning of the surgery followed by a continuous infusion of 100 ml SF (1.0 ml/kg) solution diluted by saline at a rate of 0.004 ml x Kg(-1) x min(-1) with a Grasby pump. The control group was injected with normal saline in the same volume. Gastric intramucosal pH (pHi), activity of blood diamine oxidase (DAO), and concentrations of blood LPS and IL-6 were measured before CPB (S0) and 1 h (S1) and 2 h (S2) after aortic declamping, respectively.</p><p><b>RESULTS</b>In Group C, pHi value was significantly lower at S1 and S2 than at S0 (mean P<0.01) and blood DAO and concentrations of LPS and IL-6 were significantly higher at S1 and S2 than at S0 (mean P<0.01). In Group SF, pHi was obviously lower at S1 and S2 than at S0 (P<0.05) but LPS and IL-6 levels and DAO were higher at S0 (mean P<0.05). Blood DAO and LPS level demonstrated significant negative correlations with pHi (mean P<0.01) while LPS concentration showed a positive correlation with blood DAO (P<0.01) and IL-6 concentration (P<0.05). At S1 and S2 after aortic declamping, the levels of pHi were higher in Group SF than in Group C (mean P<0.01 ) but DAO and LPS and IL-6 levels were significantly lower in Group SF than in Group C (P<0.01).</p><p><b>CONCLUSIONS</b>SF has a protective effect on gastrointestinal tract and can reduce inflammatory actions.</p>

Effect of methylprednisolone on reperfusion injury in severe uncontrolled hemorrhagic shock / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To study the effect of methylprednisolone (MP) on reperfusion injury in severe uncontrolled hemorrhagic shock and explore the possible mechanism involved.</p><p><b>METHODS</b>Twelve dogs were randomly divided into two groups, control group (Group I, n=6) and MP group (Group II, n=6). The animals were bled continuously from a femoral artery catheter to produce uncontrolled hemorrhagic shock models. Resuscitation with lactated Ringer's (LR) solution was initiated when mean arterial pressure (MAP) decreased to 20 mm Hg, and MAP was maintained at 30-40 mm Hg. MP (4 mg/kg) was injected intravenously in Group II when resuscitation began. While in Group I, normal saline (NS) was injected instead. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured before exsanguination (T(1)), when MAP decreased to 20 mm Hg (T(2)), 60 min (T(3)) and 120 min (T(4)) after resuscitation. Heart rate, MAP and cardiac output (CO) levels were recorded concomitantly.</p><p><b>RESULTS</b>Infusion volume and hemorrhage volume shed from the superior mesenteric artery in Group I were higher than those in Group II (P<0.01 and P<0.05). After reperfusion, blood SOD levels decreased progressively and MDA levels increased rapidly in Group I. In Group II, blood SOD levels at T(3) and T(4) decreased as compared with that at T(1) but a stepwise increase was present. At T(4), blood SOD level was significantly higher in Group II than in Group I (Plt;0.01). At T(3) and T(4), MDA levels were markedly lower in Group II than in Group I. During reperfusion, MAP was more steady in Group II than in Group I and survival rate after 120 min (at T(4)) was higher in Group II than in Group I (P<0.05).</p><p><b>CONCLUSIONS</b>MP has a protective effect on severe uncontrolled hemorrhagic shock and subsequent reperfusion injury. The mechanism mainly involves the anti-lipid peroxidation activity of MP.</p>