Poly[aqua-[µ(3)-N'-(carboxy-meth-yl)ethyl-ene-diamine-N,N,N'-triacetato]samarium(III)].

In the title coordination polymer, [Sm(C(10)H(13)N(2)O(8))(H(2)O)](n), each samarium(III) centre is nine-coordinated by six O and two N atoms from three N'-(carboxy-meth-yl)ethyl-enediamine-N,N,N'-triacetate ligands and one O atom of a water mol-ecule, forming polymeric chains running parallel to the a axis. The packing is governed by inter-molecular O-H⋯O hydrogen-bonding inter-actions.

Valproic Acid Treatment Inhibits Vasopermeability and Improves Survival in Rats With Lethal Scald Injury.

The aim of this study was to examine whether administration of valproic acid (VPA), a histone deacetylase inhibitor, inhibits proinflammatory mediators and ameliorate visceral vasopermeability both in a rat model of major burn, and also in rat cultured endothelial cells stimulated with permeability evoking mediators. SD rats were subjected to a 50% TBSA full-thickness scald injury, and treated with either saline or VPA (300 mg/kg) intraperitoneally. Pulmonary vascular endothelial growth factor (VEGF), myeloperoxidase (MPO), pulmonary microvascular permeability, water content, and acetylation of histone H3K9 of lungs were evaluated. In addition, pulmonary microvascular endothelial cells (PMECs) from male SD rats were cultured. With then, MPO, VEGF, histone acetylation, and the permeability of PMECs were investigated. Lethal scald injury resulted in a significant increase in microvascular permeability and water content of lung, accompanied by a significant elevation of the content of VEGF and activity of MPO, and a decrease of histone acetylation. VPA treatment significantly alleviated the microvascular permeability and water content of lung, lowered the levels of VEGF and MPO, and promoted acetylation of histone H3K9 following scald injury. Moreover, VPA reduced permeability of monolayer PMECs subjected to scald serum challenge, reduced the level of MPO and VEGF in supernatants, and promoted acetylation of histone H3K9 in PMECs. These results indicated that VPA can protect pulmonary microvascular endothelial barrier, alleviate proinflammatory mediators-evoked vascular hyperpermeability and tissue edema and improve the survival rate of rats subjected to lethal scald injury.

The effects of ulinastatin on systemic inflammation, visceral vasopermeability and tissue water content in rats with scald injury.

BACKGROUND: The aim of this study was to examine whether administration of ulinastatin inhibits pro-inflammatory mediators and ameliorate visceral vasopermeability both in a rat model of major burn, and also in rat cultured endothelial cells stimulated with permeability-evoking mediators. METHODS: Plasma levels of tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), myeloperoxidase (MPO), microvascular permeability, and water content of organ tissues were evaluated in a rodent model of a 55% TBSA full-thickness scald injury. Microvascular permeability was also evaluated with a cultured pulmonary microvascular endothelial cells (PMECs) monolayer after stimulation with trypsin, bradykinin, histamine, prostaglandin E2 and burn serum. RESULTS: We found that the plasma levels of TNF-α, CRP, MPO, vascular permeability and water content of heart, lung, kidney, and small intestine tissues were significantly increased in animals after scald injury, and administration of ulinastatin lowered the levels TNF-α, CRP, MPO, vascular permeability and water content of those organ tissues. In vitro, ulinastatin lowered the levels of TNF-α, interleukin-6 (IL-6) and attenuated permeability in PMEC monolayers after being stimulated with burn serum or trypsin, but not by bradykinin, histamine or prostaglandin E2. CONCLUSIONS: These results indicate that ulinastatin attenuates the systemic inflammatory response and visceral vasopermeability both in vivo and vitro, and may serve as a therapeutic agent for prevention of systemic inflammatory response and leakage of fluid into tissue after major burn.

[The effects of oral rehydration on ischemia injury in gut in 40% blood volume loss in rats].

OBJECTIVE: To investigate the effects of oral rehydration with glucose electrolyte solution(GES) on intestinal ischemia injury in 40% blood volume loss in rats. METHODS: SD rats were randomly divided into three groups (n=24): oral rehydration without hemorrhage (GES), hemorrhage without oral rehydration (HS), hemorrhage resuscitated with oral GES(HS + GES). About 4% of total blood volume was bled from the right common carotid artery of rats to produce a model of hemorrhagic shock. GES, which volume was three times of blood loss was given to GES group and HS + GES group in 0.5 h, 1 h and 6 h by a gastric tube post bleeding. The intestinal blood flow(IBF) were measured by laser Doppler at 2 h, 4 h and 24 h post hemorrhage. Animals were sacrificed, and specimens of intestinal tissue was taken for evaluation of Na+ -K+ -ATPase, diamine oxidase (DAO) and the rate of tissue water content, and assessment of the intestinal pathological changes. RESULTS: The IBF and the activity of Na+ -K+ -ATPase in HS+ GES group were dramatically higher than those in HS group (P < 0.05), and lower than those in GES group (P < 0.05). The water content of intestinal tissue in HS group were dramatically higher than those in GES group (P < 0.05), and lower than those at 2 h and 4 h, but dramatically higher than those at 24 h in HS + GES group. The activity of DAO at 24 h in HS+ GES group was higher than those in HS group (P < 0.05), and lower than those in GES group (P < 0.05). Less edema and hyperemia were found in HS + GES group than those in HS group at 24 h after bleeding. CONCLUSION: It is indicated that oral rehydration alleviate edema and ischemia injury in gut by increasing intestinal blood flow and the activity of Na+ -K+ -ATPase and DAO in the resuscitation of hemorrhagic shock.

[Influence of the escharectomy during stock stage on the peripheral lymphocyte apoptosis and the antigen presentation function of monocytes in peripheral blood of scalded rats].

OBJECTIVE: To investigate the influence of escharectomy at different time-points after burn injury on the lymphocyte apoptosis and the antigen presentation function of monocytes in peripheral blood of scalded rats. METHODS: One hundred and thirty-six Wistar rats were randomly divided into normal control ( C,n = 8 ), scald ( S, n = 64,without treatment after scald) , A ( n = 40, with escharectomy at 36 post-burn hour( PSH) ) , B ( n = 24, with escharectomy at 72 PSH ) groups. The rats in A , B, S groups were inflicted with 30% TBSA full-thickness scald. The rats in S group were sacrificed on 6,12,24,72,120,168,216, 288 PSH, while those in A and B groups were sacrificed at 72 -288 PSH, 168 -288PSH, respectively. The rats in C group were also sacrificed as control. The apoptotic rate of peripheral lymphocytes, the positive expression rate of MHC- II in mononuclear cells, the changes in concentration of IL-4 and gamma-IFN were determined in each group. The correlation of above indices were also analyzed. RESULTS: (1) The apoptotic rate of peripheral lymphocyte in S group were increased dramatically at 6PSH, peaking at 24 PSH( 18. 19+/-1.42% ) , then decreasing gradually, reaching the lowest level at 72 PSH(8. 25+/-0.56% ) , then it increased gradually again, approaching almost the peak value at 288 PSH( 17.81 +/- 1.99% ). The values were all obviously higher than those in C group( P <0.05). The apoptotic rates of peripheral lymphocyte in A and B groups were evidently lower than that in S group ( P <0. 01). (2) The positive expression rate of MHC-II in monocyte was decreased sharply at 6 PSH, and it was 20% lower than that in C group (37. 2 +/- 2. 4% ) at 24 PSH. It then increased gradually, but it was significantly lower than that in A, B groups at 288 PSH (18. 8 +/-2. 8, P <0.01). (3) The plasma level of y-IFN in S group increased gradually from 6 PSH on, peaking at 24 PSH(440. 8 +/-25. 1 )ng/L,then decreasing gradually , and it reached the lowest level at 288 PSH (51.3 +/-37.0) ng/L. The IL-4 level in S group was increased gradually ,peaking at 288 PSH (78. 1+/-2. 8) ng/L. (4) There was negative correlation between the expression rate of MHC- II in S group and IL-4/gamma-IFN ratio in escharectomy groups during 72 - 288 PSH ( r = - 0. 96, P < 0. 05). CONCLUSION: Eacharectomy after scald can inhibit peripheral lymphocyte apoptosis, slow down the insertional tendency of IL-4/gamma-IFN , and ameliorate the antigen presentation function of monocytes. Moreover, escharectomy during shock stage can markedly promote the immune function of monocytes.