[Effect of aloe polysaccharides pretreatment on the cerebral inflammatory response and lipid peroxidation in severe hemorrhagic shock rats first entering high altitude].

OBJECTIVE: To investigate the effect of aloe polysaccharides pretreatment on the cerebral inflammatory response and lipid peroxidation in severe hemorrhagic shock rats first entering high altitude. METHODS: Forty healthy male SD rats weighing 250-300 g were randomly divided into 5 groups (n = 8 each): sham group, shock group, AP group was further divided into 3 subgroups (AP1 0.75 mg/kg; AP2 1.50 mg/kg; AP3 3.00 mg/kg). The different doses AP were given iv respectively at 30 min before hemorrhagic shock. The mean blood pressure (MAP) was maintained at (35 ± 5) mmHg (1 mmHg = 0.133 kPa) for 60 minutes. The animals were killed at 2 hours after resuscitation. Blood samples were obtained from femoral artery for detecting tumor necrosis factor α (TNF-α), IL-6 and IL-10 concentrations; the frontal and parietal lobes brain and the hippocampus were separated from brain tissues on the ice for detecting superoxide dismutase (SOD) activity and myeloperoxidase (MPO) activity, malondialdehyde (MDA) concentration, brain Wet-dry weight ratio (W/D). RESULTS: Compared with sham group, hemorrhagic shock significantly increased serum TNF-α ((76 ± 11) ng/L), IL-6 ((1303 ± 141) ng/L) and IL-10 concentrations ((95 ± 14) ng/L), MPO activity ((20.72 ± 2.28)×10(-2) U/g) and MDA concentration ((80 ± 13) nmol/mgprot) in the brain tissue and brain W/D (6.21 ± 0.18) (t = 6.928 - 14.565, P < 0.05), while SOD activity ((56 ± 11) U/mgprot) decreased significantly (t = -5.374, P < 0.05). There were no significant difference between shock and AP1 groups. AP2 group significantly inhibited hemorrhagic shock-induced increase serum TNF-α ((54 ± 12) ng/L), IL-6 ((846 ± 78) ng/L) and IL-10 concentrations ((66 ± 11) ng/L), MPO activity ((13.13 ± 1.23)×10(-2) U/g) and MDA concentration ((56 ± 9) nmol/mgprot) in the brain tissue and brain W/D (5.71 ± 0.18) (t = -6.905 - -3.357, P < 0.05), while SOD activity ((86 ± 12) U/mgprot) increased significantly compared to shock group (t = 4.240, P < 0.05). There were no significant difference between AP2 and AP3 groups. CONCLUSION: AP pretreatment can attenuate the cerebral ischemia and reperfusion injury in severe traumatic-hemorrhagic rats first entering high altitude through inhibiting systemic inflammatory response and leukocyte aggregation and lipid peroxidation in the brain.

A microcomputer FES system for wrist moving control.

A portable close-loop control FES system, whose controller is a microcomputer, was proposed in this chapter. Considering the time-varying nonlinear of the muscle system, a self-adaptive PI control strategy was used. It included a neural network identifier (NNI) and a PI controller. NNI could get the variability of muscle working condition to identify muscle model online. Parameters of PI would be optimized by the results of NNI. Some tracking experiments had been done on able-bodied volunteers and the precision were under 4%.

[Effects of limb ischemia preconditioning on pulmonary free radicals and cytokine levels in a rabbit model of lung ischemia-reperfusion injury].

OBJECTIVE: To study the effects of limb ischemia preconditioning on pulmonary free radicals and cytokine levels during lung ischemia-reperfusion injury in rabbits. METHODS: Eighteen healthy rabbits were randomly divided into three groups: control group (group C, n = 6), ischemia/reperfusion group (group I/R, n = 6), limb ischemia preconditioning group (group L, n = 6). At the end of experiments, the wet to dry-weight ratio (W/D), activities of superoxide dismutase (SOD) and myeloperoxidase (MPO), levels of malondialdehyde (MDA) and the contents of cytokines (TNF-α, IL-6, IL-8 and IL-10) were determined in lung tissues. Protein levels of bronchoalveolar lavage fluid and serum were measured to calculate the lung permeability index. Pathologic changes of lung tissues were also observed. RESULTS: Compared to the group I/R, the lung tissue W/D ratio, MPO activity, lung permeability index, MDA and the cytokines (TNF-α, IL-6 and IL-8) levels were significantly decreased in group L (P < 0.05), while the SOD activity (P < 0.05) and IL-10 contents were significantly increased (P < 0.01). There was no statistical difference in the changes of the above parameters between group L and group C (P > 0.05). The morphologic damages were significantly reduced in group L than that in group I/R. CONCLUSION: Limb ischemia preconditioning has protective effect against lung ischemia-reperfusion injury, which may at least in part through inhibiting the release of oxygen-derived free radicals and pro-inflammatory cytokines (TNF-α, IL-6, IL-8) and increasing the production of anti-inflammatory cytokine IL-10.

[Effect of fluid resuscitation for hemorrhagic shock on oxygenation of subjects in early period of first visit of high altitude area, an experimentation on dogs].

OBJECTIVE: To investigate the effect of fluid resuscitation on oxygenation of subjects with hemorrhagic shock in early period of first visit to area of high altitude, an experiment in dogs was performed. METHODS: A model of serious hemorrhagic shock was reproduced by exsanguination resulting in a lowering of mean arterial pressure to (35+/-5) mm Hg (1 mm Hg=0.133 kPa) maintain for 1 hour. Thirteen mongrel dogs were carried to an area of 3,780 metres above sea level from an area of 1,510 metres, and they were randomly divided into three groups, namely lactated Ringer's (LR) group, 6% hydroxyethyl starch (HES) group, and control group. The dogs in LR group were infused intravenously LR in 1.5 times the volume of blood loss; those in 6% HES group were given HES in equal volume. No fluid infusion was given in the control group. After 1 hour of resuscitation, LR was intravenously given at 5 ml.kg(-1).h(-1) in all groups as maintenance dose. The changes in oxygenation were observed. RESULTS: All animals in control group were dead after 2 hours. One hour after establishment of shock, the oxygen consumption (VO(2)), oxygen delivery (DO(2)), oxygen extraction ratio (O(2)ER), arterial oxygen saturation (SaO(2)) in two resuscitation groups were significantly lower than those before shock, but venous oxygen saturation (Sv(2)) and alveolar-arterial oxygen difference (A-aDO(2)) were significantly higher (all P<0.05). In LR group, the oxygenation parameters including VO(2), DO(2), O(2)ER, SaO(2) after 2 hours of resuscitation were significantly higher than those 1 hour after shock, while A-aDO(2) was significantly lower (all P<0.05); and in HES group, VO(2), DO(2), O(2)ER were significantly higher than those 1 hour after shock, while SvO(2) was significantly lower (all P<0.05). CONCLUSION: All dogs with serious hemorrhagic shock would die of hemorrhagic shock in the early period of entering a high altitude area if fluid resuscitation is denied. Two hours after infusion of LR in 1.5 times of quantity of blood loss, oxygenation can be restored to expected normal values. Infusion of 6% HES with an equal volume of blood loss, oxygenation dose not reach expected level 2 hours after resuscitation.

Rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, reduces acute lung injury in endotoxemic rats.

OBJECTIVE: Rosiglitazone, a potent agonist of peroxisome proliferator-activated receptor (PPAR)-gamma, exerts anti-inflammatory effects in vitro and in vivo. This study was designated to determine the effects of rosiglitazone on endotoxin-induced acute lung injury in rats. DESIGN: Prospective, experimental study. SETTING: University research laboratory. SUBJECTS: Thirty-six male Wistar rats. INTERVENTIONS: All the animals were randomly assigned to one of six groups (n = 6 per group) and were given either lipopolysaccharide (6 mg/kg intravenously) or saline, pretreated with rosiglitazone (0.3 mg/kg intravenously) or vehicle (10% dimethyl sulphoxide) 30 mins before lipopolysaccharide. The selective PPAR-gamma antagonist GW9662 (0.3 mg/kg intravenously) or its vehicle (10% dimethyl sulphoxide) was given 20 mins before rosiglitazone. MEASUREMENTS AND MAIN RESULTS: Endotoxemia for 4 hrs induced evident lung histologic injury and edema, both of which were significantly attenuated by rosiglitazone pretreatment. The protective effects of rosiglitazone were correlated with the reduction by 71% of the increase of myeloperoxidase activity and the reduction by 84% of the increase of malondialdehyde in the lung tissue. The pulmonary hyperproduction of nitric oxide was reduced by 82% of the increase related to lipopolysaccharide challenge. Pretreatment with rosiglitazone also markedly suppressed lipopolysaccharide-induced expression of inducible nitric oxide synthase messenger RNA and protein in the lung, as demonstrated by reverse transcription-polymerase chain reaction or Western blot analysis. Immunohistochemical analysis revealed that rosiglitazone inhibited the formation of nitrotyrosine, a marker for peroxynitrite reactivity, in the lung tissue. In addition, the specific PPAR-gamma antagonist GW9662 antagonized the effects of rosiglitazone. CONCLUSIONS: This study provides evidence, for the first time, that the PPAR-gamma agonist rosiglitazone significantly reduces endotoxin-induced acute lung injury in rats.