Objective To improve overall value of healthcare industry through setting up critical inpatient medical services strategic plan.Methods Identify major objectives which the local government expects to achieve through strategic map; Standardize inpatient output and assign weight to each group through diagonosis related groups; Translate the objectives of strategic map and result of diagnosis related group to Balanced Score-card; Finally build up strategic map and according action plans.ResultsPreliminarily established 16 objectives、23 measures and 13 tasks in four perspectives including customer,internal work flow,learning and growing and finance.ConclusionThe strategy map and the balanced score-card can help implement full strategic plan of regional inpatient medical services; DRGs is a core management tool of patient-centred service output management; Balanced Score-card is able to realize continuous improvement of Beijing inpatient medical services from macro to micro persoetive.

AIM To investigate the role of serine/threonine protein phosphatases 1 and 2A (PP1/2A) in regulation of cell signal transduction involved in the tolerance of human umbilical vein endothelial cells (HUVEC) to hypoxia. METHODS HUVEC tolerance was established by hypoxic preconditioning. The tolerance of HUVEC was evaluated by the cell survival rate, lactic dehydrogenase (LDH) releasing and total antagonistic-oxidative capability (T-AOC). Subcellular localization of nuclear factor E2-related factor 2 (Nrf2) was determined by immunocytochemistry combined with Western blot. The expression of stress protein of heme oxygenase-1 (HO-1) was measured by Western blot. RESULTS Hypoxia 90 min decreased the survival rate and T-AOC of HUVEC significantly, increased the release of LDH in cultured HUVEC. Compared with the hypoxic group, hypoxic preconditioning (4, 8 and 24 h after hypoxia 10 min) up-regulated the tolerance against hypoxia in HUVEC, the survival rate of HUVEC and T-AOC increased and the release of LDH down-regulated when insulted with hypoxia (90 min) in HUVEC. Hypoxic preconditioning established the translocation of Nrf2 from cytoplasm to nucleus and up-regulated the expression of downstream protein HO-1. Pretreatment with okadaic acid (40 nmol·L-1), a powerful inhibitor of PP1/2A, for 10 min in hypoxic preconditioning HUVEC partly inhibited the translocation of Nrf2 from cytoplasm to nucleus and the expression of HO-1, abolished the tolerance of HUVEC established by hypoxic preconditioning. CONCLUSION PP1/2A at least partly take part in Regulation of translocation of Nrf2 and expression of HO-1, with is associated with the tolerance of HUVEC established by hypoxic preconditioning.

OBJECTIVE:To observe the effect of huoxiangzhengqi liquid on substance P(SP)of rats.METHODS:The rats were randomly divided into trial group(huoxiangzhengqi liquid)and control group(normal saline),the gastrointestinal motility of rats were observed1hour and6hours after drenched with the corresponding drugs,levels of SP in serum,sinus ventriculi,jejunum tissues homogenate and the distributions of SP positive products in sinus ventriculi and jejunum tissues of2groups of rats were also determined.RESULTS:The gastrointestinal motility of the trial group was markedly enhanced after medication,particularly1hour after medication;Compared with the control group,levels of SP in serum,sinus ventriculi,jejunum tissues homogenate and SP positive products in sinus ventriculi,jejunum tissues had a significant increase in the trial group(P

OBJECTIVETo study the mechanism of macrophage injury after trauma-hemorrhagic shock.

METHODSWistar male rats underwent trauma (closed bone fracture) and hemorrhage (mean arterial blood pressure of 35 mm Hg+/-5 mm Hg for 60 minutes, following fluid resuscitation). Rats without trauma, hemorrhage or fluid resuscitation served as controls. Peritoneal macrophages were harvested at 6 hours and 1, 2, 3, 7 days after traumatic hemorrhagic shock to determine the effects of pertussis toxin (PTX, as a specific inhibitor to Gi(alpha) and cholera toxin (CTX, as a stimulant to Gs(alpha) on macrophage-Ia expression and TNF-alpha production and levels of Gi(alpha) and Gs(alpha).

RESULTSThe macrophages from the injured rats revealed a significant decrease of Ia positive number and TNF-alpha release in response to LPS. Wi th pretreatment with PTX 10-100 ng/ml Ia positive cells and LPS-induced TNFalpha production in both control and impaired macrophages populations were dos e dependently increased. Both macrophages populations were not responding to CTX treatment (10-100 ng/ml). Western blot analyses showed that the levels of Gi(alpha) protein expression increased as much as 116.5%-148.8% of the control level fro m 6 hours through 7 days after traumatic hemorrhage. The levels of Gs protein expression were reduced at 6 hours and decreased to the lowest degree; 36% o f the control at day 1, began to return at day 2 and returned to the normal level at day 7, following traumatic hemorrhagic shock.

CONCLUSIONSPTX-sensitive G-protein may participate in th e modulation of macrophage-Ia expression and TNF-alpha release following traumatic hemorrhagic shock. Analyses of the alteration of Gi(alpha) and Gs protein express ions further supports the concept that G-protein is involved in trauma-induced macrophage signal transduction pathways.

Analysis of Variance ; Animals ; GTP-Binding Proteins ; immunology ; metabolism ; Histocompatibility Antigens Class II ; immunology ; Immunoblotting ; Lipopolysaccharides ; pharmacology ; Macrophages, Peritoneal ; immunology ; metabolism ; Male ; Rats ; Rats, Wistar ; Shock, Hemorrhagic ; blood ; immunology ; Signal Transduction ; Tumor Necrosis Factor-alpha ; biosynthesis

Objective　To investigate the mechanisms of Pinacidil prec onditioning protection of hemorrhagic shock rats. 　Methods　The rats were divided into 3 groups: a normal group ( n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditio ning was processed 24 h before making the hemorrhagic shock model. The cPLA 2 expression in myocardium was observed at different time points with western blot; Pinacidil preconditioning was processed 24, 48 and 72 h before making th e hemorrhagic shock model to observe hsp70 expression in myocardium and liver tissue with western blot. 　Results　Pinacidil preconditioning could increase hsp70 expres sion and decrease cPLA2 expression. 　Conclusions　Pinacidil preconditioning protects "shock cell" by inducing hsp70 overexpression and inhibiting cPLA2 expression, which is re sponsible for protecting myocardial and liver tissues of the hemorrhagic shock rats.

Objective　To investigate the role of β-endorphin (β-EP) in conA-induced spleen cell proliferation after traumatic hemorrhagic shock. Methods　①Wistar rats with traumatic hemorrhagic shock were used and killed 0, 1, 3, 6,12 and 24 h after traumatic hemorrhagic shock. Plasma specimens were collected and β-EP levels in plasma were detected. Rats with sham-operation served as the control. ②Spleen cells isolated from normal rats were cultured in shock plasma (group Ⅰ), inactivated shock plasma (group Ⅱ) and shock plasma+β-EP antiserum (group Ⅲ) respectively. Con A-induced spleen cell proliferation was observed. Results　①The plasma β-EP level was elevated significantly immediately after shock, and reached the peak 1 h later, then showed a deceasing tendency and restored to the level as before shock at 24 h. ②Shock plasma remarkedly suppressed spleen cell response to the mitogen conA (P<0.01) compared with control; ConA-induced spleen cell proliferative function in group Ⅱ was significantly increased than that in group Ⅰ (P<0.01), so did in group Ⅲ, which still lower than in control. Conclusion　The significantly elevated β-EP in the plasma after hemorrhagic shock might play an important role in inhibiting the proliferation of spleen cells.

AIM: To study the effects of hemorrhagic shock on BK Ca channel tyrosine phosphorylation in rat superior mesenteric artery and the role of nitric oxide (NO) in BK Ca channel tyrosine phosphorylation. METHODS: The hemorrhagic shock model [(35?5) mmHg] was established in rats and the whole lysate of superior mesenteric artery were extracted and analyzed by immune precipition (IP) and immunoblotting. The tyrosine phosphorylation levels of BK Ca channel alpha-subunit in mesenteric artery in hemorrhagic shock rats were investigated, and the modulation of BK Ca channel alpha-subunit tyrosine phosphorylation by NO and its dose-and time-dependended relationships were observed. RESULTS: The tyrosine phosphorylation level of BK Ca channel alpha-subunit in mesenteric artery in rats increased significantly after hemorrhagic shock 2 h and 4 h (P

AIM:To explore whether A3 adenosine receptor plays a role in the modulation of vascular reactivity after hemorrhagic shock in rat,and to find out the prospective drug target to restore the decreased vascular reactivity following hemorrhagic shock. METHODS:The hemorrhagic shock (40 mmHg) model was established in rat,and the reactivity of superior mesenteric artery (SMA) to norepinephrine (NE) was observed. A3AR expression at protein level and mRNA level were measured by Western blotting and RT-PCR respectively. RESULTS:The vascular reactivity of SMA to NE after hemorrhagic shock (40 mmHg) was decreased significantly in a biphasic response manner. The expression of A3AR mRNA in SMA after hemorrhagic shock decreased without significant difference. The expression of A3AR protein has a slight increase without statistical difference after 30 min of hemorrhagic shock and then has a significant decrease (especially at 2 h and 4 h after hemorrhagic shock). The usage of IB-MECA,a selective A3AR agonist,significantly increased the responsiveness of SMA to NE in hemorrhagic shock in rat. MRS1523,the selective A3AR antagonist,significantly abolished the restoration of the vascular reactivity to NE by IB-MECA in hemorrhagic shock in rat. CONCLUSION:A3AR plays a role in the modulation of vascular responsiveness to NE in hemorrhagic shock in rat,and the selective agonist of A3AR could restore the reactivity of SMA to NE in hemorrhagic shock in rat.

OBJECTIVE: To elucidate which one of &mgr;, delta and kappa opioid receptors is involved in the cardiovascular depression following traumatic hemorrhagic shock. METHODS: With traumatic hemorrhagic shock rat models, the changes of myocardial and brain &mgr;, delta and kappa opioid receptors and cardiovascular functions and their relationship with hemodynamic parameters were observed. The effects of delta and kappa opioid receptor antagonists on hemodynamic parameters of traumatic hemorrhagic shock rats were observed. RESULTS: Following traumatic hemorrhagic shock, the number of myocardial and brain delta and kappa opioid receptors significantly increased, their affinity did not alter, and the increased number of delta and kappa opioid receptors was significantly associated with the decreased hemodynamic parameters. However, &mgr; opioid receptor in heart and brain did not obviously change. delta opioid receptor antagonist ICI174,864 and kappa opioid receptor antagonist Nor-binaltorphimine (50 &mgr;g, Icv) could significantly reverse those decreased hemodynamic parameters. CONCLUSIONS: It suggests that opioid receptors, especially delta and kappa opioid receptors are closely related to the pathogenesis of traumatic hemorrhagic shock, and they play important roles in the depression of cardiovascular function following traumatic hemorrhagic shock.

Objective To explore the mechanism of adenosine triphosphatase (ATPase) of calcium overload in vascular smooth muscle cell (VSMC) in hemorrhagic shock rats. Methods Twenty-four male Wistar rats were randomly divide into four groups: control (Group C), shock start (Group S0), 2 hours post-shock (Group S2) and 4 hours post-shock (Group S4). The rat models with hemorrhage shock were produced by means of modified Wigger's method through bloodletting from femoral artery and keeping blood pressure at 40 mm Hg for 2 hours. The changes of cytosolic free Ca 2+ concentration (i) and the activities of Ca 2+ - ATPase and Na +-K +- ATPase in VSMC membrane and mitochondrial membrane were monitored in rats after shock. Results Mean channel fluorescence values of VSMC i in the Groups C, SO, S2 and S4 were 2.03?0.15, 2.37? 0.32 , 2.55?0.46 and 2.80?0.43 respectively and increased in a time-dependent fashion. Mean channel fluorescence values of VSMC i in the Groups S0, S2 and S4 was significantly higher than that in the Group C ( P