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.

Thyrotropin releasing hormone (TRH) and naloxone were compared in their antagonism to the effects of analgesia,addicton-induction,movement restatraining,respiration depression,LD50:etc of morphine.It was found that TRH was entirely different from naloxone in that it was not antagonistic at all to the morphine effects mentioned above.So TRH would be a better choice than naloxone in the treatment of traumatic shock.

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

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

OBJECTIVE:To observe the therapeutic effect of Herba Agastachis-Zhenqi liquid(HAZL)on the patients with functional dyspepsia.METHODS:Adult patients with functional dyspepsia were divided into HAZL treated group(67cases,10ml HAZL,t.i.d)and domperidone control group(34cases,domperidone10mg,t.i.d);30healthy volunteers served as normal control group.The clinical symptoms,the electrogastrogram,the serum motilin and gastrin were observed before and after HAZL administration.RESULTS:In HAZL group,the total effective rate of HAZL was61.2%(compared with control group,P

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

Objective To study the therapeutic effects of hypertonic sodium acetate dextran (HAD) in combination with dopamine (DA) on hemorrhagic shock complicated by pulmonary edema in the rats first entering high altitude. Methods Forty-two SD rats, first transported to Lhasa, Tibet (3 760 meters above the sea level), were anesthetized with sodium pentobarbital (30 mg/kg, ip). Hemorrhagic shock model with pulmonary edema was induced by hemorrhage (blood pressure at 50 mm Hg) plus intravenous injection of oleic acid (5 _l/100 g) for 1 hour. All the rats were equally divided into 6 groups, ie, normal control (no hemorrhage or oleic acid), hemorrhagic shock with pulmonary edema (HSPE), HSPE plus lactated Ringer's solution (LR, 4 ml/kg), HAD (4 ml/kg) alone, DA (2 mg/kg) alone and the combined use of HAD and DA groups. After drug administration, the hemodynamic parameters including mean arterial blood pressure (MAP), left intraventricular systolic pressure (LVSP) and the changes of intraventricular pressure (?dp/dt max) were observed at the 15th, 30th, 60th and 120th minutes respectively, blood gases at the 30th and 120th minutes respectively and the water content of the lung and the brain at the 120th minutes. Results As compared with LR control group, HAD (4 ml/kg) or DA (2 mg/kg) used alone significantly increased MAP, LVSP and ?dp/dt max ( P

To investigate the alterations of contractile function of VSM and it's primary mechanism in hemorrhagic shock rats, contractile tension of vascular rings induced seperately by NE,PE,Caffeine and K + was measured with tension conductor and physiological recorder. The results showed that after 2h and 4h of shock, contractile tension of vascular rings to NE was 76 17% and 66 50% as compared to the control group; contractile tension to 20 mmol/L caffeine and over 20 mmol/L K + was significantly decreased after 2h of shock;and decreased to 3?10 -6 M PE after 4h of shock. The data suggested that contractile tension of VSM would decrease after shock and it maybe at least in part related to the decreased function of both calcium influx from ex cells and calcium release from sarcoplasmic reticulum of vascular smooth muscle cells.

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.