Mitochondrial Drp1 recognizes and induces excessive mPTP opening after hypoxia through BAX-PiC and LRRK2-HK2.

Mitochondrial mass imbalance is one of the key causes of cardiovascular dysfunction after hypoxia. The activation of dynamin-related protein 1 (Drp1), as well as its mitochondrial translocation, play important roles in the changes of both mitochondrial morphology and mitochondrial functions after hypoxia. However, in addition to mediating mitochondrial fission, whether Drp1 has other regulatory roles in mitochondrial homeostasis after mitochondrial translocation is unknown.

Enhanced hemostatic performance of tranexamic acid-loaded chitosan/alginate composite microparticles.

Novel microparticles based on chitosan and sodium alginate were prepared using emulsification and cross-linking technologies. The spherical microparticles had a porous surface and a diameter of 2 ~ 40 μm. In simulated body fluid, these microparticles quickly swelled but gradually degraded.

[Study on the haemostatic efficiency of composite bio-particles].

A porous composite particle (CP) was fabricated by the methods of emulsification and cross-link based on chitosan, alginate and collagen protein, and the tranexamic acid-loaded composite particles (TACP) was prepared by immersing the composite particle into the solution of tranexamic acid and by freeze drying. In the hepatic and splenic hemorrhage model of rabbits, CP and TACP were randomly used as haemostatic agents, and the Suxiaozhixuefen (Flashclot) was used as control. The corresponding hemostatic time and bleeding amount were observed respectively.

[Effect of poly-adenosine diphosphate ribosyl-polymerase on vascular hyporeactivity in rats with hemorrhagic shock].

Objective: To study the effects of poly-adenosine diphosphate ribosyl-polymerase (PARP) on vascular hyporeactivity during hemorrhagic shock in rats.

Methods: Sprague-Dawley (SD) rats were randomly divided into three groups: shock, 3-aminobenzamide (3-AB) pretreatment+shock, and sham operation. Bleeding from the femoral artery to induce hemorrhagic shock model.

Mechanisms of Rho kinase regulation of vascular reactivity following hemorrhagic shock in rats.

Our previous research showed that Rho kinase took part in the regulation of vascular hyporeactivity after shock. The objective of the present study was to investigate its mechanism. With isolated superior mesenteric artery (SMA) from hemorrhagic shock rats, we studied the relationship of Rho kinase regulating vascular reactivity to calcium sensitivity and myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK).

[Regulatory effect of protein kinase C and protein kinase G on calcium sensitivity of vascular smooth muscle cells following hemorrhagic shock].

Objective: To observe the effect of protein kinase C (PKC) and protein kinase G (PKG) on calcium desensitization following hemorrhagic shock in rats.

Methods: The model of hemorrhagic shock was replicated by blood letting and maintaining mean arterial pressure at 40 mm Hg (1 mm Hg=0.133 kPa) for 2 hours.

Gene damages of mitochondrial DNA encoding cytochrome oxidase of intestinal epithelial cells in hemorrhagic shock rats.

Objective: To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells.

Methods: Wistar rats were used and divided into two groups: hemorrhagic shock group and control group. Hemorrhagic shock model of rats was utilized in this experiment.

Effects of seawater immersion on the functions of mitochondria of myocardium and hepatocyte in hemorrhagic shock rats.

Objective: To investigate the effects of seawater immersion on the function of myocardium and hepatocyte mitochondria in experimental hemorrhagic shock rats.

Methods: Twenty-four male Wistar rats were divided into three groups (n=8 in each group): control group, HSL group (hemorrhagic shock group on land) and HSS group (hemorrhagic shock group in seawater). The hemodynamic parameters, activities of H(+)-ATPase (adenosinetriphosphatase), succinate dehydrogenase (SDH) and Ca(2+)-Mg(2+)-ATPase, the calcium contents in myocardium and hepatocyte mitochondria were measured and the changes of proton translocation across the inner mitochondrial membrane were analyzed.

[Changes in systemic and local vascular reactivity in hemorrhagic shock and the therapeutic effect of delta opioid receptor antagonist ICI174,864].

Objective: To investigate the changes in systemic and local vascular reactivity following hemorrhagic shock of different severity and the therapeutic effect of alpha opioid receptor antagonist ICI174,864.

Methods: Fifty-six Wistar rats were used in two experiments. In experiment I, 32 rats were equally divided into sham operation group, 1 hour, 2 hours and 3 hours hypotension groups.

Changes of proton transportation across the inner mitochondrial membrane and H(+)-ATPase in endotoxic shock rats.

Objective: To investigate the changes of proton transportation across the inner mitochondrial membrane (IMM) and H(+)-ATPase of hepatocytes in endotoxic shock rats.

Methods: Endotoxin from E. Coil of 5.

[Effect of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat].

Objective: To study the effects of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat.

Methods: One hundred and twenty-six SD rats transported to Lasa, Tibet, 3 760 meters above the sea level, were anesthetized one week later with sodium pentobarbital (30 mg/kg, intraperitoneal). Hemorrhagic shock with pulmonary edema model was induced by hemorrhage (50 mm Hg for 1 hour, 1 mmHg=0.

[Beneficial effect of thyrotropin-releasing hormone in combination with HSD on hemorrhagic shock with pulmonary edema at high altitude in the rat].

Objective: To study the effects of thyrotropin-releasing hormone (TRH) in combination with hypertonic saline/dextran (7.5% NaCl + 6% Dextran 40, HSD ) on hemorrhagic shock with pulmonary edema in the rats which were recently brought to high altitude.

Methods: Forty-nine SD rats, transported to Lasa, Tibet, which was 3,760 meters above the sea level, were anesthetized one week later with sodium pentobarbital (30 mg/kg, intraperitoneal).

Effects of LPS, PLA(2) and OFR on proton translocation across inner mitochondrial membrane and H(+)-ATPase in the liver.

OBJECTIVE: To elucidate the effects of lipopolysaccharide (LPS), phospholipase A(2) (PLA(2)) and oxygen free radical (OFR) on proton transmembrane translocation and H(+)-ATPase. METHODS: The normal rats were sacrificed for preparetion liver mitochondria and submitochondrial particles for experiments in vitro. Submitochondrial particles were incubated with LPS (100 &mgr;g/mL), PLA(2) (10 u/mL) and FeSO(4)/Vit C (30/90 &mgr;mol/L) at 30 degrees C for 30 min.