Dysregulated renin-angiotensin system contributes to acute lung injury caused by hind-limb ischemia-reperfusion in mice.

The mechanism of acute lung injury (ALI) following limb ischemia-reperfusion (LIR) is not yet clear. We speculate that the unbalanced expression of angiotensin-converting enzymes (ACE and ACE2) and angiotensins [Ang II and Ang-(1-7)] in the renin-angiotensin system (RAS) is a major cause of ALI. To prove this hypothesis, pathological changes, lung edema, and permeability of wild-type mice at different time points within 12 h of reperfusion after 2 h of hind-limb ischemia were first detected by morphological method, measurements of wet-to-dry weight ratio, and bronchoalveolar lavage fluid.

[Preventive effects of Salvia miltiorrhiza on multiple organ edema in the rats of limb ischemia/reperfusion].

Objective: To investigate the preventive effects of Salvia miltiorrhiza (SM) on multiple organ edema in the rats which suffered from hind limb ischemia/reperfusion( LI/R).

Methods: Twenty four Wistar rats were randomly divided into 3 groups (n = 8): control group (C group), ischemia/reperfusion group (I/R group ), Salvia miltiorrhiza group (SM group). Referring to Tourniquet method, the model rats which underwent 4 hours ischemia and 4 hours reperfusion of hind limbs were made.

Role of angiotensin-converting enzyme (ACE and ACE2) imbalance on tourniquet-induced remote kidney injury in a mouse hindlimb ischemia-reperfusion model.

In this study, the relationship between the local imbalance of angiotensin converting enzymes ACE and ACE2 as well as Ang II and Ang (1-7) and renal injury was observed in the different genotypes mice subjected to tourniquet-induced ischemia-reperfusion on hind limbs. In wild-type mice, renal ACE expression increased while renal ACE2 expression decreased significantly after reperfusion, accompanied by elevated serum angiotensin II (Ang II) level and lowered serum angiotensin (1-7) (Ang (1-7)) level. However, renal Ang (1-7) also increased markedly while renal Ang II was elevated.

[Effects of taurine on TNF-alpha and NF-kappaB expression of liver injury after limbs ischemia/reperfusion in rats].

Aim: To investigate the effect of pretreatment with taurine on liver injury changes and the change of tumor necrosis factor alpha and NFkappaB expression following rats limbs ischemia/reperfusion.

Methods: The model of limbs ischemia/reperfusion injury on rats was adopted in the experiment. Wistar rats were randomized into 4 groups (n = 10): Control group, T group, I/R group and TR group.

[Effect of ischemic preconditioning on lung injury induced by ischemia/reperfusion in the hind limbs of rats].

Aim: To study the effect of ischemic preconditioning on lung injury following ischemia/reperfusion (I/R) in the hind limbs of rats.

Methods: Wistar rats were randomly divided into four groups (n=8): control group,limbs ischemia/reperfusion (LI/R) group, ischemia preconditioning (IPC) group and L-NAME group. At the end of the experiment, blood/gas analysis and the contents of serum MDA, NO, ET and lung tissue MDA, NO, ET, MPO were measured.

[The affection and significance of NO on the expression of P-selectin in renal injury following hind limb ischemia/reperfusion in rats].

Aim: To probe into the affection and significance of NO on the expression of P-selectin in renal injury following hind limb ischemia/reperfusion in rats.

Methods: In accordance with the conventional approaches of our department, the model rats were prepared after they were made to undergo 4 hours or ischemia followed by 4 hours of reperfusion of hind limbs. The Wistar rats were divided into four groups randomly: Control group, LI/R group, L-Arg group and L-NAME group.

[Effect of MK801 on apoptosis in the development of brain injury after hind limbs ischemia/reperfusion in rats].

Aim: To evaluate development of brain injury after hind limbs ischemia/reperfusion (LI/R) in rats, and the effect of MK801 on the brain injury following LI/R.

Methods: The limbs ischemia/reperfusion model was established in rats. The MDA contents were evaluated in each group, apoptotic cells were detected with TUNEL, the expression of apoptosis-associated protein, such as bcl-2, cytoC and caspase-3 were determined with immunohistochemistry and Western-blot.

[Expression NOS in acute lung injury following limb ischemia/reperfusion and its significance in rats].

Aim: To investigate the expression and role of inducible NOS (iNOS) and endothelial NOS (eNOS) in acute lung injury following limb ischemia/reperfusion (4h/4h).

Methods: Wistar rats were randomized into four groups: control group, ischemia/reperfusion (I/R) group, L-Arginine (L-Arg) pretreatment group, Aminoguanidine (AG) pretreatment group. The lung tissue of each group was subjected to assay of content of MDA, MPO, W/D and NO2-/NO3-.

[Therapeutic effect of zinc sulfate on lung injury during superior mesenteric artery occlusion(SMAO) shock].

Aim: To study preventive and therapeutic effect of zinc sulfate on lung injury during superior mesenteric artery occlusion (SMAO) shock and their mechanism of action.

Methods: Model of rabbit SMAO shock was made. The effect of zinc sulfate on the malondialdehyde (MDA) in erythrocyte membrane and plasma, oxidase (XOD) in plasma, superoxide dismutase (SOD) in erythrocyte and MDA, SOD and pulmonary surfactant (PS) in lung tissues homogenate were observed.

[The protect effect of ischemic preconditioning on the gastric mucosal injury following ischemia/reperfusion of hind limbs of rats].

Aim: To observe the degree of gastric mucosal injury following limb ischemia/reperfusion (LI/R), and to investigate the mechanism of gastric mucosal injury and the protection of ischemic preconditioning (IPC) on gastric mucosal injury.

Methods: The model rats which underwent 4 hours of ischemia and 4 hours of reperfusion of hind limbs were made. Then we respectively observed and determined the histologic lesion score after I/R and IPC + I/R.

[Effects of PKC activation on apoptosis during ischemia/reperfusion in L-6TG rat skeletal myoblasts].

Aim: To study the effects of PKC activation on apoptosis during ischemia/reperfusion in L-6TG rat skeletal myoblasts.

Methods: Cultured L-6TG cells were divided into 3 groups: control group (C), ischemia/reperfusion group (I/R), PMA + ischemia/ reperfusion group (PMA), SOD, XOD and free calcium and mitochondrial respiration in L-6TG cell were evaluated in each group. Apoptosis was detected by flow cytometer with PI staining method and agarose gel electrophoresis, the immunohistochemical method was used to determine the expression of caspase-3.

[A cell model of ischemia/reperfusion injury on skeletal muscle].

Aim: To establish a model of ischemia/reperfusion injury on L-6TG cell.

Methods: Cultured L-6TG cells were divided into 2 groups: control group (C), ischemia/reperfusion group (I/R), LDH in culture fluid, SOD, XOD, free calcium in L-6TG cell and mitochondria respiration were evaluated in each group, the micromorphologic changes were observed with microscope.

Results: Compared with control group, after L-6TG cell suffered ischemia 4 hours and reperfusion 4 hours, LDH in culture fluid, XOD, free calcium in L-6TG cell all increased significantly, while SOD in L-6TG cell and mitochondrial respiration decreased, structural damage to L-6TG cell was severe.

[The effect of NO, ET-1 on brain injury after hind limbs ischemia/reperfusion in rats].

Aim: To study the roles of nitric oxide (NO) and ET-1 in brain injury after hind limbs ischemia/reperfusion in rats and to investigate the effect of NO/ ET-1 balance on brain injury.

Methods: On a model of the hind limbs ischemia/reperfusion (LI/R) of rats, we used L-Arg(L-arginine, L-Arg), one of the substrates in the process of nitric oxide, aminoguanidine (AG) which inhibits nitric oxide synthase(NOS) and ETA receptor antagonist BQ123, to observe the changes of NO, ET-1, MDA, XOD, SOD, LDH in plasma and tNOS, iNOS, cNOS, NO, ET-1, MDA, XOD, MPO, SOD in brain tissue.

Results: Compared with the control group, the content of MDA, XOD, LDH in plasma and MDA, XOD, MPO in brain tissue increased.

[The protective effect of taurine on lung injury following limbs ischemia/reperfusion of rats].

Aim: On the model of limb ischemia/reperfusion (LIR), the effects of taurine on pulmonary morphological changes in rats were observed.

Methods: Wistar rats were divided into three groups (n=8): control group, ischemia/reperfusion group (IR) and taurine + IR (Tau + IR). Then macroscopic inspection and optical and transmission electron microscopies (TEM) were performed to assess the morphological changes of the lung tissues and their lung index (LI) and lung permeability index (LPI) and reactive oxygen species (ROS), malondialdehyde (MDA) were measured as well.

[The effect of nitric oxide on acute lung injury following ischemia/reperfusion of hind limbs in the rat].

On a model of reperfusion after ischemia in the hind limbs (LIR) of rats, we used aminoguanidine (AG) which inhibits nitric oxide synthase (NOS) and L-arginine (L-Arg), one of the substrates in the process of nitric oxide synthesis, to observe the changes in NO, NOS, malondialdehyde (MDA), myeloperoxidase (MPO) and wet/dry ratio (W/D) in both skeletal muscles and the lung as well as the changes in phosphatidyl choline (PC) of lung surfactant. The morphologic changes were observed with microscopy. It was observed that the values of NOS, MPO, MDA of the muscle and lung in LIR group increased significantly and the content of PC decreased obviously compared with those of the normal control.