[The protective effects of ischemia preconditioning on the lung injury following with limbs ischemia/reperfusion].

OBJECTIVE: To explore the protective effects of ischemic preconditioning (IPC) on the lung injury following with limbs ischemia /reperfusion (LI/R). METHODS: The models of LI/R injury were constructed in rabbits. The blood from right external jugular vein and left common carotid artery, into and out-flowing pulmonary blood (IPB, OPB) respectively. Superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) in IPB and OPB and lung tissues were measured, as well as total nitric oxide synthase (tNOS) and inducible nitric oxide synthase (iNOS) in lung tissues were detected in different groups. The effects of IPC on the lung injury were observed. RESULTS: Compared with sham and before ischemic, the activity of SOD decreased and the content of MDA and NO increased after 4 h ischemia followed by 4 h reperfusion in IPB, OPB and lung tissues. The activity of tNOS and iNOS in lung tissues increased remarkably as well, there was statistical significance (P < 0.05, P < 0.01). SOD increased and MDA, NO, tNOS, iNOS decreased significantly by IPC before ischemia/reperfusion. The correlation analysis indicated that MDA was negatively correlated with SOD and was positively correlated with MDA, NO, iNOS (P < 0.01). CONCLUSION: Oxygen free radicals metabolic confusion of lung occurred in the course of LI/R, IPC could strengthen the resistance of peroxidation in lung and had protective effects on the lung injury following with LI/R.

[The protective effects of ischemic preconditioning on the kidney injury following with ischemia/reperfusion of limbs and the possible mechanisms].

AIM: To explore the protective effects of ischemic preconditioning on the kidney injury following with ischemia/reperfusion (I/R) of limbs. METHODS: The models of I/R injury of limbs were constructed in rabbits. The blood from right external jugular vein, renal artery and renal vein represent the peripheral blood, into and out-flowing kidney blood (IKB, OKB) respectively. Superoxide dismutase (SOD), malondialdehyde (MDA), blood uria nitrogen (BUN) in peripheral blood and SOD, MDA, nitric oxide (NO) in IKB and OKB were measured, as well as SOD, MDA, induced nitric oxide synthase (iNOS) in kidney were detected in different groups. The effects of ischemic preconditioning (IPC) on the kidney injury were observed. RESULTS: Compared with control group, the activity of SOD in peripheral blood, IKB, OKB and kidney decreased, and the content of MDA increased after 4 h ischemia followed by 4 h reperfusion. The content of BUN in peripheral blood, NO in IKB, OKB and iNOS in kidney increased remarkably as well. SOD increased and MDA, NO, BUN, iNOS decreased significantly by ischemic preconditioning (IPC) before ischemia/reperfusion. The correlation analysis indicated that MDA was negatively correlated with SOD and positively correlated with NO, BUN. CONCLUSION: Oxygen free radicals metabolic confusion of kidney occurred in the course of I/R of limbs, IPC could strengthen the resistance of peroxidation in kidney and had protective effects on the kidney injury following with ischemia/reperfusion (I/ R) of limbs

[Experimental research of prevention and therapy effect of anisodamine on acute respiratory distress syndrome (ARDS)].

AIM: To study preventive and therapeutic effect of anisodamine on acute respiratory distress syndrome(ARDS) induced by oleic acid and their mechanism of action. METHODS: Model of ARDS was made in rabbits by oleic acid (OA). The effect of anisodamine on the malondialdehyde (MDA), fibronectin (FN), lactate dehydrogenase (LDH) and acid phosphatase (ACP) in plasma, and superoxide dismutase (SOD) in erythrocyte and MDA, SOD and pulmonary surfactant (PS) in lung tissues homogenate and pathological examination of lung were observed. RESULTS: The administration of anisodamine before and after 30 minutes of injection OA decreased MDA, LDH and ACP, prevented the reduction of SOD, FN and PS. Compared with ARDS group, there was marked difference between the two, and alleviated lung injury. CONCLUSION: Anisodamine possesses preventive and therapeutic effects on ARDS by inhibiting lipid peroxidation and stabilizing membranes.

[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. RESULTS: The administration of zinc sulfate decreased MDA and XOD, prevented the reduction of SOD and PS, and alleviated lung injury. CONCLUSION: It is suggested that lung is injured during SMAO shock and zinc sulfate possesses preventive and therapeutic effect, through stabilized membrane.

[Function of endothelin-1 in neurogenic pulmonary edema].

AIM: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. METHODS: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. RESULTS: After heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. CONCLUSION: The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

[Influence of astragalus and zinc sulfate on the viscosity in erythrocyte membrane during intestinal ischemia - reperfusion(I/R) injury].

AIM: To study the influence of astragalus and zinc sulfate on the viscosity in erythrocyte membrane during intestinal I/R and their mechanism of action. METHODS: Models of rabbits intestinal I/R injury were made. The effect of astragalus and zinc sulfate on the viscosity and malondialdehyde (MDA) in erythrocyte membrane, superoxide dismutase (SOD) in erythrocyte, oxidase (XO) in plasma and MDA tissues homogenate were observed. RESULTS: The administration of astragalus and zinc sulfate decreased viscosity and MDA and XO, prevented the reduction of SOD, and alleviated I/R injury. CONCLUSION: Lipid peroxidation injury of the erythrocyte membrane was one of the pathogenesis of I/R injury, and astragalus and the zinc sulfate possessed effects of anti-lipid peroxide, stabilized erythrocyte membrane, increased red blood cell deform ability and raised microcircular perfusion.