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1.
Journal of Biomedical Engineering ; (6): 132-137, 2010.
Article in Chinese | WPRIM | ID: wpr-341667

ABSTRACT

This experimental study was designed to explore the possible mechanisms of Cariporide, a kind of Na+/H+ exchanger inhibitor, for protecting the lung from warm ischemia/reperfusion injury (WI/RI) of isolated rat lung model. Thirty isolated rat lungs were established on the Langendorff apparatus and randomly divided to three groups (n = 10, each): control group (C group), ischemia/reperfusion group (IR group) and Cariporide group (CP group). Mean pulmonary artery pressure (MPAP) and peak airway pressure (pAwP) were monitored continuously. At the end of reperfusion, right bronchoalveolar lavage was performed, bronchoalveolar lavage fluid (BALF) recovery rate (BALFRR) was recorded, and protein content in BALF was measured. Lung water content (LWC), malondialdehyde (MDA) and superoxide dismutase (SOD)of left lung tissue were measured; histomorphology evaluation was performed under light microscope and transmission electron microscope. In comparison with the data from IR group, BALF protein concentration, LWC, MDA content and MPAP content of reperfusion were significantly decreased, but SOD activity was increased in CP group. Histomorphologic feature also showed that pathological change significantly reduced in CP group. In this rat WI/RI model, the mechanism by which the selective Na+/H+ exchanger inhibitor (Cariporide) attenuates lipid peroxidation induced by WI/IR may be: preventing Ca2+ overload via inhibiting the transport of Na+/H2 exchanger-1 (NHE1) in the context of the coupled exchanger, thereby reducing the activation of xanthine oxidase pathway and oxygen free radical liberation which is dependent on certain intracellular Ca2+ concentration, and lastly promoting the endogenous antioxidative mechanism.


Subject(s)
Animals , Male , Rats , Antioxidants , Pharmacology , Guanidines , Pharmacology , In Vitro Techniques , Ischemic Preconditioning , Lung , Rats, Sprague-Dawley , Reperfusion Injury , Sodium-Hydrogen Exchangers , Sulfones , Pharmacology , Superoxide Dismutase , Metabolism , Warm Ischemia
2.
Chinese Journal of Anesthesiology ; (12)1994.
Article in Chinese | WPRIM | ID: wpr-674154

ABSTRACT

Objective To assess the effect of leukocyte fihration on systemic inflammatory response to cardiopulmonary bypass.Methods Twelve mongrel dogs weighing 25-30 kg were randomly divided into 2 groups (n=6 each):control group(C)and leukocyte depletion group(LD).The dogs were anesthetized with intraperitoneal pentobarbital 25 mg?kg~(-1).The trachea was intubated.The arterial line of CPB was connected with aortic cannula and the venous line with a cannula inserted into right atrium.The leukocyte-depletion filter LD-1 was positioned in the venous line of CPB circuit.Aorta was clamped at 10 min of CPB and St.Thomas cardioplegic solution 20 ml?kg~(-1) was injected into the root of aorta.The filter was used for 5 min starting from 2 min of CPB. Aorta was clamped for 60 min.Blood samples were taken from femoral vein before CPB(T_0,baseline), immediately after aortic clamping(T_1)at 30 min of aortic clamping(T_2)5 min after aortic unclamping(T_3)at the termination of CPB(T_4)and 2 h after termination of CPB(T_5)for leukocyte count and determination of plasma L-selectin,IL-6 and IL-8 concentrations and MPO activity.The IL-6 and IL-8 concentrations in the filter LD-1 were measured at 30,60 and 90 rain after leukocyte filtration.The membrane of filter LD-1 was taken at 90 min after filtration for microscopic examination.Results The leukocyte count was significantly lower at T_1 in LD group than in C group.The plasma L-selectin,IL-6,IL-8 concentrations and MPO activity were significantly increased during CPB as compared to the baseline at T_0 in both groups but were lower at T_5 in LD group than in C group.The IL-6 and IL-8 concentrations in LD-1 filter were increased at 60 and 90 min after filtration as compared to those at 30 min.The filter membrane was covered with enormous number of leukocytes.Conclusion Leukocyte filtration can decrease systemic inflammatory response to CPB in dogs.

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