| As important message molecule and effect molecule in biology, nitric oxide(NO) takes part in many physiological and pathological regulationsJvfO plays an important role in Endotoxin-induced pulmonary injury among them.The main purpose of the present work is to investigate the effects of nitric oxide sythase(NOS) inhibitors aminoguanidine(AG) and NG-mtro-L-arginine(L-NA) and NO donor L-arginine on endotoxin induced pulmonary injury in rats. 1 Forty healthy male SD rats weighing 300±20g were used The animals were anesthetized with 20% urethane Ig · kg-1 .Common carotid artery (CAA) and common carotid vein (CAV) were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into five groups: group 1: control; group 2: LPS (5 mg · kg-1 intravenous injectionJV) group 3: high dose AG (100mg · kg-1 intraperitoneal injectionJP); group 4: middle dose AG (50mg · kg-1 IP); group 5: low dose AG (25mg · kg-1 IP). Group 1: 0.9% saline solution was given and the animals were killed 6 h after the saline solution. Group 2: 0.9% saline solution was given 3 h after LPS iv and the animals were killed 3 h after medication. Group 3,4 and 5: AG was given 3 h after LPS iv and the animals werekilled 3 h after medication respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured.2 Forty healthy male SD rats weighing 300±20g were randomly divided into five groups: group 1: control; group 2: LPS (5 mg · kg-1 intravenous injection, IV); group 3: high dose L-NA (20mg · kg-1 intraperitoneal injection, IP); group 4: middle dose L-NA (lOmg · kg-1 IP); group 5: low dose L-NA (5mg *kg"' IP). In each therapeutic group, L-NA 20mg · kg-1, 10mg · kg-1. 5mg · kg-1 was given 3 h after LPS iv respectively and the other methods used in this section is same as the first section.3 Forty eight healthy male SD rats weighing 300±20g were randomly divided into six groups: group 1: control; group 2: LPS (5 mg · kg"1 intravenous injection, iv); group 3: AG(50mg · kg-1 intraperitoneal injection, IP); group 4: high dose L-arginine (500mg · kg-1,IP); group 5: low dose L-arginine (250mg · kg-1 IP). Group 6: L-arginine+AG(500nig · kg-1,50mg · kg-1,IP). In each therapeutic group, AG^ L-argunine^ L-arginine+AG was given 3h after LPS iv respectively and the other methods used in this section is same as the first section.1 The effects of NOS inhibitor AG on endotoxin induced pulmonary injury in ratsThe studies we have performed showed: 1.1 The MAP of the rats was significantly lower in the LPS group(57.88 ± 7.54mmHg) than in the control group (96.29+3.96mmHg) at 6h after LPS (P<0.01).After the AG(100mg/kg and 50mg/kg) were administrated respectively,the MAP of the rats in AG groups (96.90 ± 3.62,93.65±10.49mmHg) were markedly higher than that of LPS group(P<0.01) at 6h after LPS.1.2 The NO content in the plasma of the rats was much increased in the LPS group than that in the control group at 3h,6h after LPS (P<0.01). After the AG(100mg/kg and 50mg/kg) were administrated respectively, the NO content in the plasma of the rats in AG groups was much lower than that of LPS group at 6h after LPS(P<0.01). In low dose AG(25mg/kg) group, the NO content in the plasma of the rats was not significantly different from that of LPS group.1.3 The NOS activity in the lung tissue of the rats in the LPS group was significantly higher than that in the control group at 6h after LPS (PO.01); In contrasting with LPS group, NOS activitiy in the lung tissues of the rats in high dose AG group and middle dose AG group was significantly inhibited (PO.01) at 6h after LPS;In low dose AG, NOS activity in the lung tissue of the rats was not significantly different from that of LPS group (PX).05).1.4...
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