ABSTRACT
<p><b>AIM</b>To study preventive and therapeutic effect of zinc sulfate on lung injury during superior mesenteric artery occlusion (SMAO) shock and their mechanism of action.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>The administration of zinc sulfate decreased MDA and XOD, prevented the reduction of SOD and PS, and alleviated lung injury.</p><p><b>CONCLUSION</b>It is suggested that lung is injured during SMAO shock and zinc sulfate possesses preventive and therapeutic effect, through stabilized membrane.</p>
Subject(s)
Animals , Female , Male , Rabbits , Lung , Metabolism , Lung Injury , Drug Therapy , Metabolism , Mesenteric Artery, Superior , Pathology , Mesenteric Vascular Occlusion , Drug Therapy , Metabolism , Shock , Drug Therapy , Metabolism , Zinc Sulfate , Therapeutic UsesABSTRACT
<p><b>AIM</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>Compared with the control group, the content of MDA, XOD, LDH in plasma and MDA, XOD, MPO in brain tissue increased. The activity of SOD decreased (P < 0.01). The content of tNOS, iNOS in brain tissue increased, cNOS decreased (P < 0.01). The content of NO, ET-1 in I/R group in plasma and brain tissue increased, the ratio of NO/ET-1 decreased. The brain injury was deteriorated. After using L-Arg and BQ123, the ratio of NO/ET-1 in plasma and brain tissue increased, the brain injury lightened. Whereas after using AG, the ratio of NO/ET-1 decreased, brain injury became more serious.</p><p><b>CONCLUSION</b>The NO/ET-1 ratio decreased after LI/R, brain injury became more serious.</p>
Subject(s)
Animals , Male , Rats , Brain Injuries , Pathology , Endothelin-1 , Metabolism , Extremities , Nitric Oxide , Metabolism , Rats, Wistar , Reperfusion Injury , Metabolism , PathologyABSTRACT
<p><b>AIM</b>To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.</p>