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作 者:张洪伟[1] 曾泽戎[2] 宋俊峰[3] 贾斌[2] 温光楠[2]
机构地区:[1]第四军医大学西京医院胃肠外科,陕西西安710032 [2]第四军医大学病理生理教研室,陕西西安710032 [3]第四军医大学神经生物研究所,陕西西安710032
出 处:《中国病理生理杂志》2002年第5期510-513,共4页Chinese Journal of Pathophysiology
摘 要:目的 :观察高浓度氯气染毒时肺血流动力学和呼吸功能变化并探讨其在肺损伤中的作用。方法 :35只家兔 ,随机分为 :离体肺组 :10只离体兔肺在稳定后吸入氯气 (5 0× 10 -4,2 0min)。在回流压力恒定的条件下 ,测定灌流压力、气道压力、潮气量、肺重量等变化。另 9只离体兔肺设为正常对照 ;整体动物组 :8只动物自气管插管吸入氯气 (5 0× 10 -4,2 0min) ;另 8只为对照组。检测肺动脉压力、呼吸频率、气道压力、潮气量等的变化 ;实验结束时均测定肺湿 /干重比值。结果 :离体肺组 :控制回流压力与灌流液流速 (133mL/min)不变 ,染毒后灌流压力即有缓慢而持续的升高 ;染毒开始 10min离体肺肺重量有一过性的降低 ,后开始持续增高 ,染毒后 6 0min肺重量显著大于对照组、出现肺水肿 ,继而灌流压力也显著升高 ,潮气量减少 ,灌流液血球压积值显著增高 ;整体动物染毒后肺动脉压力也有缓慢的升高 ,但没有剧烈的改变 ;呼吸频率加快 ,气道内压力波动幅度加大 ,潮气量减少。染毒后 6 0min出现明显的肺水肿。结论 :高浓度氯气染毒可导致肺动脉 /灌流压力升高及肺水肿。但肺动脉 /灌流压力的改变并不是导致肺水肿的主要原因。氯气染毒后引起动物的呼吸频率加快、气道内压增大 ,潮气量减少。AIM: To investigate the effect of high concentration of chlorine gas(Cl 2) exposure on lung haemodynamic and respiratory function in intact and isolated perfused rabbit lungs (IPLs). METHODS: 8 intact and 10 IPLs were exposed to Cl 2 at high concentration(50×10 -4 )for 20 min, as measured group, 8 additional intact and 9 IPLs, which were similarly treated but not exposed to Cl 2, served as controls. The changes of lung weigh of IPL(△W)?pressure of pulmonary artery(Pa)and venous pressure(Pv)?airway pressure and tidal volume(TV) were continuously measured and recorded simultaneously. RESULTS: In IPL group: While the perfusing blood flow was kept constant (133.3 mL/min), and Pv did not change, following the exposure, the Pa increased slightly, then the lung weight were increased significantly and the TV decreased . Hematocrit of perfusate of EIPL and parameters of lung water increased also. In intact group : Pa increased slightly, respiratory rate accelerated immediately, and TV decreased. CONCLUSION:Although mean Pa increased continuously and slightly in both intact and IPL group following the exposure to high concentration of Cl 2, the primary cause of edema was most likely to alter pulmonary capillary permeability. The respiratory rate accelerated and TV decreased due to exposure to Cl 2 enhanced hypoxia of intact rabbits.
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