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研究生:彭詩琪
研究生(外文):Shih-Chi, Peng
論文名稱:低氧影響肺血管活動性及血流分布的機轉
論文名稱(外文):The regional pulmonary vascular activity and flow distribution during hypoxia.
指導教授:黃坤崙黃坤崙引用關係
指導教授(外文):Kun-Lun, Huang
學位類別:碩士
校院名稱:國防醫學院
系所名稱:海底醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2007
畢業學年度:95
語文別:中文
中文關鍵詞:ㄧ氧化氮缺氧性肺動脈收縮肺血管活動性
外文關鍵詞:Nitric oxideNOHypoxic pulmonary vasoconstrictionHPVPulmonary vascular activity
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缺氧對於身體的影響非常大,而在多種型態缺氧中低氧性缺氧最為常見。局部缺氧時會產生缺氧性肺動脈血管收縮,肺部血管以收縮的方式來改變肺部血流的分佈,以維持一定的通氣/灌流比值達到最好的氧氣交換吸收狀態。但吸入低氧空氣時缺氧性肺動脈血管收縮並不明顯,表示整體肺部血管的確會自行調控,可能由於一氧化氮的釋放平衡了原本缺氧時所引起的血管收縮作用。因此本實驗目的是探討整體缺氧時局部肺血管活動性的變化及一氧化氮在低氧呼吸下對於肺血管活動所扮演的角色。本實驗以每組6-8隻雄性紐西蘭大白兔,給予吸入12%之低濃度氧氣半小時(低氧組),或利用一氧化氮酶抑制劑L-NAME將內生性一氧化氮生成抑制後,再同時給予吸入12%之低濃度氧氣半小時(L-NAME+低氧組),觀察其生理血液動力學之改變及肺部通氣血流分佈的變化,利用「多重惰性氣體排除技術」觀察肺部通氣/灌流分佈,及「螢光微顆粒分析技術」觀察肺部血流分佈狀態。實驗結果顯示低氧狀態會導致動脈平均血壓降低,而在低氧組的肺動脈壓沒有明顯變化,而L-NAME+低氧組產生缺氧性肺動脈血管收縮,並明顯看到肺動脈高壓及肺血管阻力都上升。多重惰性氣體排除技術測量顯示,各組在肺內分流、無效腔比例及高低通氣/灌流比值各肺區分部狀態沒有明顯變化。螢光微粒分析結果顯示,無論是否將內生性一氧化氮抑制,低氧並未造成肺部背至腹側或頭至尾端之顯著血流重新分佈,但是一氧化氮抑制後給予低氧明顯造成同一肺解剖平面上血流分佈較離散,亦即某些細小區域內的血流增加,而其鄰近區域則顯著下降,造成肺血管舒張及收縮的活動性增加,但此時的血管活動性變化比例與單純低氧時並無顯著差異。本研究得到的結論為在低氧的情況下,內生性的一氧化氮會影響缺氧性缺氧性肺動脈血管收縮的產生,但體內仍有其他血管舒張的物質產生,使當有肺動脈高壓時肺內血管並不會完全收縮。
Humans encounter hypoxia thoughout their lives. The vasoconstriction of the hypoxia area in the lung plays an important role in shunting away the blood flow and in maintaining a matched ventilation/perfusion. This redistribution of pulmonary blood flow improves arterial oxygenation. Hypoxic hypoxia is the most frequently to see in many types of hypoxia. The purpose of this study are the regional pulmonary vascular activity and the role of nitric oxide in pulmonary blood flow distribution during hypoxia. There are 6 to 8 of New Zealand rabbits in each group were selected to observe the hemodynamics and lung perfusion distribution changing, under the low FiO2 inspiration or low FiO2 inspiration moreover restrain nitric oxide by administration of L-NAME. We use multiple inner gas elimination technique (MIGET) to evaluate ventilation / perfusion and fluorescents microsphere technique to evaluate pulmonary perfusion. Our study result in physical parameters: exposure to 12%O2 reduce the mean arterial pressure from 91±6 to 71±4 mmHg and systemic vascular resistance from 180±20 to 166±18 mmHg/l/min in hypoxia 30 mins(n=8). In hypoxia group acute hypoxia did not elevate mean pulmonary arterial pressure. L-NAME pretreatment significantly enhanced the increase in pulmonary vascular resistance during acute hypoxia and attenuated the decrease in systemic vascular resistance. MIGET parameters: There is no significant changing in pulmonary shunting, the ratio of dead space and the region of high-low ventilation / perfusion distribution in all segment of lung in control groups and hypoxia group. L-NAME pretreatment increase the ratio of dead space during acute hypoxia. The status of fluorescents microsphere technique: there is no L-NAME pretreatment or not significant difference of total blood flow distribution in dorsal to ventral during acute hypoxia. Height separated from regression line mean raise pulmonary vascular activity in L-NAME+hypoxia group. Relavine of perfusion decrease mean vasoconstriction percentage increase. The vasoconstriction percentage in L-NAME+hypoxia group higher than the other two group. In conclusion, exogenous nitric oxide is an impotant vasodilator in pulmonary circulation. That nitric oxide lead vasodilation to balance hypoxic pulmonary vasoconstriction during hypoxia. But the other unknown vasoconstrictor or vasodilator to mediate pulmonary circulation during hypoxia.
正文目錄
【碩士論文目次】 頁次
正文目錄 Ⅰ
表目錄 Ⅱ
圖目錄 Ⅲ
中文摘要 Ⅴ
英文摘要 Ⅶ
第一章 緒論 1
第二章 實驗材料與方法 21
第三章 實驗結果 37
第四章 討論 75
第五章 結論 87
第六章 參考資料 88
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