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Inhalation of Nitric Oxide in Acute Respiratory Distress Syndrome

成人呼吸窘迫症候群患者吸入一氧化氮

摘要


一氧化氮吸入選擇性擴張具高血管張力的可通氣肺部。非通氣肺部的氧合作用常因為相對血流減少而改善。一氧化氮的大部分效應是經由激發腺嘌呤環酵素所產生的CGMP所媒介。成人呼吸窘迫症候群病患吸入一氧化氮(選擇性肺部血管擴張劑),減少肺部動脈血壓及增加氧合作用,因為分流減少,減少右心室舒張末期和收縮末期容積,增加右心室收縮分率,但平均全身血壓及心臟指數並不改變。一氧化氮吸入能夠迅速增加氧合作用,一旦停止使用,這個效應馬上消失。一氧化氮吸入能夠因為減少肺部靜脈血管張力,而減少肺部微血管的靜水壓力。一氧化氮吸入能夠因為抑制氧化傷害,而減少肺部微血管的通透性,一氧化氮吸入能夠扮演自由基清除者,而減少氧化傷害。成人呼吸窘迫症候群病患的處理並不一致,少數特殊病患的生存,不容易在多數異質病患發現。氣體交換的改善並不一致,可能也不具意義。良好反應常和基礎肺部血管張力、肺泡容積增加、初期分流增加、心輸出量增加、和ABO血型有關。一氧化氮吸入結合增加肺部血管張力或增加一氧化氮吸入效應的方法,可能得到比一氧化氮吸入更好的結果。一氧化氮吸入可能改善成人呼吸窘迫症候群病患通氣的新方案,例如高頻通氣和液體通氣。

並列摘要


Inhalation of nitric oxide (INO) selectively vasodilates ventilated lung regions with increased vascular tone. The oxygenation of nonventilated regions often improves due to a reduction in relative blood flow. Most effects of NO are mediated by cyclic GMP (cGMP) resulting from the activation of adenylate cyclase by NO. Selective pulmonary vasodilation by INO in acute respiratory distress syndrome (ARDS) reduced pulmonary artery pressure (PAP) with increased PaO2/FiO2 as the shunt decreased, lowered right ventricle end-diastolic volume (RVEDV) and right ventricle end-systolic volume (RVESV), and increased the right ventricle ejection fraction (RVEF), but the mean artery pressure (MAP) and cardiac index (CI) did not change. With INO, there was a rapid improvement in PaO2/FiO2, and this effect was immediately lost on discontinuation. INO may reduce hydrostatic forces in pulmonary capillaries by decreasing pulmonary venous tone. INO may also reduce pulmonary capillary permeability by inhibiting oxidant injury, and INO acts as a free radical scavenger and attenuates oxidative damage. Management of ARDS was not standardized between groups, and survival benefits to small subgroups were lost within large groups of heterogenous ARDS patients. Improvement in gas exchange was variable and may not be meaningful. A favorable response is related to baseline pulmonary vascular tone, alveolar recruitment, high initial venous admixture, increased cardiac output (CO), and ABO blood type. The combination of INO with other agents that increase pulmonary vascular tone or prolong or accentuate the effect of INO may lead to better results than INO. INO may improve new modalities, such as high frequency ventilation and partial liquid ventilation (PLV), to ventilate ARDS patients.

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