Semigran M J, Cockrill B A, Kacmarek R, Thompson B T, Zapol W M, Dec G W, Fifer M A
Department of Medicine, Massachusetts General Hospital, Boston 02114.
J Am Coll Cardiol. 1994 Oct;24(4):982-8. doi: 10.1016/0735-1097(94)90859-1.
This study was performed to assess the utility of inhaled nitric oxide as a selective pulmonary vasodilator in patients with severe chronic heart failure and to compare its hemodynamic effects with those of nitroprusside, a nonselective vasodilator.
Preoperative pulmonary vascular resistance is a predictor of right heart failure after heart transplantation. Non-selective vasodilators administered preoperatively to assess the reversibility of pulmonary vasoconstriction cause systemic hypotension, limiting their utility.
Systemic and pulmonary hemodynamic measurement were made at baseline, during oxygen inhalation and with the addition of graded doses of inhaled nitric oxide or intravenous nitroprusside in 16 patients with New York Heart Association class III or IV heart failure referred for heart transplantation.
Pulmonary vascular resistance decreased to a greater extent with 80 ppm nitric oxide (mean +/- SEM 256 +/- 41 to 139 +/- 14 dynes.s.cm-5) than with the maximally tolerated dose of nitroprusside (264 +/- 49 to 169 +/- 30 dynes.s.cm-5, p < 0.05, nitric oxide vs. nitroprusside). Pulmonary capillary wedge pressure increased with 80 ppm nitric oxide (26 +/- 2 to 32 +/- 2 mm Hg, p < 0.05). Mean arterial pressure did not change with nitric oxide but decreased with nitroprusside. Seven of the 16 patients, including 1 patient who did not have an adequate decrease in pulmonary vascular resistance with nitroprusside but did with nitric oxide, have undergone successful heart transplantation.
Inhaled nitric oxide is a selective pulmonary vasodilator in patients with pulmonary hypertension due to left heart failure and may identify patients with reversible pulmonary vasoconstriction in whom agents such as nitroprusside cause systemic hypotension. Inhaled nitric oxide causes an increase in left ventricular filling pressure by an unknown mechanism.
本研究旨在评估吸入一氧化氮作为选择性肺血管扩张剂在重度慢性心力衰竭患者中的效用，并将其血流动力学效应与非选择性血管扩张剂硝普钠的效应进行比较。
术前肺血管阻力是心脏移植后右心衰竭的一个预测指标。术前使用非选择性血管扩张剂评估肺血管收缩的可逆性会导致全身性低血压，限制了它们的效用。
对16例纽约心脏病协会III或IV级心力衰竭且转诊接受心脏移植的患者，在基线、吸氧期间以及添加不同剂量的吸入一氧化氮或静脉注射硝普钠时进行全身和肺血流动力学测量。
与最大耐受剂量的硝普钠相比，80 ppm一氧化氮使肺血管阻力下降幅度更大（平均±标准误，从256±41降至139±14达因·秒·厘米⁻⁵）（硝普钠从264±49降至169±30达因·秒·厘米⁻⁵，p<0.05，一氧化氮与硝普钠相比）。80 ppm一氧化氮使肺毛细血管楔压升高（从26±2升至32±2 mmHg，p<0.05）。一氧化氮使平均动脉压未发生变化，但硝普钠使其下降。16例患者中有7例，包括1例使用硝普钠时肺血管阻力未充分下降但使用一氧化氮时下降的患者，已成功接受心脏移植。
吸入一氧化氮是因左心衰竭导致肺动脉高压患者的选择性肺血管扩张剂，可能识别出使用硝普钠等药物会引起全身性低血压的可逆性肺血管收缩患者。吸入一氧化氮通过未知机制导致左心室充盈压升高。
