Reimold S C, Byrne J G, Caguioa E S, Lee C C, Laurence R G, Peigh P S, Cohn L H, Lee R T
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
J Am Coll Cardiol. 1991 Oct;18(4):1085-90. doi: 10.1016/0735-1097(91)90771-z.
Treatment of patients with aortic regurgitation with vasodilators reduces regurgitant volume, ventricular dilation and left ventricular mass. Although these effects are presumably due to afterload reduction, it is also possible that the aortic regurgitant orifice area is not constant. To test the latter hypothesis, aortic regurgitation was created in 10 open chest sheep by partial resection of the noncoronary leaflet under direct visualization. Regurgitant flow was measured with an aortic supravalvular electromagnetic probe; aortic and left ventricular pressures were measured with catheter-tipped micromanometer pressure transducers. The effective regurgitant orifice area was calculated by a modification of the continuity equation in a manner similar to the Gorlin equation. The regurgitant orifice area was measured three times: after aortic regurgitation was created, after mean arterial pressure was increased by 15 to 25 mm Hg with intravenous dopamine and after mean arterial pressure was reduced by 15 to 25 mm Hg with intravenous sodium nitroprusside. Comparison of regurgitant volumes and areas obtained after creation of aortic regurgitation and at the conclusion of the experiment in the absence of dopamine or sodium nitroprusside demonstrated no significant change over time. Dopamine administration was associated with an 86 +/- 81% increase in regurgitant volume (p less than 0.01) and a 38 +/- 44% increase in regurgitant orifice area (p less than 0.01). Sodium nitroprusside administration resulted in a 51 +/- 14% decrease in regurgitant volume (p less than 0.001) and a 28 +/- 21% reduction in regurgitant orifice area (p = 0.007). In this model of acute aortic regurgitation, the effective regurgitant orifice area was altered by increasing or decreasing the aortic transvalvular pressure gradient.(ABSTRACT TRUNCATED AT 250 WORDS)
用血管扩张剂治疗主动脉瓣关闭不全患者可减少反流量、心室扩张和左心室质量。虽然这些作用可能是由于后负荷降低,但主动脉反流口面积也有可能并非恒定不变。为验证后一种假设,在10只开胸绵羊中通过直视下部分切除无冠瓣造成主动脉瓣关闭不全。用主动脉瓣上电磁探头测量反流量;用导管顶端微测压压力传感器测量主动脉和左心室压力。有效反流口面积通过对连续性方程进行修改后计算得出,计算方式类似于戈林方程。反流口面积测量三次:在造成主动脉瓣关闭不全后、静脉注射多巴胺使平均动脉压升高15至25毫米汞柱后以及静脉注射硝普钠使平均动脉压降低15至25毫米汞柱后。比较造成主动脉瓣关闭不全后以及在未使用多巴胺或硝普钠的实验结束时获得的反流量和面积,结果显示随时间无显著变化。给予多巴胺后反流量增加86±81%(p<0.01),反流口面积增加38±44%(p<0.01)。给予硝普钠后反流量减少51±14%(p<0.001),反流口面积减少28±21%(p = 0.007)。在这个急性主动脉瓣关闭不全模型中,通过增加或降低主动脉跨瓣压力梯度可改变有效反流口面积。(摘要截取自250词)