Bittner H B, Chen E P, Kendall S W, Van Trigt P
Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Chest. 1997 Mar;111(3):706-11. doi: 10.1378/chest.111.3.706.
Right ventricular (RV) failure, which is a leading cause of early morbidity and mortality following cardiac transplantation, is attributed to the inability of the donor RV to acutely compensate for the recipient's elevated pulmonary vascular resistance (PVR). Furthermore, the effect of donor brain death (BD) on RV function is unclear. The purpose of this study was to investigate the effects of donor BD on RV function in the setting of elevated PVR. The interactions of the RV and its afterload, the pulmonary vasculature, and left atrial pressure were assessed by measurements of pulmonary vascular energetics and their oscillatory nature using proximal ultrasonic pulmonary artery (PA) flow probe and micromanometers in the proximal and distal PA in 20 mongrel dogs (25.8 +/- 0.4 kg, five control animals). A band was placed around the distal PA (PA-systolic gradient > 15 mm Hg). BD was induced by rising intracranial pressure and was validated neuropathologically. Data were collected at 0, 2, 4, and 6 h after BD in both banded and control animals. Fourier analysis was used to calculate RV oscillatory power, mean power, and total power (TP). Comparison of changes due to banding were made to baseline measurements using multivariate analysis and paired Student's t test (p < 0.05). A significant twofold to fourfold increase in pulmonary impedance and PVR occurred with an acute rise in PA gradient. Control animals tolerated acute increases in PVR without significant changes in TP. There was a significant increase of RV TP from 73 (+/-11) to 98 (+/-10) mW at baseline after the acute rise in PVR and impedance. After BD, the response to increased PVR and impedance was abolished significantly compared with baseline and control animals, suggesting a significant loss of compensatory TP to sustain pulmonary vascular blood flow. The data indicate that BD is detrimental to RV mechanical function.
右心室(RV)衰竭是心脏移植后早期发病和死亡的主要原因,这归因于供体右心室无法急性代偿受体升高的肺血管阻力(PVR)。此外,供体脑死亡(BD)对右心室功能的影响尚不清楚。本研究的目的是调查在PVR升高的情况下供体BD对右心室功能的影响。通过使用近端超声肺动脉(PA)流量探头和微压计测量近端和远端PA的肺血管能量学及其振荡性质,评估右心室及其后负荷、肺血管系统和左心房压力之间的相互作用,研究对象为20只杂种犬(25.8±0.4 kg,五只对照动物)。在远端PA周围放置一条束带(PA收缩压差>15 mmHg)。通过升高颅内压诱导脑死亡,并经神经病理学验证。在束带动物和对照动物脑死亡后的0、2、4和6小时收集数据。采用傅里叶分析计算右心室振荡功率、平均功率和总功率(TP)。使用多变量分析和配对学生t检验(p<0.05),将束带引起的变化与基线测量值进行比较。随着PA梯度的急性升高,肺阻抗和PVR显著增加了两倍至四倍。对照动物能够耐受PVR的急性升高,TP无显著变化。在PVR和阻抗急性升高后,基线时右心室TP从73(±11)显著增加到98(±10)mW。与基线和对照动物相比,脑死亡后对PVR和阻抗增加的反应显著消失,表明维持肺血管血流的代偿性TP显著丧失。数据表明,脑死亡对右心室机械功能有害。