De Luca Fabio A, Cruz Ruy J, Garrido Alejandra Del Pilar Gallardo, Prist Ricardo, Rocha-E-Silva Mauricio
Division of Applied Physiology, Heart Institute (InCor), University of Sao Paulo School of Medicine, Sao Paulo, Brazil.
Ann Transplant. 2009 Jan-Mar;14(1):38-46.
Organs from the so-called marginal donors have been used with a significant higher risk of primary non function than organs retrieved from the optimal donors. We investigated the early metabolic changes and blood flow redistribution in splanchnic territory in an experimental model that mimics marginal brain-dead (BD) donor.
MATERIAL/METHODS: Ten dogs (21.3+/-0.9 kg), were subjected to a brain death protocol induced by subdural balloon inflation and observed for 30 min thereafter without any additional interventions. Mean arterial and intracranial pressures, heart rate, cardiac output (CO), portal vein and hepatic artery blood flows (PVBF and HABF, ultrasonic flowprobe), and O(2)-derived variables were evaluated.
An increase in arterial pressure, CO, PVBF and HABF was observed after BD induction. At the end, an intense hypotension with normalization in CO (3.0+/-0.2 vs. 2.8+/-2.8 L/min) and PVBF (687+/-114 vs. 623+/-130 ml/min) was observed, whereas HABF (277+/-33 vs. 134+/-28 ml/min, p<0.005) remained lower than baseline values.
Despite severe hypotension induced by sudden increase of intracranial pressure, the systemic and splanchnic blood flows were partially preserved without signs of severe hypoperfusion (i.e. hyperlactatemia). Additionally, the HABF was mostly negatively affected in this model of marginal BD donor. Our data suggest that not only the cardiac output, but the intrinsic hepatic microcirculatory mechanism plays a role in the hepatic blood flow control after BD.
与从最佳供体获取的器官相比，使用所谓边缘供体的器官出现原发性无功能的风险显著更高。我们在一个模拟边缘脑死亡（BD）供体的实验模型中研究了内脏区域的早期代谢变化和血流重新分布。
材料/方法：10只犬（21.3±0.9千克），通过硬膜下球囊充气诱导脑死亡，此后在无任何额外干预的情况下观察30分钟。评估平均动脉压和颅内压、心率、心输出量（CO）、门静脉和肝动脉血流量（PVBF和HABF，超声血流探头）以及氧衍生变量。
脑死亡诱导后观察到动脉压、CO、PVBF和HABF升高。最后，观察到严重低血压，CO（3.0±0.2对2.8±2.8升/分钟）和PVBF（687±114对623±130毫升/分钟）恢复正常，而HABF（277±33对134±28毫升/分钟，p<0.005）仍低于基线值。
尽管颅内压突然升高导致严重低血压，但全身和内脏血流部分得以保留，无严重灌注不足迹象（即高乳酸血症）。此外，在这个边缘BD供体模型中，HABF大多受到负面影响。我们的数据表明，不仅心输出量，而且肝脏内在微循环机制在脑死亡后的肝血流控制中起作用。
