Larsen F S, Ejlersen E, Strauss G, Rasmussen A, Kirkegaard P, Hansen B A, Secher N
Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark.
Transplantation. 1999 Nov 27;68(10):1472-6. doi: 10.1097/00007890-199911270-00007.
We determined whether the coupling between cerebral blood flow (CBF) and oxygen metabolism (CMRO2) is preserved during liver transplantation. Because of cerebrovascular dilatation, we hypothesized that cerebral metabolic autoregulation is impaired, because CBF becomes uncoupled from CMRO2 during the reperfusion phase of the operation.
In a prospective study, 13 patients (8 women, median age 46, range 21-6) with liver failure (10 with end-stage chronic liver disease and 3 with acute liver failure) were enrolled. Catheters were placed in a femoral artery and in the internal jugular vein for calculation of the cerebral arteriovenous oxygen content difference (AVDO2). CBF was recorded by the 133Xenon injection technique, and by transcranial Doppler sonography determined mean flow velocity (Vmean) in the middle cerebral artery. The CMRO2 was calculated as the AVDO2 times CBF and the cerebrovascular resistance (CVR) as the mean arterial pressure to CBF ratio. An index of large cerebral artery diameter was expressed by the CBF to Vmean ratio.
From induction of anesthesia to the anhepatic period, CBF decreased from a median of 47 (interquartiles 31-55) to 41 (37-48) ml 100 g(-1) min(-1), whereas the CMRO2 remained unchanged (1.3 [0.9-2.5] vs. 1.7 [0.9-2.3] ml 100 g(-1) min(-1)). In the reperfusion phase, the CBF increased to 51 (45-54) ml 100 g(-1) min(-1), whereas the CMRO2 remained unchanged at 1.1 (1.0-2.5) ml 100 g(-1) min(-1). The CVR decreased from 2.0 mm Hg (1.4-2.1) to 1.4 (1.1-1.8) mm Hg(-1) min 100 g ml. In the anhepatic phase, mean arterial pressure decreased from 92 mm Hg (84-98) to 85 (80-92) mm Hg and at reperfusion it was 80 (71-105) mm Hg. From the anhepatic to the reperfusion phase, the CBF increased 7% (0 to 26) for each mm Hg concomitant increase in PaCO2. The CBF to Vmean ratio remained stable (1.0 [0.8-1.2] vs. 0.9 [0.7-1.1] ml 100 g(-1) min(-1) cm(-1) sec).
During the reperfusion phase of liver transplantations, cerebrovascular dilatation uncouples cerebral oxidative metabolism from blood flow. The increase in CBF is beyond what can be explained by changes in arterial carbon dioxide tension and arterial pressure.
我们确定了肝移植期间脑血流量（CBF）与氧代谢（CMRO2）之间的耦合是否得以保留。由于脑血管扩张，我们推测脑代谢自动调节功能受损，因为在手术的再灌注阶段CBF与CMRO2出现了解耦。
在一项前瞻性研究中，纳入了13例肝功能衰竭患者（8例女性，中位年龄46岁，范围21 - 6岁）（10例为终末期慢性肝病，3例为急性肝功能衰竭）。将导管置于股动脉和颈内静脉以计算脑动静脉氧含量差（AVDO2）。通过133氙注射技术记录CBF，并通过经颅多普勒超声测定大脑中动脉的平均血流速度（Vmean）。CMRO2通过AVDO2乘以CBF计算得出，脑血管阻力（CVR）通过平均动脉压与CBF的比值计算得出。大脑大动脉直径指数通过CBF与Vmean的比值表示。
从麻醉诱导到无肝期，CBF从中位值47（四分位间距31 - 55）降至41（37 - 48）ml 100 g⁻¹ min⁻¹，而CMRO2保持不变（1.3 [0.9 - 2.5] 与1.7 [0.9 - 2.3] ml 100 g⁻¹ min⁻¹）。在再灌注阶段，CBF增至51（45 - 54）ml 100 g⁻¹ min⁻¹，而CMRO2保持不变，为1.1（1.0 - 2.5）ml 100 g⁻¹ min⁻¹。CVR从2.0 mmHg（1.4 - 2.1）降至1.4（1.1 - 1.8）mmHg⁻¹ min 100 g ml。在无肝期，平均动脉压从92 mmHg（84 - 98）降至85（80 - 92）mmHg，再灌注时为80（71 - 105）mmHg。从无肝期到再灌注阶段，随着PaCO₂每升高1 mmHg，CBF增加7%（0至26）。CBF与Vmean的比值保持稳定（1.0 [0.8 - 1.2] 与0.9 [0.7 - 1.1] ml 100 g⁻¹ min⁻¹ cm⁻¹ sec）。
在肝移植的再灌注阶段，脑血管扩张使脑氧化代谢与血流解耦。CBF的增加超出了动脉二氧化碳张力和动脉压变化所能解释的范围。
