Sequential Preoperative Ipsilateral Portal and Arterial Embolization in Patients with Colorectal Liver Metastases

Background Preoperative portal vein embolization (PVE) induces ipsilateral atrophy of the hepatic parenchyma to be resected, as well as contralateral compensatory hypertrophy of the residual liver. However, there are two potential problems with this technique: inadequate contralateral hypertrophy and tumor progression while waiting for the non-embolized liver to hypertrophy. We devised a strategy to deal with these two problems by performing an ipsilateral hepatic artery embolization 6 weeks after an unsatisfactory PVE in an effort to accelerate the hypertrophy of the remnant liver. Materials and Methods Two patients with colorectal liver metastases underwent to this sequential preoperative treatment in order to achieve resectability of their metastatic disease. Results Both patients successfully underwent major hepatic resection. Conclusions In our experience sequential ipsilateral portal vein and hepatic artery embolization extended the indications for liver resection for metastatic colorectal cancer.     

Mechanism of liver regeneration after liver resection and portal vein embolization (ligation) is different?

Whether or not liver regeneration after portal branch embolization (PE) (ligation, PVL) in the non-embolized (ligated) lobe is by the same mechanism as regeneration in the remnant lobe after liver resection has been reviewed. Portal vein branch embolization and heat shock protein are then discussed. Tumor growth accelerated in the remnant liver after hepatectomy. In contrast, PE or PVL resulted in marked contralateral hepatic hypertrophy and significant reduction of tumor growth in the non-embolized (non-ligated) lobes. Follistatin administration significantly increased liver regeneration after hepatectomy in rats. In contrast, regeneration of non-ligated lobes after PVL was not accelerated by exogenous follistatin. Tumor growth also was not accelerated. The liver regeneration rate peaked at 48–72 h in the nonligated lobe after PVL, a delay of 24 h compared with the remnant liver after hepatectomy. In the postoperative early stage, the expression of activin βA, βC, and βE mRNAs was stronger in PVL than in hepatectomy. At 72 h the expression of activin receptor type IIA mRNA reached a peak in hepatectomy, but was significantly lower in PVL. Thus, regulation of activin signaling through receptors is one of the factors determining liver regeneration after hepatectomy and PVL. These serial experimental results imply that the mechanism of liver regeneration after portal branch ligation (embolization) is different from that after hepatectomy. Heat shock protein was induced in the liver experimentally by intermittent ischemic preconditioning and could play some beneficial role in the recovery of liver function after hepatectomy, even in cirrhotic patients. When heat shock protein following right portal vein embolization in both the embolized and non-embolized hepatic lobes was investigated in clinical cases, a two to fourfold increase in HSP70 was induced in the non-embolized lobe compared with the embolized lobe. Oral administration of geranylgeranylacetone (a non-toxic HSP inducer) suppressed inflammatory responses and improved survival after 95% hepatectomy by induction of HSP70 in rats.     

门静脉栓塞术在二期精准肝切除中的应用

目的: 探讨门静脉栓塞术在二期精准肝切除的应用。方法: 分析7例在超声扫描及X线数字减影血管造影引导下,经皮经肝穿刺门静脉栓塞术后,行二期精准肝切除术的肝癌病人临床资料。分成肝硬化组3例和无肝硬化组4例,分别检测门静脉栓塞术前和术后肝功能指标及肝体积变化,总结二期手术切除。结果: 7例病人均成功实施经皮经肝穿刺门静脉栓塞术,其中6例病人达到肝脏体积代偿增大的预期效果,顺利完成二期精准肝切除术。1例结肠直肠癌肝转移病人在门静脉栓塞8周后,未栓塞肝脏代偿性增大体积未达到精准肝切除的条件,转外院顺利行拯救性联合肝脏离断和门静脉结扎的二步肝切除术。两组经皮经肝穿刺门静脉栓塞术后1 d,肝功能指标较术前升高（P<0.05）,予护肝治疗3~7 d后降至术前水平。未发生严重并发症。结论: 门静脉栓塞技术成功率高、安全可行。剩余肝脏代偿性增大明显,可显著提高二期精准肝切除手术率。     

门静脉栓塞术临床应用研究进展

选择性门静脉栓塞术（PVE）可使栓塞侧肝叶萎缩，未栓塞侧肝叶代偿性增生，从而增加了剩余肝组织（FLR），扩大了肝切除术的手术适应范围，达到降低术后肝衰竭发生率的目的。笔者就PVE相关问题及最新研究进展做一综述。

     

Beneficial effect of hyperbaric oxygenation on liver regeneration in cirrhosis

BACKGROUND: Underlying hepatic injury and cirrhosis are leading factors that interfere with the post-operative liver regeneration and function. Hyperbaric oxygenation (HBO) has been reported to ameliorate the ischemia-reperfusion injury of the liver, to induce compensatory hypertrophy of the predicted remnant liver in rats after portal vein ligation and to augment liver regeneration after hepatectomy in non-cirrhotic rats. Our aim was to determine the effect of HBO treatment on liver regeneration after partial hepatectomy in normal and cirrhotic mice in this experimental study. MATERIALS AND METHODS: The effect of HBO on liver regeneration was studied in a mice model combining carbon tetrachloride induced cirrhosis and partial hepatectomy. Mice were divided into four groups: Control, cirrhotic, non-cirrhotic HBO-treated, and cirrhotic HBO-treated. All animals underwent 40% hepatectomy. Liver regeneration was evaluated by the proliferating cell nuclear antigen-labeling index. Serum aspartate aminotransferase and alanine aminotransferase levels were measured to evaluate liver injury. RESULTS: Serum alanine aminotransferase and aspartate aminotransferase levels were significantly decreased in HBO-treated cirrhotic group compared to cirrhosis group after hepatectomy (P = 0.001 and P = 0.014, respectively). The proliferating cell nuclear antigen labeling index was significantly higher in HBO treated cirrhotic group than in cirrhotic group after hepatectomy (P = 0.022). CONCLUSIONS: Our results suggest that HBO treatment improves liver functions and augments hepatocyte regeneration in cirrhotic mice after hepatectomy. Post-operative HBO treatment may have a beneficial effect on post-operative liver function and regeneration in cirrhotic patients.     

Recovery of hepatic function determined by cytochrome P450-dependent drug metabolism lags after compensatory hepatic volume changes after portal vein ligation in rats

BACKGROUND: Clinically, portal vein embolization has been proven to be useful as a preoperative treatment for major hepatic surgeries with impaired liver function. However, its effects on the metabolism and elimination of various drugs after portal vein embolization or ligation remain to be elucidated. MATERIALS AND METHODS: A portal vein branch that perfuses the central and left lobes of the liver of male Wistar rat was ligated, and changes in the weights of ligated and nonligated lobules as well as hepatic levels and activities of cytochrome P450 (CYP) isoforms, such as CYP3A2 and CYP2C11, were determined. To evaluate in vivo the effect of PVL on hepatic drug metabolism, the narcotic activity (sleep time) of midazolam, a specific substrate for CYP3A2, was measured. RESULTS: Although plasma levels of alanine aminotransferase and hepatic weight returned to basal levels at day 7 after the portal vein ligation, hepatic activities of CYP3A2 and CYP2C11 still remained low (53% and 54% of control levels, respectively), and returned to their initial levels after about day 14. The metabolism of midazolam was prolonged by approximately three times at day 7 after ligation and returned to basal levels at day 14. CONCLUSIONS: Because hepatic CYP-dependent drug metabolism by CYP isoforms recovered more slowly than the apparent recovery of hepatic volume and plasma alanine aminotransferase levels, the therapeutics of drugs metabolized by the CYP isoforms should be used carefully in patients who receive major hepatectomy with portal vein branch embolization.     

Extension of right portal vein embolization to segment IV portal branches

HYPOTHESIS: Routine embolization of segment IV, combined with right portal vein embolization (PVE), has been suggested in patients who are candidates for right trisegmentectomy to induce higher and faster hypertrophy of segments II-III. Our objective was to compare hypertrophy of segments II-III induced by PVE with and without extension to segment IV in patients undergoing major hepatectomy. METHODS: Twenty-six consecutive patients were prospectively evaluated; the future remnant liver volume was calculated using the portal phase of spiral computed tomographic scans before and 3 to 4 weeks after right PVE (group R, n = 13), which was extended to segment IV branches in 13 patients (group L). RESULTS: Twenty patients (76.9%) underwent the scheduled hepatic resection. Of the 6 patients who did not undergo the planned operation, 5 showed disease progression; in 1 patient (group L), there was an insufficient increase of the future remnant liver volume due to the presence of embolizing material in the left lobe. The mean +/- SD time between PVE and volume measurements was 31.8 +/- 9.3 days. The overall mean +/- SD future remnant liver volume increase was 53.1% +/- 24.8%; the increase for segment IV was significantly higher in group R than group L. The mean +/- SD post-PVE volumes of segments II-III and the rate of volume increase were similar in the 2 groups: group R, 348.4 +/- 83.1 cm3 and 67.8% +/- 30.8%, respectively, vs group L, 391.2 +/- 78.05 cm3 and 56.1% +/- 35.1%, respectively (P = .20 and P = .40). CONCLUSION: Extension of embolization to segment IV portal branches should not be routinely used because a similar volume increase of segments II-III can be simply achieved by right PVE.     

Hepatocyte growth factor supply accelerates compensatory hypertrophy caused by portal branch ligation in normal and jaundiced rats.

BACKGROUND: Hepatocyte growth factor (HGF), first identified as the most potent mitogen for hepatocytes, significantly stimulates liver regeneration after hepatectomy. In this report, we examined whether HGF is also useful in accelerating compensatory hypertrophy caused by portal branch ligation in normal and jaundiced rats. MATERIALS AND METHODS: Normal and reversible obstructive jaundiced rats underwent portal ligation of the left lateral and median branches, which supply approximately 70% of the total volume of the liver. Simultaneously, the animals were continuously treated with either recombinant human HGF (rhHGF) or vehicle alone via an intraperitoneally implanted osmotic pump. Two and four days after portal ligation, the degree of compensatory hypertrophy in unoccluded lobes was examined by measuring the wet weight ratios of the unoccluded lobes to the whole liver and the 5-bromo-2'-deoxyuridine labeling index of hepatocytes in each group. RESULTS: The HGF treatment significantly increased the wet weight ratios and the DNA synthesis in nonoccluded lobes 2 and 4 days after portal ligation in both normal and jaundiced rats. Moreover, rhHGF supply promptly decreased serum total bilirubin level in jaundiced rats. CONCLUSIONS: Continuous rhHGF administration not only accelerates compensatory hypertrophy in normal and jaundiced rats but also ameliorates hyperbilirubinemia in jaundiced rats.     

A predictive scoring system for insufficient liver hypertrophy after preoperative portal vein embolization

Background

The factors which affect hypertrophy of the future liver remnant after portal vein embolization remain unclear. The aim of this study was to clarify the clinical factors affecting the hypertrophy rate after portal vein embolization and to develop a scoring system predicting insufficient liver hypertrophy.

Doppler estimation of portal blood flow after percutaneous transhepatic portal vein embolization.

OBJECTIVE: To elucidate changes in portal blood flow (PBF) after percutaneous transhepatic portal vein embolization and their possible association with hypertrophy of the nonembolized hepatic segments. SUMMARY BACKGROUND DATA: The increase in PBF of the nonembolized hepatic segments after embolization is presumed to trigger hypertrophy of these segments. However, changes in PBF after embolization have not been investigated, and their extent remains unknown. METHODS: The authors prospectively measured PBF velocity, using color Doppler ultrasound, in 21 patients without cirrhosis who underwent embolization of the right portal vein or the right portal vein plus the left medial portal branch. Liver hypertrophy was assessed with a volumetric study using computed tomography. RESULTS: The PBF velocity significantly increased, from 11.1+/-3.6 cm/sec before embolization to 20.1+/-7 cm/sec 1 day after embolization. Subsequently, the velocity gradually decreased, but it remained significantly elevated until postembolization day 14. The volume of the nonembolized segments significantly increased from 370+/-141 cm3 to 488+/- 145 cm3. The hypertrophy rate (cm3/day) of the nonembolized segments after embolization correlated closely with the extent of increase in the PBF velocity, expressed as the velocity on day 1 divided by the velocity before embolization. The hypertrophy rate had a significant correlation with the absolute value of the PBF velocity on day 1, but its correlation coefficient was low. No significant correlations were observed between the hypertrophy rate and other clinical variables. CONCLUSIONS: The hypertrophy rate of nonembolized hepatic segments after embolization is predictable from the extent of the increase in the PBF velocity. This can be estimated easily and noninvasively with Doppler ultrasound 1 day after embolization.     

Compensatory hepatic hypertrophy after occlusion of branches of the portal vein or bile duct

The effect on the liver of portal or bile duct branch occlusion was examined in rabbits by measuring hepatic tissue blood flow and cellular kinetics, using the bromodeoxyuridine labeling index. The portal branch bile duct branch, or both, to the main lobe and caudate lobe (80.4% of total liver weight) were ligated or embolized just above the right posterior lobe (19.6%), resulting in compensatory hypertrophy of the right posterior lobe and atrophy of the main and caudate lobes. Twenty-four days after ligation, the degree of compensatory hypertrophy in the different groups was comparable. There were significant differences in the pattern of the development of hypertrophy. Ligation of both a portal branch and the corresponding bile duct resulted in more rapid hypertrophy and atrophy than ligation of a portal branch alone. Ligation of a branch of the bile duct resulted in slow development of hypertrophy and atrophy. In the embolization group, the increase in the right posterior lobe stopped 6 days after the operation, resulting that it was about 40% thereafter. Histological findings showed that the fibrin clot had contracted and was floating in the portal branch to the main lobe. These results suggested that portal blood flow to the main lobe had resumed and was gradually increasing as the clot contracted. Portal branch ligation gave results superior to those with portal branch embolization with regard to application to preoperative procedure in extended hepatobiliary surgery.     

Preoperative portal vein embolization for major liver resection: a meta-analysis

INTRODUCTION: Preoperative portal vein embolization (PVE) is used clinically to prevent postoperative liver insufficiency. The current study examined the impact of portal vein embolization on liver resection. METHOD: A comprehensive Medline search to identify all registered literature in the English language on portal vein embolization. Meta-analysis was performed to assess the result of PVE and its impact on major liver resection. RESULT: A total of 75 publications met the search criteria but only 37 provided data sufficiently enough for analysis involving 1088 patients. The overall morbidity rate for PVE was 2.2% without mortality. Four weeks following PVE, 85% patients underwent the planned hepatectomy (n = 930). Twenty-three patients had transient liver failure following resection after PVE (2.5%) but 7 patients developed acute liver failure and died (0.8%).The reason for nonresection following PVE (n = 158, 15%) included inadequate hypertrophy of remnant liver (n = 18), severe progression of liver metastasis (n = 43), extrahepatic spread (n = 35), refusal to surgery (n = 1), poor general condition (n = 1), altered treatment to transcatheter artery embolization or chemotherapy (n = 24), complete remission after treatment with 3 cycles of fluoracil and interferon alpha in a patient with hepatocellular carcinoma (n = 1), incomplete pre- or postembolization scanning (n = 8). Of those who underwent laparotomy without resection, (n = 27) reasons included intraoperative finding of peritoneal dissemination (n = 15), portal node metastasis (n = 2), severe invasion of the tumor to the hepatic artery and portal vein (n = 1), and gross tumoral extension precluding curative resection (n = 9).Two techniques were used for portal vein embolization: percutaneous transhepatic portal embolization, (PTPE) and transileocolic portal embolization, (TIPE). The increase in remnant liver volume was much greater in PTPE than TIPE group (11.9% vs. 9.7%; P = 0.00001). However, the proportion of patients who underwent resection following PVE was 97% in TIPE and 88% PTPE, respectively (P = <0.00001). Although there was no significant difference in patients who had major complications post-PVE, the rate for minor complications was significantly higher among patients who had PTPE (53.6% vs. 0%, P = <0.0001). CONCLUSION: PVE is a safe and effective procedure in inducing liver hypertrophy to prevent postresection liver failure due to insufficient liver remnant.     

Preoperative Portal Embolization in Patients with Hepatocellular Carcinoma

The factors that contribute to the effect of portal vein embolization before hepatectomy for hepatocellular carcinoma are unclear. Sixty-six patients with hepatocellular carcinoma were enrolled in the study. Changes in liver function, portal vein pressure, and liver volume after embolization were examined. A multiple linear regression analysis was performed to identify factors that independently contributed to the effects of portal vein embolization. The acceptable volume ratio of the remnant liver was calculated from liver function and compared with the volume ratio of the non-embolized liver. No postoperative deaths were observed after portal vein embolization or hepatectomy. Serum total bilirubin and prothrombin time did not change significantly after portal vein embolization. In patients who underwent arterial embolization before portal vein embolization, aminotransferase levels increased significantly. The only factor that could significantly predict the atrophy effects of portal vein embolization was previous arterial embolization. The volume ratio of the non-embolized liver was smaller than the acceptable volume ratio of the remnant liver in 18 of 40 patients and increased over the acceptable volume ratio in all cases after portal vein embolization. Portal vein embolization induced atrophy or hypertrophy of the embolized or non-embolized liver sufficiently, even when the liver was dysfunctional or cirrhotic. The atrophy effects were significant, especially when arterial embolization had been performed before portal vein embolization.     

Chemotherapy does not impair hypertrophy of the left liver after right portal vein obstruction

In patients with multiple colorectal liver metastases, the technical limits of curative surgery can be overcome by both reducing tumor volume with preoperative chemotherapy and by increasing the future remnant liver with portal vein embolization. Chemotherapy is generally discontinued before the embolization because it is alleged to impair hypertrophy of the future remnant liver. We have tested this assumption by comparing two groups of patients who had undergone right portal vein obstruction: 10 patients in whom chemotherapy was maintained until surgery and 10 patients in whom it was interrupted at least 1 month prior to portal obstruction. The two groups, with and without chemotherapy, were comparable for patient’s age (60 ± 9 versus 61 ± 9 years), number of metastases (7.7 ± 3 versus 6.2 ± 3), and future remnant liver volume (25 ± 9% versus 23 ± 5% of the total liver). After right portal vein obstruction, the increase of the future remnant liver was comparable in the two groups (33 ± 26% versus 25 ± 7%). Liver resection was performed in 14 patients (7 in each group) with a similar morbidity rate (57% in each group). In conclusion, continuing chemotherapy while portal vein obstruction is performed did not impair the hypertrophy of the future remnant volume nor the postoperative course after liver resection. Therefore, chemotherapy can be safely continued until liver surgery, when portal vein obstruction is indicated.     

Nonsuperiority of technetium-99m-galactosyl human serum albumin scintigraphy over conventional volumetry for assessing the future liver remnant in patients undergoing hepatectomy after portal vein embolization

BackgroundTechnetium-99m-galactosyl human serum albumin scintigraphy is preferred for assessing the liver functional reserve in patients undergoing hepatectomy, but its superiority over computed tomography volumetry after portal vein embolization and subsequent hepatectomy remains elusive. We aimed to compare technetium-99m-galactosyl human serum albumin scintigraphy with conventional computed tomography volumetry for predicting posthepatectomy liver failure in patients after portal vein embolization.MethodsThis retrospective study analyzed 152 consecutive patients who underwent hepatobiliary cancer resection after portal vein embolization between 2006 and 2021. Posthepatectomy liver failure was graded according to the International Study Group of Liver Surgery criteria. The predictive abilities for posthepatectomy liver failure were compared between the future remnant uptake (%) by technetium-99m-galactosyl human serum albumin scintigraphy and the future remnant volume (%) by computed tomography volumetry.ResultsFuture remnant uptake (%) was significantly greater than future remnant volume (%) after portal vein embolization (47.9% vs 40.8%; P < .001), while the values were comparable before portal vein embolization (32.7% vs 31.2%; P = .116). Receiver operating characteristic curve analysis revealed that post–portal vein embolization future remnant volume (%) had a significantly higher area under the curve than post–portal vein embolization future remnant uptake (%) (0.709 vs 0.630; P = .046) for predicting posthepatectomy liver failure. Multivariable analysis revealed that post–portal vein embolization future remnant volume (%) independently predicted posthepatectomy liver failure, but future remnant uptake (%) did not. Although the incidence of posthepatectomy liver failure grade ≥B was 17.8% when indocyanine green–clearance of the future liver remnant based on both future remnant volume (%) and future remnant uptake (%) was ≥0.05, it was higher in other combinations: 55.6% for indocyanine green clearance of the remnant volume ≥0.05/indocyanine green clearance of the remnant uptake ≤0.05; 50.0% for indocyanine green clearance of the remnant volume ≤0.05/indocyanine green clearance of the remnant uptake ≥0.05; and 50% for indocyanine green clearance of the remnant volume ≤0.05/indocyanine green clearance of the remnant uptake ≤0.05.ConclusionsTechnetium-99m-galactosyl human serum albumin scintigraphy is not superior to computed tomography volumetry for assessing the future liver remnant in patients undergoing major hepatectomy after portal vein embolization.     

Resección en 2 tiempos de tumores hepáticos perihiliares con torniquete en la cisura umbilical y embolización portal secuencial al cuarto día postoperatorio (ALTPS modificado)

Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) achieves the hypertrophy of the future liver remnant in seven days. We achieved the same hypertrophy placing a tourniquet in the parenchimal transection line associating a right portal vein ligation (associating liver tourniquet and right portal vein ligation for staged hepatectomy-ALTPS). In perihiliar tumors a«non touch» technique should be performed. ALPPS y ALTPS do not comply with this technical aspect because a dissection of the hilum is carried out in both procedures during the portal dissection. To avoid this problem we devised a new method called sequential ALTPS. It consists of placing a tourniquet in the umbilical fissure without ligation of the right portal vein during the first stage. Subsequently, on the 4^th postoperative day we perform a percutaneous right portal vein embolization. We present the first case of this new technique in which we have obtained a hypertrophy of 77% of the future liver remnant seven days after portal vein embolization. In the second stage a right trisectionectomy was performed with inferior vena cava resection with a goretex graft replacement.     

Resection for multiple metastatic liver tumors after preoperative portal embolization

Surgical resection has been recognized as the most effective treatment for patients with colorectal liver metastases. However, hepatectomy can be performed in only approximately 10% to 20%. Among the factors that are contraindications for hepatectomy, insufficient functional volume of the remnant liver after hepatic resection can cause postoperative hepatic failure and is still an obstacle to major hepatic resection. As one of the solutions to this dilemma and to be able to expand the indications for major hepatectomy, preoperative portal embolization (PVE) was proposed to induce compensatory hypertrophy of the contralateral remnant liver in patients with metastatic disease as well as in those with injured hepatic parenchyma, i.e., hepatocellular carcinoma and hilar cholangiocarcinoma. Currently, PVE allows more patients with previously unresectable liver tumors to benefit from resection. Long-term survival is comparable to that after resection without PVE.     

Preoperative hepatic venous embolization for partial hepatectomy combined with segmental resection of major hepatic vein

BACKGROUND: Liver resection of segments VII and/or VIII sometimes requires segmental resection of the right hepatic vein in patients with liver tumours invading or located close to the hepatic vein. In this situation, hepatic vein reconstruction is thought to have an important role in the postoperative function of segment VI. This study investigated whether preoperative embolization of the major hepatic vein could obviate the need for hepatic vein reconstruction after cranial partial resection of the liver including the major hepatic vein trunk in a preclinical model. METHODS: Sixteen beagles were divided into two groups of eight: control group (hepatectomy alone) and hepatic venous embolization (HVE) group (hepatectomy after HVE). HVE was performed 2 weeks before hepatectomy. All dogs underwent resection of the cranial third of the left lateral liver lobe together with the major trunk of the left hepatic vein. Following hepatectomy, survival, histological features, portal venous pressure and serum aspartate aminotransferase (AST) levels were determined. RESULTS: Six control animals and seven in the HVE group were alive 1 week after hepatectomy. Immediately after hepatectomy, portal venous pressure was significantly higher in the control group compared with the HVE group (mean(s.d.) 14.0(1.1) versus 8.1(1.0) mmHg; P < 0.01). Histological examination of the remnant left lateral lobe demonstrated patchy parenchymal haemorrhage in the control group and normal parenchymal architecture in the HVE group. Peak AST levels were observed on day 1 in both groups and were significantly higher in the control group (mean(s.d.) 182(42) versus 67(40) units/l; P < 0.01). CONCLUSION: In this model, preoperative HVE facilitated interlobar venous collateral formation and minimized the untoward effects of segmental hepatic vein resection. This procedure may obviate the need for hepatic vein reconstruction after cranial partial liver resection including the major hepatic vein.     

Hepatic blood flow in rats with portal branch ligation

Hepatic arterial blood flow (HABF) in the liver lobes and splanchnic nonhepatic arterial blood flow were measured in rats with and without right portal branch ligation for 1 month using 57Co microspheres. Portal branch ligation led to 60% atrophy of the ligated lobe and to hypertrophy of the nonligated lobe. In nonligated lobes of the portal branch ligation model and in the lobes of controls, HABF expressed per gram liver was comparable. In both models splanchnic non-HABF was also comparable. In the atrophic lobe, HABF remained constant; expressed per gram liver, it increased. In this lobe the net result was a significant decrease in total hepatic blood flow (ml/min/g liver).