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Portal Hyperperfusion after Extended Hepatectomy Does Not Induce a Hepatic Arterial Buffer Response (HABR) but Impairs Mitochondrial Redox State and Hepatocellular Oxygenation.

Dold S, Richter S, Kollmar O, von Heesen M, Scheuer C, Laschke MW, Vollmar B, Schilling MK, Menger MD - PLoS ONE (2015)

Bottom Line: This, however, did not provoke a hepatic arterial buffer response.Nonetheless, portal hyperperfusion and constant hepatic arterial blood flow were associated with a reduced mitochondrial redox state and a decreased hepatic tissue pO2 after 70% and 90% hepatectomy.This was associated with a 2-fold increase of bromosulfophthalein excretion.

View Article: PubMed Central - PubMed

Affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.

ABSTRACT

Background & aims: Portal hyperperfusion after extended hepatectomy or small-for-size liver transplantation may induce organ dysfunction and failure. The underlying mechanisms, however, are still not completely understood. Herein, we analysed whether hepatectomy-associated portal hyperperfusion induces a hepatic arterial buffer response, i.e., an adaptive hepatic arterial constriction, which may cause hepatocellular hypoxia and organ dysfunction.

Methods: Sprague-Dawley rats underwent 30%, 70% and 90% hepatectomy. Baseline measurements before hepatectomy served as controls. Hepatic arterial and portal venous flows were analysed by ultrasonic flow measurement. Microvascular blood flow and mitochondrial redox state were determined by intravital fluorescence microscopy. Hepatic tissue pO2 was analysed by polarographic techniques. Hepatic function and integrity were studied by bromosulfophthalein bile excretion and liver histology.

Results: Portal blood flow was 2- to 4-fold increased after 70% and 90% hepatectomy. This, however, did not provoke a hepatic arterial buffer response. Nonetheless, portal hyperperfusion and constant hepatic arterial blood flow were associated with a reduced mitochondrial redox state and a decreased hepatic tissue pO2 after 70% and 90% hepatectomy. Microvascular blood flow increased significantly after hepatectomy and functional sinusoidal density was found only slightly reduced. Major hepatectomy further induced a 2- to 3-fold increase of bile flow. This was associated with a 2-fold increase of bromosulfophthalein excretion.

Conclusions: Portal hyperperfusion after extended hepatectomy does not induce a hepatic arterial buffer response but reduces mitochondrial redox state and hepatocellular oxygenation. This is not due to a deterioration of microvascular perfusion, but rather due to a relative hypermetabolism of the remnant liver after major resection.

No MeSH data available.


Related in: MedlinePlus

Hepatic blood flow.Portal venous blood flow (PVF; A), hepatic arterial blood flow (HAF; B), and total hepatic blood flow (THF; C) per 100g liver wet weight under baseline conditions (con) and after 30%, 70% and 90% hepatectomy (PHx). Flow measurements were performed with ultrasonic flow probes. Mean values ± SEM, *p<0.05 vs. con.
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pone.0141877.g001: Hepatic blood flow.Portal venous blood flow (PVF; A), hepatic arterial blood flow (HAF; B), and total hepatic blood flow (THF; C) per 100g liver wet weight under baseline conditions (con) and after 30%, 70% and 90% hepatectomy (PHx). Flow measurements were performed with ultrasonic flow probes. Mean values ± SEM, *p<0.05 vs. con.

Mentions: Hepatectomy resulted in a distinct portal hyperperfusion. This was indicated by a massively increased blood flow in the portal vein after 70% and, in particular, after 90% hepatectomy when compared to baseline. In contrast, hepatic arterial blood flow did not significantly change throughout the experiment, indicating the lack of a HABR. As a consequence, 70% liver resection resulted in a 2-fold increased total hepatic blood flow and 90% resection provoked an almost 4-fold increase of liver perfusion (Fig 1).


Portal Hyperperfusion after Extended Hepatectomy Does Not Induce a Hepatic Arterial Buffer Response (HABR) but Impairs Mitochondrial Redox State and Hepatocellular Oxygenation.

Dold S, Richter S, Kollmar O, von Heesen M, Scheuer C, Laschke MW, Vollmar B, Schilling MK, Menger MD - PLoS ONE (2015)

Hepatic blood flow.Portal venous blood flow (PVF; A), hepatic arterial blood flow (HAF; B), and total hepatic blood flow (THF; C) per 100g liver wet weight under baseline conditions (con) and after 30%, 70% and 90% hepatectomy (PHx). Flow measurements were performed with ultrasonic flow probes. Mean values ± SEM, *p<0.05 vs. con.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4629903&req=5

pone.0141877.g001: Hepatic blood flow.Portal venous blood flow (PVF; A), hepatic arterial blood flow (HAF; B), and total hepatic blood flow (THF; C) per 100g liver wet weight under baseline conditions (con) and after 30%, 70% and 90% hepatectomy (PHx). Flow measurements were performed with ultrasonic flow probes. Mean values ± SEM, *p<0.05 vs. con.
Mentions: Hepatectomy resulted in a distinct portal hyperperfusion. This was indicated by a massively increased blood flow in the portal vein after 70% and, in particular, after 90% hepatectomy when compared to baseline. In contrast, hepatic arterial blood flow did not significantly change throughout the experiment, indicating the lack of a HABR. As a consequence, 70% liver resection resulted in a 2-fold increased total hepatic blood flow and 90% resection provoked an almost 4-fold increase of liver perfusion (Fig 1).

Bottom Line: This, however, did not provoke a hepatic arterial buffer response.Nonetheless, portal hyperperfusion and constant hepatic arterial blood flow were associated with a reduced mitochondrial redox state and a decreased hepatic tissue pO2 after 70% and 90% hepatectomy.This was associated with a 2-fold increase of bromosulfophthalein excretion.

View Article: PubMed Central - PubMed

Affiliation: Department of General-, Visceral-, Vascular- and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany.

ABSTRACT

Background & aims: Portal hyperperfusion after extended hepatectomy or small-for-size liver transplantation may induce organ dysfunction and failure. The underlying mechanisms, however, are still not completely understood. Herein, we analysed whether hepatectomy-associated portal hyperperfusion induces a hepatic arterial buffer response, i.e., an adaptive hepatic arterial constriction, which may cause hepatocellular hypoxia and organ dysfunction.

Methods: Sprague-Dawley rats underwent 30%, 70% and 90% hepatectomy. Baseline measurements before hepatectomy served as controls. Hepatic arterial and portal venous flows were analysed by ultrasonic flow measurement. Microvascular blood flow and mitochondrial redox state were determined by intravital fluorescence microscopy. Hepatic tissue pO2 was analysed by polarographic techniques. Hepatic function and integrity were studied by bromosulfophthalein bile excretion and liver histology.

Results: Portal blood flow was 2- to 4-fold increased after 70% and 90% hepatectomy. This, however, did not provoke a hepatic arterial buffer response. Nonetheless, portal hyperperfusion and constant hepatic arterial blood flow were associated with a reduced mitochondrial redox state and a decreased hepatic tissue pO2 after 70% and 90% hepatectomy. Microvascular blood flow increased significantly after hepatectomy and functional sinusoidal density was found only slightly reduced. Major hepatectomy further induced a 2- to 3-fold increase of bile flow. This was associated with a 2-fold increase of bromosulfophthalein excretion.

Conclusions: Portal hyperperfusion after extended hepatectomy does not induce a hepatic arterial buffer response but reduces mitochondrial redox state and hepatocellular oxygenation. This is not due to a deterioration of microvascular perfusion, but rather due to a relative hypermetabolism of the remnant liver after major resection.

No MeSH data available.


Related in: MedlinePlus