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Ultrasonic characterization of the nonlinear properties of canine livers by measuring shear wave speed and axial strain with increasing portal venous pressure.
Rotemberg V, Byram B, Palmeri M, Wang M, Nightingale K
(2013) J Biomech 46: 1875-81
MeSH Terms: Animals, Biomechanical Phenomena, Dogs, Liver, Liver Circulation, Models, Cardiovascular, Nonlinear Dynamics, Portal Pressure, Portal Vein, Ultrasonography, Vascular Stiffness
Show Abstract · Added May 29, 2014
Elevated hepatic venous pressure is the primary source of complications in advancing liver disease. Ultrasound imaging is ideal for potential noninvasive hepatic pressure measurements as it is widely used for liver imaging. Specifically, ultrasound based stiffness measures may be useful for clinically monitoring pressure, but the mechanism by which liver stiffness increases with hepatic pressure has not been well characterized. This study is designed to elucidate the nonlinear properties of the liver during pressurization by measuring both hepatic shear wave speed (SWS) and strain with increasing pressure. Tissue deformation during hepatic pressurization was tracked in 8 canine livers using successively acquired 3-D B-mode volumes and compared with concurrently measured SWS. When portal venous pressure was increased from clinically normal (0-5mmHg) to pressures representing highly diseased states at 20mmHg, the liver was observed to expand with axial strain measures up to 10%. At the same time, SWS estimates were observed to increase from 1.5-2m/s at 0-5mmHg (baseline) to 3.25-3.5m/s at 20mmHg.
Copyright © 2013 Elsevier Ltd. All rights reserved.
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11 MeSH Terms
How to handle a huge portosystemic shunt in adult living donor liver transplantation with a small-for-size graft: report of a case.
Shirouzu Y, Ohya Y, Tsukamoto Y, Yamamoto H, Lee KJ, Okajima H, Asonuma K, Inomata Y
(2009) Surg Today 39: 637-40
MeSH Terms: Adult, Humans, Ligation, Liver, Liver Circulation, Liver Cirrhosis, Liver Transplantation, Living Donors, Male, Organ Size, Splanchnic Circulation, Splenic Vein, Vascular Diseases
Show Abstract · Added February 11, 2015
Little attention has been paid to a ligation of the spontaneous portosystemic shunt in adult living donor liver transplantation (LDLT). A 33-year-old Japanese man with cryptogenic liver cirrhosis accompanied by a huge splenorenal shunt underwent LDLT. Acute cellular rejection produced "to and fro" portal venous flow on postoperative day (POD) 10. Steroid bolus therapy reversed the rejection, but the recovery of the portal venous flow was incomplete and the recipient subsequently started to have episodes of encephalopathy. Angiography showed portal hypoperfusion and portal flow steal via a huge splenorenal shunt. The patient underwent a shunt occlusion on POD 58. Portography showed marked improvement of the portal hypoperfusion. The encephalopathy thereafter dramatically reversed and the patient was discharged with no complications related to shunt ligation on POD 110. This case suggested that a ligation of a huge portosystemic shunt should therefore be considered at the time of transplantation, even when a relatively small graft is implanted.
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13 MeSH Terms
Intraportal administration of neuropeptide Y and hepatic glucose metabolism.
Nishizawa M, Shiota M, Moore MC, Gustavson SM, Neal DW, Cherrington AD
(2008) Am J Physiol Regul Integr Comp Physiol 294: R1197-204
MeSH Terms: Alanine, Animals, Blood Glucose, Blood Pressure, Dogs, Fatty Acids, Nonesterified, Female, Glucagon, Glucose, Glycerol, Heart Rate, Homeostasis, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Liver Circulation, Male, Neuropeptide Y, Portal Vein, Postprandial Period, Somatostatin, Time Factors
Show Abstract · Added December 10, 2013
We examined whether intraportal delivery of neuropeptide Y (NPY) affects glucose metabolism in 42-h-fasted conscious dogs using arteriovenous difference methodology. The experimental period was divided into three subperiods (P1, P2, and P3). During all subperiods, the dogs received infusions of somatostatin, intraportal insulin (threefold basal), intraportal glucagon (basal), and peripheral intravenous glucose to increase the hepatic glucose load twofold basal. Following P1, in the NPY group (n = 7), NPY was infused intraportally at 0.2 and 5.1 pmol.kg(-1).min(-1) during P2 and P3, respectively. The control group (n = 7) received intraportal saline infusion without NPY. There were no significant changes in hepatic blood flow in NPY vs. control. The lower infusion rate of NPY (P2) did not enhance net hepatic glucose uptake. During P3, the increment in net hepatic glucose uptake (compared with P1) was 4 +/- 1 and 10 +/- 2 micromol.kg(-1).min(-1) in control and NPY, respectively (P < 0.05). The increment in net hepatic fractional glucose extraction during P3 was 0.015 +/- 0.005 and 0.039 +/- 0.008 in control and NPY, respectively (P < 0.05). Net hepatic carbon retention was enhanced in NPY vs. control (22 +/- 2 vs. 14 +/- 2 micromol.kg(-1).min(-1), P < 0.05). There were no significant differences between groups in the total glucose infusion rate. Thus, intraportal NPY stimulates net hepatic glucose uptake without significantly altering whole body glucose disposal in dogs.
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23 MeSH Terms
Intraportally delivered GLP-1, in the presence of hyperglycemia induced via peripheral glucose infusion, does not change whole body glucose utilization.
Johnson KM, Edgerton DS, Rodewald T, Scott M, Farmer B, Neal D, Cherrington AD
(2008) Am J Physiol Endocrinol Metab 294: E380-4
MeSH Terms: Animals, Blood Glucose, Dogs, Enzyme-Linked Immunosorbent Assay, Female, Glucagon, Glucagon-Like Peptide 1, Glucose, Hyperglycemia, Infusions, Intravenous, Insulin, Liver Circulation, Male
Show Abstract · Added December 10, 2013
After a meal, glucagon-like peptide-1 (GLP-1) and glucose levels are significantly greater in the hepatic portal vein than in the artery. We have previously reported that, in the presence of intraportal glucose delivery, a physiological increase of GLP-1 in the hepatic portal vein increases nonhepatic glucose uptake via a mechanism independent of changes in pancreatic hormone secretion. The aim of the present study was to determine whether intraportal glucose delivery is required to observe this effect. Experiments consisted of a 40-min basal period, followed by a 240-min experimental period, during which conscious 42-h fasted dogs received glucose peripherally to maintain arterial plasma glucose levels at approximately 160 mg/dl. In addition, either saline (n = 6) or GLP-1 (1 pmol.kg(-1).min(-1); GLP-1, n = 6) was administered intraportally during the experimental period. As in the previous study, the presence of GLP-1 did not alter pancreatic hormone levels; however, in the present study, intraportal GLP-1 infusion did not result in an increase in whole body glucose utilization. This is despite the fact that arterial and hepatic portal vein GLP-1 levels were maintained at the same level as the previous study. Therefore, a physiological elevation of GLP-1 in the hepatic portal vein does not increase whole body glucose uptake when hyperglycemia is induced by peripheral glucose infusion. This indicates that a physiological increase in GLP-1 augments glucose utilization only when GLP-1 and glucose gradients conditions mimic the postprandial state.
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13 MeSH Terms
Effects of the nitric oxide donor SIN-1 on net hepatic glucose uptake in the conscious dog.
An Z, DiCostanzo CA, Moore MC, Edgerton DS, Dardevet DP, Neal DW, Cherrington AD
(2008) Am J Physiol Endocrinol Metab 294: E300-6
MeSH Terms: Animals, Blood Glucose, Blood Pressure, Carbon, Dogs, Fatty Acids, Nonesterified, Glucagon, Glucose, Glycerol, Heart Rate, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Liver Circulation, Molsidomine, Nitric Oxide Donors, Portal Vein
Show Abstract · Added December 10, 2013
To determine the role of nitric oxide in regulating net hepatic glucose uptake (NHGU) in vivo, studies were performed on three groups of 42-h-fasted conscious dogs using a nitric oxide donor [3-morpholinosydnonimine (SIN-1)]. The experimental period was divided into period 1 (0-90 min) and period 2 (P2; 90-240 min). At 0 min, somatostatin was infused peripherally, and insulin (4-fold basal) and glucagon (basal) were given intraportally. Glucose was delivered intraportally (22.2 mumol.kg(-1).min(-1)) and peripherally (as needed) to increase the hepatic glucose load twofold basal. At 90 min, an infusion of SIN-1 (4 mug.kg(-1).min(-1)) was started in a peripheral vein (PeSin-1, n = 10) or the portal vein (PoSin-1, n = 12) while the control group received saline (SAL, n = 8). Both peripheral and portal infusion of SIN-1, unlike saline, significantly reduced systolic and diastolic blood pressure. Heart rate rose in PeSin-1 and PoSin-1 (96 +/- 5 to 120 +/- 10 and 88 +/- 6 to 107 +/- 5 beats/min, respectively, P < 0.05) but did not change in response to saline. NHGU during P2 was 31.0 +/- 2.4 and 29.9 +/- 2.0 mumol.kg(-1).min(-1) in SAL and PeSin-1, respectively but was 23.7 +/- 1.7 in PoSin-1 (P < 0.05). Net hepatic carbon retention during P2 was significantly lower in PoSin-1 than SAL or PeSin-1 (21.4 +/- 1.2 vs. 27.1 +/- 1.5 and 26.1 +/- 1.0 mumol.kg(-1).min(-1)). Nonhepatic glucose uptake did not change in response to saline or SIN-1 infusion. In conclusion, portal but not peripheral infusion of the nitric oxide donor SIN-1 inhibited NHGU.
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3 Members
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18 MeSH Terms
The effect of vagal cooling on canine hepatic glucose metabolism in the presence of hyperglycemia of peripheral origin.
DiCostanzo CA, Dardevet DP, Williams PE, Moore MC, Hastings JR, Neal DW, Cherrington AD
(2007) Metabolism 56: 814-24
MeSH Terms: Animals, Blood Glucose, Cold Temperature, Dogs, Glucose, Hyperglycemia, Lactic Acid, Liver, Liver Circulation, Vagus Nerve
Show Abstract · Added December 10, 2013
We examined the role of vagus nerves in the transmission of the portal glucose signal in conscious dogs. At time 0, somatostatin infusion was started along with intraportal insulin and glucagon at 4-fold basal and basal rates, respectively. Glucose was infused via a peripheral vein to create hyperglycemia ( approximately 2 fold basal). At t = 90, hollow coils around the vagus nerves were perfused with -10 degrees C or 37 degrees C solution in the vagally cooled (COOL) and sham-cooled (SHAM) groups, respectively (n = 6 per group). Effectiveness of vagal blockade was demonstrated by increase in heart rate during perfusion in the COOL vs SHAM groups (183 +/- 3 vs 102 +/- 5 beats per minute, respectively) and by prolapse of the third eyelid in the COOL group. Arterial plasma insulin (22 +/- 2 and 24 +/- 3 micro U/mL) and glucagon (37 +/- 5 and 40 +/- 4 pg/mL) concentrations did not change significantly between the first experimental period and the coil perfusion period in either the SHAM or COOL group, respectively. The hepatic glucose load throughout the entire experiment was 46 +/- 1 and 50 +/- 2 mg . kg(-1) . min(-1) in the SHAM and COOL groups, respectively. Net hepatic glucose uptake (NHGU) did not differ in the SHAM and COOL groups before (2.2 +/- 0.5 and 2.9 +/- 0.8 mg . kg(-1) . min(-1), respectively) or during the cooling period (3.0 +/- 0.5 and 3.4 +/- 0.6 mg . kg(-1) . min(-1), respectively). Likewise, net hepatic glucose fractional extraction and nonhepatic glucose uptake and clearance were not different between groups during coil perfusion. Interruption of vagal signaling in the presence of hyperinsulinemia and hyperglycemia resulting from peripheral glucose infusion did not affect NHGU, further supporting our previous suggestion that vagal input to the liver is not a primary determinant of NHGU.
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2 Members
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10 MeSH Terms
Splanchnic cortisol production in dogs occurs primarily in the liver: evidence for substantial hepatic specific 11beta hydroxysteroid dehydrogenase type 1 activity.
Basu R, Edgerton DS, Singh RJ, Cherrington A, Rizza RA
(2006) Diabetes 55: 3013-9
MeSH Terms: 11-beta-Hydroxysteroid Dehydrogenase Type 1, Animals, Dogs, Female, Hydrocortisone, Kinetics, Liver, Liver Circulation, Male, Portal System, Splanchnic Circulation, Viscera
Show Abstract · Added December 10, 2013
Eight dogs underwent combined hepatic/portal vein catheterization and infusion of D4-cortisol in order to determine the relative contributions of the viscera and liver to splanchnic cortisol production. D4-cortisol concentrations progressively decreased from 2.6 +/- 0.1 to 2.4 +/- 0.1 to 1.7 +/- 0.1 microg/dl (P < 0.001 by ANOVA) from hepatic artery to portal vein to hepatic vein, respectively, indicating 8 +/- 3 and 28 +/- 3% extraction across the viscera and liver, respectively. On the other hand, hepatic artery, portal vein, and hepatic vein cortisol concentrations did not differ (0.31 +/- 0.12 vs. 0.28 +/- 0.11 vs. 0.27 +/- 0.10 microg/dl, respectively), indicating zero net cortisol balance. This meant that 1.0 +/- 0.1 microg/min of cortisol was produced within the splanchnic bed, all of which occurred within the liver (1.2 +/- 0.1 microg/min). On the other hand, visceral cortisol production did not differ from zero (-0.2 +/- 0.2 microg/min; P < 0.001 vs. liver). Flux through the 11beta hydroxysteroid dehydrogenase (HSD) type 1 pathway can be measured by determining the rate of conversion of D4-cortisol to D3-cortisol. D3-cortisol concentrations were lower in the portal vein than hepatic artery (0.45 +/- 0.03 vs. 0.48 +/- 0.02, respectively; P < 0.01) but did not differ in the portal vein and hepatic vein, indicating net uptake across the viscera but zero balance across the liver. D3-cortisol production with the viscera and liver averaged 0.2 +/- 0.1 microg/min (P = NS vs. zero production) and 0.6 +/- 0.1 microg/min (P < 0.001 vs. zero production; P < 0.001 vs. viscera production), respectively. We conclude that most, if not all, of splanchnic cortisol production occurs within the liver. Taken together, these data suggest that the high local cortisol concentrations generated via the 11beta HSD type 1 pathway within the liver likely contribute to the regulation of hepatic glucose, fat, and protein metabolism.
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12 MeSH Terms
Role of the hepatic sympathetic nerves in the regulation of net hepatic glucose uptake and the mediation of the portal glucose signal.
Dicostanzo CA, Dardevet DP, Neal DW, Lautz M, Allen E, Snead W, Cherrington AD
(2006) Am J Physiol Endocrinol Metab 290: E9-E16
MeSH Terms: Animals, Blood Glucose, Dogs, Glucagon, Glucose, Glycerol, Hyperglycemia, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Liver Circulation, Norepinephrine, Portal System, Somatostatin, Sympathectomy, Sympathetic Nervous System
Show Abstract · Added December 10, 2013
Portal glucose delivery enhances net hepatic glucose uptake (NHGU) relative to peripheral glucose delivery. We hypothesize that the sympathetic nervous system normally restrains NHGU, and portal glucose delivery relieves the inhibition. Two groups of 42-h-fasted conscious dogs were studied using arteriovenous difference techniques. Denervated dogs (DEN; n=10) underwent selective sympathetic denervation by cutting the nerves at the celiac nerve bundle near the common hepatic artery; control dogs (CON; n=10) underwent a sham procedure. After a 140-min basal period, somatostatin was given along with basal intraportal infusions of insulin and glucagon. Glucose was infused peripherally to double the hepatic glucose load (HGL) for 90 min (P1). In P2, glucose was infused intraportally (3-4 mg.kg(-1).min(-1)), and the peripheral glucose infusion was reduced to maintain the HGL for 90 min. This was followed by 90 min (P3) in which portal glucose infusion was terminated and peripheral glucose infusion was increased to maintain the HGL. P1 and P3 were averaged as the peripheral glucose infusion period (PE). The average HGLs (mg.kg(-1).min(-1)) in CON and DEN were 55+/-3 and 54+/-4 in the peripheral periods and 55+/-3 and 55+/-4 in P2, respectively. The arterial insulin and glucagon levels remained basal in both groups. NHGU (mg.kg(-1).min(-1)) in CON averaged 1.7+/-0.3 during PE and increased to 2.9+/-0.3 during P2. NHGU (mg.kg(-1).min(-1)) was greater in DEN than CON (P<0.05) during PE (2.9+/-0.4) and failed to increase significantly (3.2+/-0.2) during P2 (not significant vs. CON). Selective sympathetic denervation increased NHGU during hyperglycemia but significantly blunted the response to portal glucose delivery.
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1 Members
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17 MeSH Terms
Modulation of mitochondrial calcium management attenuates hepatic warm ischemia-reperfusion injury.
Anderson CD, Pierce J, Nicoud I, Belous A, Knox CD, Chari RS
(2005) Liver Transpl 11: 663-8
MeSH Terms: Alanine Transaminase, Animals, Apoptosis, Aspartate Aminotransferase, Mitochondrial, Calcium, Disease Models, Animal, Ischemia, Liver, Liver Circulation, Male, Necrosis, Probability, Rats, Rats, Sprague-Dawley, Reperfusion, Reperfusion Injury, Risk Factors, Ruthenium Red, Sensitivity and Specificity
Show Abstract · Added January 10, 2014
Hepatic warm ischemia and reperfusion (IR) injury occurs in many clinical situations and has an important link to subsequent hepatic failure. The pathogenesis of this injury involves numerous pathways, including mitochondrial-associated apoptosis. We studied the effect of mitochondrial calcium uptake inhibition on hepatic IR injury using the specific mitochondrial calcium uptake inhibitor, ruthenium red (RR). Rats were subjected to 1 hour of 70% warm hepatic ischemia following RR pretreatment or vehicle injection. Sham-operated animals served as controls. Analysis was performed at 15 minutes, 1 hour, 3 hours, or 6 hours after reperfusion. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations were determined. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining was performed to assess apoptosis, and hepatocellular necrosis was semiquantitated from hematoxylin and eosin-stained tissue sections. RR pretreatment significantly decreased both AST and ALT serum levels after 6 hours of reperfusion (AST: 1,556 +/- 181 U/L vs. 597 +/- 121 U/L, P = 0.005; ALT: 1,118 +/- 187 U/L vs. 294 +/- 39 U/L, P = 0.005). Apoptosis was observed within 15 minutes of reperfusion in vehicle-pretreated animals and peaked after 3 hours of reperfusion (98 +/- 21 cells/high-power field [hpf]). Apoptosis was inhibited at all time points by RR pretreatment. Histologic evidence of necrosis was not observed prior to 3 hours of reperfusion (23% +/- 4%), and maximal necrosis was observed after 6 hours of reperfusion (26% +/- 1% percent area). RR pretreatment significantly decreased the necrotic percent area at both the 3-hour and the 6-hour time points (4.2% +/- 2%; 3.7% +/- 1%, respectively). Hepatic IR injury resulted in both apoptotic and necrotic cell death, which were attenuated by RR pretreatment. In conclusion, these observations implicate mitochondrial calcium uptake in the pathogenesis of hepatic IR injury.
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19 MeSH Terms
Interaction of a selective serotonin reuptake inhibitor with insulin in the control of hepatic glucose uptake in conscious dogs.
Moore MC, DiCostanzo CA, Dardevet D, Lautz M, Farmer B, Cherrington AD
(2005) Am J Physiol Endocrinol Metab 288: E556-63
MeSH Terms: Animals, Blood Flow Velocity, Blood Glucose, Carbon, Consciousness, Dogs, Drug Interactions, Fatty Acids, Nonesterified, Female, Fluvoxamine, Glucagon, Glucose, Glycerol, Glycogen, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Liver Circulation, Male, Serotonin, Serotonin Uptake Inhibitors, Somatostatin
Show Abstract · Added December 10, 2013
Whether hyperinsulinemia is required for stimulation of net hepatic glucose uptake (NHGU) by a selective serotonin reuptake inhibitor (SSRI) was examined in four groups of conscious 42-h-fasted dogs, using arteriovenous difference and tracer ([3-3H]glucose) techniques. Experiments consisted of equilibration (-120 to -30 min), basal (-30 to 0 min), and experimental periods (Exp; 0-240 min). During Exp, somatostatin, intraportal insulin [at basal (Ins groups) or 4-fold basal rates (INS groups)], basal intraportal glucagon, and peripheral glucose (to double hepatic glucose load) were infused. In the Fluv-Ins (n = 7) and Fluv-INS groups (n = 6), saline was infused intraportally from 0 to 90 min (P1), and fluvoxamine was infused intraportally at 2 microg x kg(-1) x min(-1) from 90 to 240 min (P2). Sal-Ins (n = 9) and Sal-INS (n = 8) received intraportal saline in P1 and P2. NHGU during P2 was 8.4 +/- 1.4 and 6.9 +/- 2.3 micromol x kg(-1) x min(-1) in Sal-Ins and Fluv-Ins, respectively (not significant), and 13.3 +/- 2.2 and 20.9 +/- 3.1 micromol x kg(-1) x min(-1) (P < 0.05) in Sal-INS and Fluv-INS. Unidirectional (tracer-determined) hepatic glucose uptake was twofold greater (P < 0.05) in Fluv-INS than Sal-INS. Net hepatic carbon retention during P2 was significantly greater in Fluv-INS than Sal-INS (18.5 +/- 2.7 vs. 12.2 +/- 1.9 micromol x kg(-1) x min(-1)). Nonhepatic glucose uptake was reduced in Fluv-INS vs. Sal-INS (20.0 +/- 1.3 vs. 38.4 +/- 5.4 micromol x kg(-1) x min(-1), P < 0.05). Intraportal fluvoxamine enhanced NHGU and net hepatic carbon retention in the presence of hyperinsulinemia but not euinsulinemia, suggesting that hepatocyte-targeted SSRIs may reduce postprandial hyperglycemia.
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23 MeSH Terms