Difference in Hepatic Tissue Oxygenation between Total Vascular Exclusion and Inflow Occlusion of the Liver and the Possible Role of Hepatic Venous Blood under Liver Ischemia

1998 ◽  
Vol 15 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Tsutomu Sato ◽  
Yoshihiro Asanuma ◽  
Tomoyuki Kusano ◽  
Noriaki Sasaki ◽  
Yoshiaki Shindo ◽  
...  
1999 ◽  
Vol 32 (3) ◽  
pp. 805-811
Author(s):  
Tsutomu Sato ◽  
Tomoyuki Kusano ◽  
Toshiaki Kurokawa ◽  
Hiroshi Nanjo ◽  
Koichi Kawamura ◽  
...  

1964 ◽  
Vol 206 (6) ◽  
pp. 1304-1308 ◽  
Author(s):  
William A. Reed ◽  
Robert T. Manning ◽  
Lenly T. Hopkins

This work was done to evaluate the effects of hepatic hypoxia and hyperthermia in the dog. Hepatic temperature changes were produced by portal vein perfusion and hypoxia by hepatic arterial inflow occlusion. The extracorporeal circuit consisted of a heat exchanger, plastic tubing, pump, and heating jacket. Blood passed from the femoral artery or jugular vein through the extracorporeal circuit and returned to the portal vein. Forty-two animals were studied. Simple arterial inflow occlusion for 1 hr caused death in three of five animals. Perfusion of the liver with venous blood during hepatic artery occlusion was followed by death in all animals while survival was obtained when arterial blood perfusate was utilized. Death occurred if hepatic temperature exceeded 43 C, with one exception. Portal vein infusion without hepatic anoxia resulted in survival of animals following short periods of hepatic hyperthermia up to 46 C. The greatest increase in serum transaminase and alkaline phosphatase followed hepatic hyperthermia or anoxia, or both. Enzyme values gradually returned to normal within 21 days. It is concluded that hepatic anoxia augments the toxic effect of hepatic hyperthermia. The cause of death was not definitely identified.


1984 ◽  
Vol 62 (9) ◽  
pp. 1086-1091 ◽  
Author(s):  
Denis Garceau ◽  
Nobuharu Yamaguchi ◽  
Robert Goyer ◽  
Francine Guitard

The metabolic role of neurally released noradrenaline (NA) was studied in the liver of anesthetized dogs. Sustained stimulation with various frequencies was directly applied on the anterior plexus of hepatic nerves. Stimulation-induced changes in plasma concentrations of endogenous catecholamines in hepatic venous blood were determined in correlation with concomitant changes in those of glucose (GL). Mean basal values for hepatic venous NA, adrenaline, dopamine, and GL were 0.062, 0.022, 0.032 ng/mL, and 97.9 mg%, respectively. Among these catecholamines, NA was the only one being released significantly during stimulation. While hepatic venous NA increased rapidly during stimulation, being maximum within 3 min, hepatic venous GL increased gradually, reaching a maximum value 5 min after the onset of stimulation. A highly significant correlation (r = 0.90, P < 0.001) was found between changes in hepatic venous NA and GL concentrations observed during stimulation at various frequencies (2–16 Hz). However, hepatic vasoconstricting responses to stimulation were not correlated with increased hepatic venous GL. An α-blockade with phentolamine (2 mg/kg, iv) resulted in diminished release of GL by approximately 50% (P < 0.05) and reduced hepatic arterial vasoconstriction by approximately 47% (P < 0.01) upon stimulation (8 Hz, 5 min), even though NA release was markedly enhanced. We conclude that in the dog, NA is the sole catecholamine released within the liver in response to direct hepatic nerve stimulation, and NA thus released mediates the hepatic glycogenolysis via α-adrenoceptors.


Surgery Today ◽  
2021 ◽  
Author(s):  
Atsushi Nanashima ◽  
Yukinori Tanoue ◽  
Tatefumi Sakae ◽  
Isao Tsuneyoshi ◽  
Masahide Hiyoshi ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Reina Hirooka ◽  
Kyoji Ito ◽  
Nobuyuki Takemura ◽  
Fuminori Mihara ◽  
Norihiro Kokudo

Abstract Background The mortality of abdominal vena caval injuries is as high as 50–80%. Yet, there were few reports on how to repair injured inferior vena cava (IVC). This report presents a method of vena caval repair in a case of penetrating retrohepatic IVC injury, requiring hepatic resection and total vascular exclusion (TVE). Case presentation The patient was a 20-year-old man with a stab wound in the epigastrium. An emergency laparotomy was performed in the emergency room, and a stab incision on the left liver was detected. As the Pringle’s maneuver did not reduce bleeding, hepatic vein injury was suspected, and left hemihepatectomy was performed to confirm the bleeding point. After the hepatectomy, laceration was still evident deeper into the resection, and IVC injury was suspected. The bleeding was temporarily controlled by tentative hepatorrhaphy and gauze packing, and the initial damage control surgery was terminated. Definitive surgery was performed on the third postoperative day. The lacerated point was observed under TVE, and the laceration penetrated the retrohepatic IVC through its posterior wall. The slit of the posterior wall was sutured first, followed by suturing of the anterior wall of the IVC. Finally, the lacerated liver was closed with hepatorrhaphy. TVE was removed, and the massive bleeding was successfully controlled. Conclusion In severe liver injuries involving the retrohepatic IVC, hepatic resection and TVE may be useful for ensuring an optimized surgical field for repairing the injured IVC.


2021 ◽  
pp. 1-3
Author(s):  
Renate Kaulitz ◽  
Gerhard Ziemer ◽  
Michael Hofbeck

Abstract Direct hepatic veins-to-hemiazygos connection offers the balanced distribution of hepatic venous blood to both lungs, not requiring anticoagulation. We report a 13-year follow-up after this type of off-pump Fontan completion. Patient’s hepatic veins-to-hemiazygos confluence increased with growth to allow for unobstructed flow. This unique technique can be recommended in heterotaxy patients, if atrial hepatic venous drainage and hemiazygos vein are in close proximity.


2021 ◽  
pp. 1-16
Author(s):  
Marcin Adamczak ◽  
Stanisław Surma

<b><i>Background:</i></b> Metabolic acidosis in CKD is diagnosed in patients with plasma or venous blood bicarbonate concentration lower than 22 mmol/L. Metabolic acidosis occurs in about 20% of patients with CKD. Metabolic acidosis may lead to dysfunction of many systems and organs as well as CKD progression. Currently, sodium bicarbonate is mainly used for pharmacological treatment of metabolic acidosis in patients with CKD. Veverimer is a new drug dedicated to treatment of metabolic acidosis in patients with CKD. Orally given veverimer binds hydrogen ions in the intestines and subsequently is excreted from the body with feces. Clinical studies have shown that veverimer is effective in increasing serum bicarbonate concentrations in CKD patients with metabolic acidosis. Here, we present review of the epidemiology, pathogenesis, diagnosis, treatment, and prevention of metabolic acidosis in CKD patients. <b><i>Summary:</i></b> Metabolic acidosis is common in patients with CKD and contributes to CKD progression and many complications, which worsen the prognosis in these patients. Currently, sodium bicarbonate is mainly used in metabolic acidosis treatment. The role of the new drug veverimer in the metabolic acidosis therapy needs further studies. <b><i>Key Message:</i></b> The aim of this review article is to summarize the current knowledge concerning the epidemiology, pathogenesis, diagnosis, treatment, and prevention of metabolic acidosis in CKD patients.


Development ◽  
1971 ◽  
Vol 26 (3) ◽  
pp. 481-495
Author(s):  
Par Elisabeth Houssaint ◽  
Nicole Le Douarin

Cholinesterases in the chick liver. The role of the endoderm in the appearance of the activity of cholinesterases in the hepatic mesenchyme The histochemical method of Koelle & Friedenwald (1949), as modified by Gerebtzoff (1953), has been used to investigate the distribution of cholinesterases in the chick embryonic and adult liver. Non-specific cholinesterases and, in a lower proportion acetylcholinesterase, have been detected in the endothelial cells of blood sinusoids of both adult and embryonic hepatic tissue. The hepatocytes do not show any cholinesterase activity. Cholinesterases appear precociously in the liver mesenchyme, since they already occur in the septum transversum of the 3-day-old chick embryo. An experimental procedure preventing the invasion of the hepatic mesenchymal Anlage by the endodermic cords has been used. The experimentally isolated hepatic mesenchyme shows an important cholinesterase activity; therefore this activity does not depend on the presence of the hepatocytes. The grafting of the determined hepatic endodern in the somatopleura of the 3-day-old chick embryo results in the development of hepatic tissue in the body wall. In this experimentally produced liver, cholinesterase activities are present in the endothelial cells which have arisen from somatopleura mesenchymal cells, though normally somatopleural mesenchyme does not possess these enzymes. The role of the endoderm in the appearance of this enzymic activity in the somatopleural mesenchyme is discussed.


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