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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
The liver receives blood from two sources: the hepatic artery carries oxygenated blood (approximately 30% of liver blood flow), and the hepatic portal vein carries deoxygenated blood (approximately 70% of blood flow). The venous blood from the hepatic portal vein contains newly absorbed nutrients, drugs, microbes and toxins from the gastrointestinal tract. Branches of both of these blood vessels carry blood into the liver sinusoids where oxygen, most of the nutrients and some toxic substances are processed by the hepatocytes. The resulting venous blood drains into the hepatic vein to return to the systemic venous circulation.
Hepatic Dearterialization and Infusion Treatment of Liver Tumors
Published in Hans-Inge Peterson, Tumor Blood Circulation: Angiogenesis, Vascular Morphology and Blood Flow of Experimental and Human Tumors, 2020
Stig Bengmark, Eva Peterson-Dahl, Per E. Fredlund
Occlusion of the hepatic artery can also be performed with various catheterization procedures. A balloon catheter can be selectively placed into the hepatic artery,57 but remaining collateral circulation will probably make this method less useful for tumor treatment.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
The liver receives blood through the portal vein and hepatic artery. The former accounts for 75–80% and the latter 20–25% of the total hepatic blood flow (1500 ml/min), which is about one-quarter of cardiac output (Figure 1).
Excellent outcome following emergency deceased donor ABO-incompatible liver transplantation using rituximab and antigen specific immunoadsorption
Published in Scandinavian Journal of Gastroenterology, 2022
Ulrika Skogsberg Dahlgren, Gustaf Herlenius, Bengt Gustafsson, Johan Mölne, Lennart Rydberg, Andreas Socratous, William Bennet
In total, four ABOi recipients had biopsy proven T-cell mediated rejection (Table 4). Two adult patients had steroid resistant T-cell mediated rejection and both responded to anti-thymocyte globuline treatment. One patient developed AMR (Pat#12, Table 4). This patient was retransplanted with an ABOi graft due to acute-on-chronic liver failure, in turn due to therapy resistant chronic rejection. In addition to anti-AB antibody rebound, high MFI DSA (Class II DSA, MFI 12201) was detected post-transplantation. Multiple IA-, and PP-sessions were performed but were unsuccessful in controlling the Ab rebound (Figure 2(A,B)). A liver biopsy at POD 12 showed histological features of AMR (AMR-score 2, Figure 3(B)) with a strong C4d-deposition (C4d-score 3, Figure 3(C)). Several surgical complications also complicated the clinical course. During the first post-operative weeks the patient was re-operated three times, twice for bleeding with circulatory shock and once due to bile leakage. After the second bleeding episode a partial thrombosis in the hepatic artery proper was diagnosed. Thereafter intrahepatic necrosis developed followed by multiple intrahepatic biliary strictures. Septicemia contraindicated intensified immunosuppression and re-transplantation and the patient died four months post-transplantation.
Anatomic Variation of the Cystic Artery: New Findings and Potential Implications
Published in Journal of Investigative Surgery, 2021
Li Li, Qiang Li, Mingguo Xie, Wenwei Zuo, Bin Song
Awareness of variant anatomy, such as a zero angle between the cystic artery and right hepatic artery injury, could also be useful in preventing right hepatic artery injury. In some reports, authors had described right hepatic artery or its branches injury was present in 7% (5/71) of cadavers that had undergone cholecystectomy and had no abnormality of the liver or bile ducts [36]. Consequences of right hepatic artery injury include hemorrhage, right lobe atrophy, hemophilia, infection, and hepatic ischemia. Some of these complications have necessitated hepatectomy or even hepatic transplantation, particularly if accompanied by biliary injury [4,14,21,22,16]. A classification of laparoscopic biliary injuries mechanisms exists (the Stewart-Way classification), which groups injuries based on anatomic pattern and mechanism of laparoscopic injury [37]. Having the right hepatic artery mistaken for the cystic artery is one of causes (Stewart-Way class IV) [14,36]. It is conceivable that a zero-angle cystic artery is more likely to be mistakenly identified as the right hepatic artery, because the straight-line course of the cystic artery and right hepatic artery does not reveal an obvious boundary during cystic artery dissection; and boundary detection is more difficult due to the lack of depth perception and inherent visual limitations of laparoscopic procedures [4]. Although it was unclear how often right hepatic artery injury were associated with such variant anatomy, it is conceivable that awareness such variant anatomy may decrease the potential risk of accidental the right hepatic artery injury during LC.
Effect of carvedilol versus propranolol on acute and chronic liver toxicity in rats
Published in Drug and Chemical Toxicology, 2021
At the end of the rats were anesthetized with pentobarbital (50 mg/kg), and the liver was perfused in situ via the portal vein, using a non-recirculating system (Matsumoto et al. 2000). Briefly, the abdomen was opened, and the bile duct was cannulated with a polyethylene PE-10 tubing (i.d. 0.28 mm). The hepatic artery was ligated. A ligature was passed around the inferior vena cava (IVC) above the renal vein. The portal vein was then cannulated with a polyethylene PE-205 catheter. The liver was immediately perfused with Krebs–Henseleit bicarbonate solution (KHS) oxygenated with 95% O2–5% CO2 through silastic tubing (Hamilton et al. 1974) at 37 °C. The KHS had the following composition (mM): 118 NaCl, 4.7 KCl, 1.2 KH2PO4, 1.2 MgSO4, 2.5 CaCl2, 25 NaHCO3, and 11.0 glucose; pH 7.4. The IVC was cut below the ligature, thus allowing the perfusate to escape. Thereafter, the thorax was opened and supradiaphragmatic part of IVC was cannulated using a PE-240 catheter, and a ligature around the infrarenal IVC was tied. The liver was then perfused at 20, 40 and 60 ml/min through the portal vein, and the effluent escaped through the IVC cannula. The perfusion pressure was measured by continuously monitoring the height of perfusate in an open vertical capillary column (i.d.=2 mm) attached to the perfusion system just proximal to the inflow cannula when the perfusate was infused.