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Liver Blood Flow
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The portal vein is a valveless vein and drains blood from the large and small intestines, spleen, stomach, pancreas and gall bladder to the liver. The hepatic portal vein contributes 70% of total liver blood flow and 50%–60% of basal oxygen supply. In the fasting state, the oxygen saturation of portal venous blood is approximately 85%, but this decreases with increased gut activity. The higher O2 saturation in portal venous blood at resting conditions, compared with mixed venous O2 saturation, is due to the high mesenteric arterial shunting through the intestinal capillaries draining into the portal system. The velocity of blood flow in the portal system is 9 cm/s – approximately half that in the hepatic artery. Thus, the hepatic portal system is a low-pressure (5–10 mmHg), low-resistance and low-velocity system. The portal venous pressure depends on the state of constriction/dilatation of mesenteric arterioles and on intrahepatic resistance. The resistance in the portal system is approximately 6%–12% of that in the hepatic artery.
Disorders of the digestive tract
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
The liver is the most important metabolic organ in the body. The hepatic portal system brings venous blood from the intestine where absorbed nutrients are processed, stored and detoxified by the liver. Box 9.9 outlines the numerous functions of the liver.
Disorders of the digestive tract
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
The liver is the most important metabolic organ in the body. The hepatic portal system brings venous blood from the intestine, and the absorbed nutrients are then processed, stored and detoxified by the liver. Box 7.3 outlines the numerous functions of the liver in addition to its role in digestion.
Factors determining the oral absorption and systemic disposition of zeaxanthin in rats: in vitro, in situ, and in vivo evaluations
Published in Pharmaceutical Biology, 2022
Seong‑Wook Seo, Dong‑Gyun Han, Eugene Choi, Min‑Jeong Seo, Im‑Sook Song, In‑Soo Yoon
The absorption of zeaxanthin from the gut lumen into the systemic circulation occurs via two different routes: the hepatic portal system and the lymphatic system via chylomicron formation (Deming and Erdman 1999; Murillo et al. 2019). In the latter route, a drug absorbed from the gut lumen bypasses hepatic first‑pass elimination. The results shown in Table 4 clearly indicate that the lymphatic pathway plays a significant role in the oral absorption of zeaxanthin. It is also suggested that the lymphatic absorption and bioavailability of zeaxanthin were not affected by the concomitant use of the lipids tested in this study. However, the use of more advanced and sophisticated formulation systems with other lipids and excipients could lead to different results, which warrants further research.
Clinical pharmacology of antiplatelet drugs
Published in Expert Review of Clinical Pharmacology, 2022
Georg Gelbenegger, Bernd Jilma
COX-1 occurs ubiquitously in the human body and is also present in platelets [7]. Acetylsalicylic acid (ASA) irreversibly acetylates serine 530 of platelet-bound COX-1, and thereby prevents arachidonic acid from reaching the active site of COX-1 [8,9]. This precludes the production of TxA2, a platelet-activating and vasoconstrictory agent, producing an overall inhibitory effect on platelet aggregation (concurrent inhibition of TxA2 and PGI2 has opposing effects on hemostasis, but the antithrombotic effect of TxA2 inhibition prevails at low doses) [10]. Platelets are anucleate, which disables them to newly synthesize COX-1. Therefore, platelet inhibition by ASA is permanent and is sustained for the remainder of the platelet’s life span (7–10 days). Acetylsalicylic acid shows a high first-pass effect with up to 50% being deacetylated in the intestinal walls and the liver [11], and its antiplatelet effect is therefore carried out in the presystemic circulation (hepatic portal system). Acetylsalicylic acid shows a 170-fold more potent inhibition of COX-1 than COX-2 [11]. Other nonsteroidal anti-inflammatory drugs also bind to COX-1 and affect platelet function but do so in a reversible manner, leading to a lesser pronounced pharmacodynamic effect [12].
An overview of current advancements in pancreatic islet transplantation into the omentum
Published in Islets, 2021
Kimia Damyar, Vesta Farahmand, David Whaley, Michael Alexander, Jonathan R. T. Lakey
Type 1 Diabetes Mellitus (T1DM) is an autoimmune disorder in which insulin-producing β-cells, predominant within the islets of Langerhans in the pancreas, are destroyed. This ultimately results in blood sugar elevation and loss of glycemic control.1 The development of the Edmonton protocol in 2000 introduced islet transplantation as a method to restore glycemic control in insulin-dependent T1DM patients.2 Under the current standard of care, the liver is considered the primary site for clinical islet transplantation. The islets can be easily infused into the hepatic portal system allowing β-cells to effectively restore glycemic control to the patients. However, there are limitations associated with islet infusion into the portal system. There is a risk of portal vein thrombosis as well as the elevation of portal pressure that can lead to uncontrolled bleeding. Moreover, there is a possibility of islet loss after transplantation due to the IBMIR that can occur when islets encounter the recipient’s blood.3–6 In order to address the limitations associated with intrahepatic islet transplantation, alternative sites have been investigated including but not limited to the omentum, peritoneum, spleen, renal subcapsule, and gastric submucosa. However, some of these sites show limitations in capacity and functional outcome or introduce further complications post-transplant.3,7–12