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Hyperfibrinolysis in Liver Cirrhosis
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
The changes in fibrinolysis may result in complications during surgery in patients with liver disease. Kwaan et al.47 suggested that an increase of fibrinolytic activity during splenectomy in a patient with hepatic cirrhosis might be responsible for severe oozing during surgery. In patients undergoing a portacaval shunt operation, increased fibrinolytic activity may contribute to the hemorrhagic complications of the operation.118,119 Uncontrollable oozing associated with hypofibrinogenemia and high plasma fibrinolytic activity developed during surgery in about 10% of the patients undergoing a portacaval shunt operation.120 In patients undergoing an orthotopic H ver transplantation severe bleeding is the major cause of perioperative death.121 The hemorrhagic diathesis during the procedure may be due to DIC, hyperfibrinolysis, or a combination of these two processes. Recent studies suggest that enhancement of fibrinolysis during the anhepatic and early post-anhepatic period, due to an extensive increase of t-PA, may be the major cause of sustained bleeding.121
Shunts in the Portal Area of the Rat
Published in Waldemar L. Olszewski, CRC Handbook of Microsurgery, 2019
This is a rather complicated technique mainly due to the high tension on the anastomosis and the limited space available. Henzel et al.10 placed the corner sutures through vena cava and vena porta first, tied the vessels together next, and then performed the posterior suture line. Thereafter the vessels were clamped, incised, and the frontal suture line done last. A side-to-side portacaval shunt allows continued portal blood supply to the liver. Apparently because of this the “portacaval shunt syndrome” is tempered, or even absent.10,16
Physiology and Disorders of Human Bilirubin Metabolism
Published in Karel P. M. Heirwegh, Stanley B. Brown, Bilirubin, 1982
P. Berthelot, Ph. Duvaldestin, J. Fevery
The postoperative alterations in liver function tests seem most often related to the operative site (see below) and/or the hepatic disease involved. Nevertheless, some studies suggest specific anesthetic drug-induced changes, particularly, when halothane is repeatedly administered. The hepatic changes induced by most anesthetics are moderate and transitory. All types of anesthesia, including epidural anesthesia, cause a reduction in hepatic blood flow in man.267,268 Mild transient abnormalities of liver function tests are common after general anesthesia and surgery. They consist mainly of a decreased BSP clearance whatever the type of anesthetic used.269 Abnormal BSP retention occurred in about 50% of the patients following operation on the lower abdomen or on the extremities,270 and even in a high proportion of cases following gastrectomy or cholecystectomy. This BSP retention was not related to the type of anesthesia or to the duration of operation. Patients with hepatic diseases, and undergoing portacaval shunt operations, showed the greatest postoperative change in hepatic function.
Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
Published in Pharmaceutical Biology, 2021
Long Cheng, Xiaoying Wang, Xueni Ma, Huimei Xu, Yifan Yang, Dekui Zhang
Several recent studies have shown that inflammation including systemic inflammation, neuroinflammation, and endotoxemia, modulates HE pathogenesis (Luo et al. 2015). A previous study reported that portacaval shunt (PCS) rats exhibited increased activities of cyclooxygenase and inducible NO synthase, and increased levels of IL6 in the cerebral cortex, indicating the presence of neuroinflammation. Subsequent treatment with ibuprofen, an anti-inflammatory drug, normalised the activities of cyclooxygenase and inducible NO synthase, and completely restored the cognitive ability of the rats (Cauli et al. 2007). Another study demonstrated the importance of neuroinflammation and revealed that neuroinflammation could be caused by peripheral inflammation. It was observed that an increase in the expression of TNF-α, IL-1b, and nuclear NF-κB in the hippocampus of HE rats established by PCS exposure led to altered neurotransmission and finally impaired spatial learning and memory. However, administration of anti-TNF-α drugs, which could not cross the blood-brain barrier, reduced neuroinflammation, translocated NF-κB to the nucleoli, and normalised TNF-α and IL-1b in the hippocampus. Ultimately, spatial learning and memory were restored (Dadsetan et al. 2016). Similar results were obtained in this study where the expression of TNF-α and IL-6 were increased in the brain, suggesting that inflammatory factors modulate brain edoema caused by hepatic encephalopathy. Moreover, DMY normalised the expression of TNF-α and IL-6.
Effects of YM155 on the proliferation and apoptosis of pulmonary artery smooth muscle cells in a rat model of high pulmonary blood flow-induced pulmonary arterial hypertension
Published in Clinical and Experimental Hypertension, 2022
Bingbing Ye, Xiaofei Peng, Danyan Su, Dongli Liu, Yanyun Huang, Yuqin Huang, Yusheng Pang
Congenital heart disease (CHD) is a common cardiovascular malformation in children, with morbidity reported to be 10‰ of live births worldwide. Moreover, portacaval shunt CHD is the most common type of CHD (1–3). Individuals with portacaval shunt CHD have a chronic systemic-pulmonary circulation shunt, causing a prolonged state of continuous high blood flow. The condition results in elevated pulmonary artery pressure (PAP), and eventually progresses into pulmonary artery hypertension (PAH) induced by high pulmonary blood flow (4). PAH is a chronic condition marked by pulmonary vascular remodeling, notably in the tunica media. The tunica media is composed of pulmonary arterial smooth muscle cells (PASMCs), and the proliferation and apoptosis of PASMCs perform a direct role in pulmonary vascular remodeling. In PAH, PASMCs demonstrate cancer-like cell characteristics of increased proliferation and anti-apoptosis, which lead to arterial muscularization, intraluminal thrombosis formation, vascular wall thickening, and lumen stenosis (5). The imbalance between the formation of thrombosis mediators and the production of inflammatory cytokines, coupled with the loss of endothelial barrier integrity, enables the penetration of these circulating factors into the tunica media of the blood vessels, thus driving the migration, hypertrophy, and proliferation of PASMCs, and further resulting in vascular remodeling and disease progression (6). PAH medications are limited in efficacy and specificity and, more importantly, are unable to reverse the underlying pulmonary vascular remodeling in this disease. That is, they mitigate the symptoms of PAH, but are not a cure for it (7,8). Therefore, it’s critical to further unfold the regulatory mechanisms of PASMC proliferation and apoptosis, so to facilitate the discovery of new therapeutic strategies designed to alleviate and reverse the progression of PAH.