Serum acidosis prior to reperfusion facilitates hemodynamic recovery following liver transplantation

Fukazawa, Kyota; Vitin, Alexander A.; Pretto, Ernesto A.

doi:10.1007/s00540-015-2080-2

Cited by 8 publications

(5 citation statements)

References 21 publications

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“…After transplantation with excised liver grafts, portal blood is perfused to initiate hepatic function recovery. Although serum pH values normalize slowly after hepatic IR, the heamodynamics stabilize quickly in LT models . Losartan administered to donors and recipients before LT has been found to result in the maintenance of liver function by inhibition of multiple damaging signalling pathways .…”

Section: Pre‐conditions For Lt To Eliminate Cold Hepatic Ir Injurymentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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The liver, the largest organ with multiple synthesis and secretion functions in mammals, consists of hepatocytes and Kupffer, stem, endothelial, stellate and other parenchymal cells. Because of early and extensive contact with the external environment, hepatic ischaemia reperfusion (IR) may result in mitochondrial dysfunction, autophagy and apoptosis of cells and tissues under various pathological conditions. Because the liver requires a high oxygen supply to maintain normal detoxification and synthesis functions, it is extremely susceptible to ischaemia and subsequent reperfusion with blood. Consequently, hepatic IR leads to acute or chronic liver failure and significantly increases the total rate of morbidity and mortality through multiple regulatory mechanisms. An increasing number of studies indicate that mitochondrial structure and function are impaired after hepatic IR, but that the health of liver tissues or liver grafts can be effectively rescued by attenuation of mitochondrial dysfunction. In this review, we mainly focus on the subsequent therapeutic interventions related to the conservation of mitochondrial function involved in mitigating hepatic IR injury and the potential mechanisms of protection. Because mitochondria are abundant in liver tissue, clarification of the regulatory mechanisms between mitochondrial dysfunction and hepatic IR should shed light on clinical therapies for alleviating hepatic IR‐induced injury.

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Section: Pre‐conditions For Lt To Eliminate Cold Hepatic Ir Injurymentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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“…Cell death in the pH paradox is not oxygen-dependent. Reperfusion at low pH (<6.5) blocks increase of mitochondrial membrane permeability, which allows mitochondrial re-polarization and prevents cell death [ 31 , 32 , 33 ].…”

Section: Impact Of Anesthesia and Surgery (Liver Resection And Liver mentioning

confidence: 99%

Review. Perioperative Management of Lactic Acidosis in End-Stage Liver Disease Patient

Vitin

Azamfirei

Tomescu

et al. 2017

The Journal of Critical Care Medicine

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Lactic acidosis (LA) in end-stage liver disease (ESLD) patients has been recognized as one of the most complicated clinical problems and is associated with increased morbidity and mortality. Multiple-organ failure, associated with advanced stages of cirrhosis, exacerbates dysfunction of numerous parts of lactate metabolism cycle, which manifests as increased lactate production and impaired clearance, leading to severe LA-induced acidemia. These problems become especially prominent in ESLD patients, that undergo partial hepatectomy and, particularly, liver transplantation. Perioperative management of LA and associated severe acidemia is an inseparable part of anesthesia, post-operative and critical care for this category of patients, presenting a wide variety of challenges. In this review, lactic acidosis applied pathophysiology, clinical implications for ESLD patients, diagnosis, role of intraoperative factors, such as anesthesia and surgery-related, vasoactive agents impact, and also current treatment options and modalities have been discussed.

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“…Whereas the etiological and prognostic effects of acidosis on coagulation and blood transfusion requirements have been extensively described in adults and children submitted to prolonged surgery procedures or trauma, there are few data on the association between acidosis and coagulopathy in OLT. Previous studies suggested that metabolic acidosis may be protective during reperfusion because acidemia suppresses the activity of pH-dependent enzymes, such as proteolytic enzymes and phospholipases, limiting cell damage and tissue necrosis [15,31,32]. Here, we could demonstrate that metabolic acidosis during the reperfusion phase of OLT is directly associated with impaired coagulation and increased need of blood transfusion.…”

Section: Discussionmentioning

confidence: 53%

Association of acidosis with coagulopathy and transfusion requirements in liver transplantation

Souza

Yokoyama

Magnus

et al. 2021

J Thromb Thrombolysis

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The relationship between acidosis and coagulopathy has long been described in vitro and in trauma patients, but not yet in orthotopic liver transplantation (OLT). The association of metabolic acidosis with coagulopathy and with transfusion requirements was evaluated in patients submitted to OLT. Changes in acid-base and coagulation parameters were analyzed by repeated measures. Regression analyses [adjusted for sex, age, model for end stage liver disease (MELD) score, and baseline values of hemoglobin, fibrinogen, international normalized ratio, platelets] determined the association of acid-base parameters with coagulation markers and transfusion requirement. We included 95 patients, 66% were male, 49.5% of the patients had hepatocellular carcinoma and the mean MELD score was 20.4 (SD 8.9). The values of all the coagulation and acid-base parameters significantly changed during OLT, particularly in the reperfusion phase. After adjustments for baseline parameters, the decrease in pH and base excess (BE) values were associated with a decrease in fibrinogen levels (mean decrease of fibrinogen level = 14.88 mg/dL per 0.1 unit reduction of pH values and 3.6 mg/dL per 1 mmol/L reduction of BE levels) and an increase in red blood cells transfusion (2.16 units of RBC per 0.1 unit reduction of pH and 0.38 units of RBC per 1 mmol/L reduction of BE levels). Among multiple factors potentially associated with adverse outcomes, decreasing pH levels were independently associated with the length of hospitalization but not with in-hospital mortality. Metabolic acidosis is independently associated with decreased fibrinogen levels and increased intraoperative transfusion requirement during OLT. Awareness of that association may improve treatment strategies to reduce intraoperative bleeding risk in OLT.

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Serum acidosis prior to reperfusion facilitates hemodynamic recovery following liver transplantation

Cited by 8 publications

References 21 publications

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Review. Perioperative Management of Lactic Acidosis in End-Stage Liver Disease Patient

Association of acidosis with coagulopathy and transfusion requirements in liver transplantation

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