Effect of graft reperfusion on intracellular calcium levels in mononuclear leucocytes during human orthotopic liver transplantation

Enright, Siobhan; Srinivasa, R; Bellamy, Mark

doi:10.1046/j.1365-2168.1998.00699.x

Cited by 4 publications

(6 citation statements)

References 12 publications

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“…However, many other proinflammatory cytokines, including IL-1b, IL-2, and IL-8, which increase in the flush blood from the donor graft, are not correlated with the quantity of catecholamines used to treat the hemodynamic instability after reperfusion [ 27 ]. In addition, a variety of other mediators, including activated circulating monocytes, arginase, endotoxin, monocyte chemoattractant protein-1, and thromboxane are present during PRS but there is a lack of evidence for a causal relationship between these mediators and PRS during LT [ 24 29 30 31 32 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Postreperfusion syndrome during liver transplantation

Jeong

2015

Korean J Anesthesiol

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As surgical and graft preservation techniques have improved and immunosuppressive drugs have advanced, liver transplantation (LT) is now considered the gold standard for treating patients with end-stage liver disease worldwide. However, despite the improved survival following LT, severe hemodynamic disturbances during LT remain a serious issue for the anesthesiologist. The greatest hemodynamic disturbance is postreperfusion syndrome (PRS), which occurs at reperfusion of the donated liver after unclamping of the portal vein. PRS is characterized by marked decreases in mean arterial pressure and systemic vascular resistance, and moderate increases in pulmonary arterial pressure and central venous pressure. The underlying pathophysiological mechanisms of PRS are complex. Moreover, risk factors associated with PRS are not fully understood. Rapid and appropriate treatment with vasopressors, volume replacement, or venesection must be provided depending on the cause of the hemodynamic disturbance when hemodynamic instability becomes profound after reperfusion. The negative effects of PRS on postoperative early morbidity and mortality are clear, but the effect of PRS on postoperative long-term mortality remains a matter of debate.

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Section: Pathophysiologymentioning

confidence: 99%

Postreperfusion syndrome during liver transplantation

Jeong

2015

Korean J Anesthesiol

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“…MAC forms an ionophore in the cell membrane, which permits transit of calcium into the cell. We have previously shown an elevation in intracellular calcium in this group of patients over the same time course as complement activation (i.e., a modest rise in intracellular calcium during veno‐venous bypass followed by a major rise after graft reperfusion) 3. There are many mechanisms by which this could occur,19 consistent with the incorporation of a calcium ionophore into the cell membrane.…”

Section: Discussionmentioning

confidence: 51%

“…We have previously shown an elevation in intracellular calcium in this group of patients over the same time course as complement activation (i.e., a modest rise in intracellular calcium during veno-venous bypass followed by a major rise after graft reperfusion). 3 There are many mechanisms by which this could occur, 19 consistent with the incorporation of a calcium ionophore into the cell membrane. Increases in intracellular calcium in sinusoidal endothelial cells may also have a crucial role in mediating the expression of adhesion molecules 20 and thus contribute to the microcirculatory disturbances observed in primary graft dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…2 However, the hemodynamic changes and elevation of intracellular calcium (suggestive of membrane damage) occur much faster than the time course of cytokine expression. 3 Although some inflammatory mediators are expressed early after graft reperfusion (IL-6, IL-8) 4 the majority require more time for expression. 2 One explanation for the immediate cardiovascular response could be the involvement of an existing protein cascade.…”

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confidence: 99%

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Complement membrane attack complex and hemodynamic changes during human orthotopic liver transplantation

et al. 2004

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on behalf of the Leeds Liver GroupHemodynamic changes and elevation of intracellular calcium following reperfusion in human liver transplantation occur rapidly and do not match the time course of cytokine expression, therefore, we postulate involvement of other, pre-formed substances, such as complement. We studied 40 adult patients undergoing liver transplantation. Blood was drawn for estimation of C3, C4, C3 degradation product, membrane attack complex, and CH100 levels and elastase (a marker of neutrophil activation) at induction of anesthesia, 5 minutes before reperfusion, 5 minutes and 60 minutes after reperfusion. Cardiac output was measured by thermodilution and systemic vascular resistance was calculated at these same time points. There was a significant rise in C5b-9 membrane attack complex (P ‫؍‬ .0012) with a corresponding fall in C3 (P ‫؍‬ .0013) and C4 (P ‫؍‬ .0002) levels and a rise in C3 degradation product levels (P ‫؍‬ .0006). There was no significant change in CH100. These changes very closely followed the hemodynamic changes of a significant fall in systemic vascular resistance index (P ‫؍‬ .0024) and increase in cardiac index (P ‫؍‬ .0005). Elastase rose from 356 ؎ 53 to 557 ؎ 40 g/L (P < .0001). There is complement activation and neutrophil activation at reperfusion in liver transplantation. Dilution alone cannot explain the fall in C3 and C4 levels as there is a corresponding increase in membrane attack complex and C3 degradation product levels with time. As both C3 and C4 are consumed, the classical pathway must be active, though alternative and lectin activated pathways may also be involved. These findings may, at least in part, explain the hemodynamic changes typically seen at reperfusion in liver transplantation. (Liver Transpl 2004;10:273-278.)

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“…A variety of other mediators have been associated with the development of postreperfusion syndrome, including arginase, 22 thromboxane, 23 endotoxin, 24 monocyte chemoattractant protein-1, 25 and activated circulating monocytes. 26 While such mediators may indeed be present during the postreperfusion syndrome, mechanistic studies are thus far lacking. 26 More study in large-animal models may yield insights as to which targets are most promising for prevention and treatment of postreperfusion syndrome.…”

Section: : What Are Some Novel Strategies In the Treatment Of Postrmentioning

confidence: 99%

Postreperfusion Syndrome During Liver Transplantation

Fiegel

Zimmerman

Seres

et al. 2012

Semin Cardiothorac Vasc Anesth

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A 55-year-old male with cirrhosis and end-stage liver disease secondary to alcohol abuse and hepatitis C presents for cadaveric transplant. His current MELD (model for end-stage liver disease) score is 33. The donor is a 35-year-old male with an intracerebral hemorrhage who underwent donation after cardiac death (DCD) organ harvesting. After reperfusion of the portal vein, the patient experiences profound, sustained hypotension resistant to all standard vasopressor medications.

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Effect of graft reperfusion on intracellular calcium levels in mononuclear leucocytes during human orthotopic liver transplantation

Cited by 4 publications

References 12 publications

Postreperfusion syndrome during liver transplantation

Postreperfusion syndrome during liver transplantation

Complement membrane attack complex and hemodynamic changes during human orthotopic liver transplantation

Postreperfusion Syndrome During Liver Transplantation

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