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

细胞外 生物学中的钙 医学 细胞内 钙ATP酶 膜透性 内分泌学 移植 内科学 免疫学 药理学 生物化学 化学 ATP酶
作者
Siobhan Enright,R Srinivasa,Mark C. Bellamy
出处
期刊:British Journal of Surgery [Oxford University Press]
卷期号:85 (5): 673-676 被引量:4
标识
DOI:10.1046/j.1365-2168.1998.00699.x
摘要

Orthotopic liver transplantation (OLT) is accompanied by local and systemic manifestations of the ischaemia-reperfusion syndrome. Local effects are mediated in part through changes in intracellular calcium levels in Kupffer cells. Arachidonic acid metabolites mediate increases in intracellular calcium concentration and thus potentiate the effect of free radicals. This study was carried out to characterize white blood cell (WBC) calcium changes as a mediator for white cell activation in human OLT.Twenty consecutive patients had OLT using standard surgery and anaesthesia techniques. Blood samples were drawn for estimation of WBC cytosolic calcium content at induction of anaesthesia, 5 min before graft reperfusion and 15 min after reperfusion. The rate of rise in intracellular calcium concentration after the addition of a calcium chloride 1 mmol L(-1) solution to the extracellular milieu was used as an estimate of membrane calcium permeability.Both extracellular (P = 0.0002) and intracellular (P = 0.0008) calcium concentrations rose with time. However, at no time was there a correlation between extracellular and intracellular calcium levels or rate of calcium influx (r2 = 0.002, P = 0.78). There was a significant increase in intracellular calcium concentration (P = 0.0008) and in the rate of rise of intracellular calcium levels (P = 0.0009) after reperfusion.There was a significant increase in circulating monocyte membrane permeability for calcium and cytosolic calcium concentration following reperfusion in human OLT. This was independent of extracellular calcium concentration. These results are consistent with WBC activation by reperfusion and could be implicated in the systemic reperfusion syndrome seen in OLT in humans.
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