Background: Intermittent Pringle manoeuvre resulted in less blood loss and better preservation of liver function when it was applied for fewer than 120 minutes. The mechanism of better preservation of liver function under intermittent Pringle manoeuvre at molecular level remains unclear. Furthermore, the ultrastructural features in the liver with chronic diseases under intermittent Pringle manoeuvre have not been studied. The aim of the study is to investigate the expression of stress genes and ultrastructural change of the liver under intermittent Pringle manoeuvre.
Methods: From July 1995 to February 1998, 131 patients underwent hepatectomy for liver tumours (61 patients without Pringle manoeuvre and 70 patients with intermittent Pringle manoeuvre). Twenty-five patients (15 with Pringle manoeuvre and 10 without Pringle manoeuvre) were included in the study of hepatic stress gene expression during hepatectomy. Twenty-two patients (18 patients with intermittent Pringle manoeuvre and four patients without Pringle manoeuvre) were randomly assigned for electron microscopic examination.
Results: For the expression of stress genes, both the heat shock genes (HSP 70A and HSC 70) and acute phase genes (TNF-alpha and interleukin-6) were detected simultaneously in the patients with or without intermittent Pringle manoeuvre. The patients under intermittent Pringle manoeuvre had relatively higher mRNA levels of heat shock gene 70 family, which is related to intracellular repair and protection. Induction of TNF-alpha and interleukin-6 genes, which contributed to ischaemia-reperfusion injury and postoperative complication, was not found in the patients under intermittent Pringle manoeuvre. Under the electron microscopy, the hepatic ultrastructure was well maintained under intermittent Pringle manoeuvre whatever the liver status, even when the accumulated ischaemic duration was extended to 120 min.
Conclusion: Intermittent Pringle manoeuvre induced relatively higher expression of heat shock genes, which are related to intracellular homeostasis, and is consistent with the well maintenance of liver ultrastructure.