Protective effects of ischaemic preconditioning of remote small intestine on liver warm ischaemia-reperfusion injury in rats

Abstract

Objective To observe the protective effective of remote small intestinal ischaemic preconditioning (RIPC) on liver warm ischemia-reperfusion injury (IRI) in rats. Methods Fourty male rats were allocated to four groups: sham operated, RIPC alone, IRI alone, and RIPC plus IRI. RIPC was induced in small intestine with a vascular clip, before liver IRI, by three alternate cycles of 5 min ischaemia followed by 5 min reperfusion. Liver IRI was produced by 70% inflow occlusion for 45 min, open-reflow 3 h. Blood alanine aminotransferase (ALT), lactate dehydrogenase (LDH), nitric oxide (NO) and endothelin (ET) levels were determined, liver pathological changes were observed by HE staining, and mean arterial pressure (MAP), SaO2. Results Three h after reflow, ALT and LDH levels, MAP, SaO2 in RIPC + IR group were (434.26 ± 133.42) U/L, (2536 ± 181 ) U/L, (83. 1 ±7. 3) mmHg (1 mm Hg =0. 133 kPa) and (97.4 ±0.5)%, significantly increased (P <0.05) as compared with the IR group [(953.64 ± 114. 12) U/L, (5734 ± 296) U/L, (67. 1 ±7.4) mmHg and (93. 1 ±0. 6)% respectively]. The liver pathological changes in RIPC + IR group alleviated as compared with the IR group. Serum NO concentration in the IR group [( 15.54 ±2. 34) μmol/L]was lower than in RIPC + IR group [( 18. 10 ±1.82) μmol/L]in the portal vein blood (P <0.05). In peripheral blood, plasma ET concentration in IR group was (672.4 ± 63. 1 ) ng/L, higher than in RIPC + IR group [(451.7 ± 63.6) ng/L, ( P < 0. 05 )],and so did in portal vein blood [IR group: (612. 5 ± 48.2 ) ng/L, RIPC + IR group: (401.5 ± 51.2)ng/L]. Conclusion Small intestinal RIPC can reduce the hepatic ischemia-reperfusion injury. NO and ET may play an important role in the protection. Key words: Ischaemia-reperfusion injury; Remote ischaemic preconditioning; Liver; Small intestine