[Protective effects of hydroxyethyl starch (130/0.4) against ischemia reperfusion injury of kidney: experiment with rats].

Objective: To explore the protective effects of hydroxyethyl starch (HES)(130/0.4) against ischemia reperfusion injury of kidney and its impact on the expression of intercellular adhesion molecule-1 (ICAM-1).

Methods: Forty SD rats underwent resection of the right kidney and clamping of the left renal artery for 60 min to establish renal ischemia reperfusion model, and then were randomly divided into 4 equal groups: Group S, undergoing infusion of normal saline 20 mg/kg 20 min before the reopening of the renal artery, Group W1, undergoing infusion of HES 5 mg/kg 20 min before the reopening of the renal artery, Group W2, undergoing infusion of HES 10 mg/kg, and Group W3, undergoing infusion of normal saline 20 mg/kg. Ten rats underwent sham operation and were used as controls (Group C). 24 h after reperfusion arterial blood samples were collected to detect 6 the levels of serum creatinine (Cr) and blood urea nitrogen (BUN), and then the rats were killed with their kidneys taken out to undergo pathological examination and calculation of Paller's score. Immunohistochemistry was used to detect the expression of intercellular adhesion molecule-1 (ICAM-1).

Results: The levels of BUN and Cr of Group S were 152 +/- 22 and 3.17 +/- 1.00 mmol/L respectively, both significantly higher than those of Group C, and the levels of BUN and Cr of Groups W2 and W3 were 99 +/- 23 and 1.82 +/- 0.86 mmol/L and 92 +/- 28 and 1.57 +/- 0.70 mmol/L respectively, all significantly lower than those of Group S (P < 0. 05 or P < 0.01). The Paller's scores of W2 and W3 were 33.6 +/- 16.6 and 29.2 +/- 12.3 respectively,both significantly lower that of Group S (43.2 +/- 15. 8, both P < 0.05). The absorption levels of ICAM-1 of Groups W2 and W3 were 182 +/- 22 and 161 +/- 25 respectively, both significantly lower than that of Group S (212 +/- 32, P < 0.01).

Conclusion: Infusion of 10-20 ml/kg HES (130/0.4) significantly alleviates the ischemia-reperfusion injury, probably by reducing the ICAM-1 expression.