Exaggerated liver injury induced by ischemia-reperfusion in spontaneously hypertensive rats.

BACKGROUND: The functions of polymorphonuclear leukocytes (PMNs), which play a critical role in organ damage, are primed in patients with essential hypertension and spontaneously hypertensive rats (SHR). Hepatic ischemia-reperfusion (I/R) injury is shown to be caused and aggravated by the PMNs. We examined whether the hepatic I/R injury was exaggerated in SHR.

METHODS: The portal vein and artery were partially occluded for 60 min. Blood samples were obtained to determine the degree of liver damage during 48 h after reperfusion.

RESULTS: The increase in serum transaminase concentration and hepatic myeloperoxidase content, which reflects the number of PMNs in liver tissue, in SHR were significantly greater than those of their control rats, Wistar-Kyoto rat (WKY). However, the elevations in hepatic transaminases induced by I/R did not differ between other hypertensive animal models (N-nitro-L-arginine methyl ester [L-NAME]-treated and deoxycorticosterone acetate [DOCA]/salt-treated rats) and their controls.

CONCLUSIONS: These results suggest that the elevated PMNs, but not high blood pressure per se, contributes to the exaggerated hepatic I/R injury in SHR.