The roles of sex hormone and gender difference for spinal cord protection in spinal cord ischemia

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We evaluated the tissue oxygen partial pressure of spinal cord(PsptO2) following aortic cross-clamping and-unclamping, and then clarified the mechanism of improvement in the PsptO2 following spinal ischemia observed with remote ischemic preconditioning(RIPC) or intravenous estrogen in rabbits. In isoflurane anesthetized rabbits(n=36), we prepared for measurement of PsptO2 following aortic cross-clamping using tissue PO2 monitoring. In the first set of experiment, we allocated 18 animals into 3 groups,(a) control group ; n=6,(b) RIPC group ; n=6,(c) glibenclamide pretreatment(0. 3mg/kg) group ; n=6. In the second set of experiment, we also allocated 18 animals into 3 groups,(d) control group ; n=6,(e) estrogen(17ss estradiol : 20μg) group ; n=6,(f) fulvestrant pretreatment(1mg/kg) group ; n=6. RIPC improved deterioration of the values in PsptO2 at 20 min after aortic cross-clamping and 0, 2, 5 min after aortic unclamp. The improvement was diminished by pretreatment of glibenclamide. Administration of 17s estradiol improved deterioration of the values in PsptO2 at 20 min after aortic cross-clamping and 0, 2, 5 min after aortic unclamp. The improvement was diminished by pretreatment of fulvestrant.In conclusion, after aortic cross-clamping, the RIPC performed improves the deterioration in PsptO2 through the KATP channel activation and 17ss estradiol improves the deterioration in PsptO2 through the estrogen receptor activation.