[Objective]To investigate the effect of high energy shock waves on the expression of BMP-2 in adult rabbits with necrotic femoral head,and to explore the mechanism of avascular femoral head necrosis treated with high energy shock waves.[Methods]Thirty eight male adult New Zealand white rabbits,weighting 3.0 to 4.0 kg(average weight 3.3 kg) were used to establish animal model of avascular femoral head necrosis.Bilateral femoral head necrosis was induced by methylprednisolone and lipopolysaccharide.The left hind limbs(treatment side) of all rabbits received shock wave treatment of the femoral heads and the right limbs(control side) of all rabbits received no shock wave treatment.The animals were killed at 24 hours and 1(n=6),2(n=6),4(n=6),8(n=6),and 12(n=6) weeks after shock wave therapy.The femoral heads were harvested and freed of soft tissue and cartilage.They were assigned to immunohistochemistry and quantitative real-time reverse transcriptase PCR.[Results]Compared with the contralateral control without shock wave treatment,the BMP-2 mRNA expression levels increased to a peak at 1 week after the shock wave treatment and remained high at 24 hours and 1、 2、 4、 8 weeks after the shock wave treatment.At 4,8 and 12 weeks after shock wave treatment,the average percentage of staining area of the femoral heads in the treatment side were significantly higher than those in the control side(P

Objective To study the effect of subarachnoid hemorrhage (SAH) on voltagedependent potassium channels (Kv) currents of smooth muscle cells,which is hypothesized to be different between cerebral pial arteries and penetrating arteries.Methods Smooth muscle cells from cerebral pial arteries and penetrating arteries in rats were enzymatically isolated 72 h after SAH,and patch clamp was used to test the relative cell size,resting potential and Kv currents.Results Resting potential of either pial ((45.63 ±1.18) mV) or penetrating artery ((41.55-± 1.19) mV) was shifted positively by SAH,even more significantly in latter (F =8.24,P ＜ 0.05 ; F =9.36,P ＜ 0.01) ; Resting potential of pial artery of control ((38.76 ± 1.03) mV),penetrating artery of control ((38.53 ± 0.67) mV),pial artery of SAH ((36.87 ± 1.49) mV) and penetrating artery of SAH((37.89 ± 1.24) mV) were shifted positively to the same level by 1 μmol/L 4-aminopyridine (4AP; F =3.08,P ＞0.05).Maximum Current Density (Imax) of either pial ((20.82 ±0.59) pA/pF) or penetrating artery ((15.15 ±0.37) pA/pF) was compromised by SAH,also more significantly in latter (F =6.22,P ＜ 0.05) ; Imax of pial artery of control (9.15 ± 0.16),penetrating artery of control (9.04 ± 0.36),pial artery of SAH (8.77 ± 0.26) and penetrating artery of SAH (9.12 ± 0.17) were decreased to the same level by 1 μmol/L 4AP (F =2.96,P ＞ 0.05).Conclusions SAH probably shares the similar pathway with Kv blocker (4AP) in Kv currents inhibition.Further,SAH differently inhibits smooth muscle cells Kv currents and resting potential of cerebral pial arteries and penetrating arteries,which may be related with their different sensitivity towards cerebral vasospasm following SAH.