Introduction: The aim of this study was to investigate if steroids enhance the vasoconstrictive effect of endothe-lin-1 (ET-1) on femoral arteries.

Materials and Methods: Ten female Wistar rats 59 to 88 days of age and 238 to 310 g of body weight, were used. Forty femoral artery segments were harvested. These arterial segments were mounted as ring preparations on a small vessel myograph. Two vessels from each animal were randomized to incubation with methylprednisolone 5 μg/ml [1] while the other 2 vessels were incubated with placebo. The arteries were stimulated cumulatively with endothelin-1. Isometric wall tension was quantified by the EC50; the vasoconstrictor concentration resulting in half maximal contraction.

Results: Thirty-eight arteries could be harvested in total; 20 were randomized to steroid treatment while 18 served as controls. The endothelin-1 dose-response curve displayed a stronger contraction for the steroid group in relation to the controls with increasing doses of ET-1. The EC50 of 4.4*10⁻⁸ M ± 1.8*10⁻⁸ M for the steroid vessels was lower compared to 5.9*10⁻⁸ M ± 3.4*10⁻⁸ M for the controls (mean ±SD; n.s.).

Discussion: Endothelin-1 is a potent vasoconstrictor. This study showed that incubation with methylprednisolone enhanced ET-1 mediated contraction of femoral arteries which can diminish blood flow within the vascular bed supplying the femoral head. This may be a relevant cofactor in the early pathogenesis of steroid-associated femoral head necrosis.

Introduction: The aim of this study was to investigate if steroids enhance the vasoconstrictive effect of nor-adrenaline on femoral arteries, which may result in femoral head blood flow reduction.

Materials and Methods: Ten male Wistar rats 62 to 88 days of age, 254 to 318 g of body weight, were used. Twenty femoral artery segments were harvested. These arterial segments were mounted as ring preparations on a small vessel myograph for isometric force measurements. The arteries were stimulated cumulatively with noradrenaline before and after incubation with methylprednisolone (5 μg/ml). Isometric wall tension was plotted and quantified by the EC50, the vasoconstrictor concentration resulting in halfmaximal contraction.

Results: The noradrenaline dose-response curve displayed a shift to the left for the steroid group in relation to the controls. This was reflected by a significantly lower EC50 of 9.5*10⁻⁷ M ± 5.1*10⁻⁷ M for the steroid vessels compared to 2.5*10⁻⁶ M ± 1.1*10⁻⁶ M for the control vessels (mean ± SD; p< 0.005).

Discussion: This study showed that incubation with methylprednisolone enhanced noradrenaline-mediated contraction of femoral arteries. Enhanced contraction of femoral arteries can diminish blood flow within the vascular bed supplying the femoral head. This may be a relevant cofactor in the early pathogenesis of steroid-associated femoral head necrosis.

The treatment of osteonecrosis of the femoral head (FHN) is controversial. It mainly occurs in young patients in whom total hip replacement is best avoided because of an increased risk of revision. The objective of this long-term follow-up study was to evaluate the outcome of intertrochanteric flexion osteotomy as a hip joint preserving operation for FHN.

Over a 19-year period we carried out 70 intertrochanteric flexion osteotomies for FHN in 64 patients. The mean follow-up was 10.4 years (3.0 to 20.3). The overall mean Harris hip score increased from 51 points preoperatively to 71 points postoperatively. Six patients (9%) developed early postoperative complications. A total of 19 hips (27%) underwent total hip arthroplasty at a mean of 8.7 years after osteotomy. The five-year survival rate was 90%. Survival rates of hips in Ficat stage 2 were higher than those in stages 3 or 4. Hips with a preoperative necrotic angle of < 200° had a better survival probability than those with a necrotic angle > 200°. Our findings suggest that flexion osteotomy is a safe and effective procedure in Ficat stage 2 and 3 FHN, preferably with a necrotic angle of < 200°.