Objective To evaluate the clinical effect and complications of total hip replacement (THR) in novel femoral neck fracture,old femoral neck fracture, aseptic necrosis of femoral head and coxa degenerative osteoarthropathy. To provide instructions to surgical indications and treatment effects analysis.Methods One hundrde and four patients were divided into 4 groups by disease type: novel femoral neck fracture group (n = 32 ), old femoral neck fracture group (n = 22) ,aseptic necrosis of femoral head group (n =34) and coxa degenerative osteoarthropathy group (n = 16). These patients were followed-up for 12 - 144 months after THR, their Harris standard score and complications data, before and after operation, were analyzed retrospectively. Results After operation, the Harris standard scores were 92. 6 ± 5.8,90. 1 ± 5. 2,86. 3 ± 4. 6,81.9 ±4. 1 in novel femoral neck fracture,old femoral neck fracture,aseptic necrosis of femoral head and coxa degenerative osteoarthropathy groups respectively, which were significantly higher than the scores before operation (25.6±1.8,36.7±2.6,52.9±4.3,42. 1 ±3.8,Ps ＜0.05). Conclusion THR has good effects in the four types of diseases. Short length of stay and high healing rate are marked characteristics of THR. More attention shoud be paid to the complications of THR.

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (α2-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of 10⁻⁸~10⁻⁶ mol/L, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or 3×10⁻⁹ mmol/L) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial α₂-adrenoceptor and nitric oxide synthase.
Arteries ; Dexmedetomidine* ; Endothelium ; Humans ; Indomethacin ; Lung ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type III* ; Pulmonary Artery ; Serotonin ; Vasoconstriction* ; Yohimbine