Mosier H D, Jansons R A, Hill R R, Dearden L C
Endocrinology. 1976 Aug;99(2):580-9. doi: 10.1210/endo-99-2-580.
The uptake of sulfate by rib cartilage in vitro and in vivo and the serum somatomedin activity by bioassay were determined in male rats during and after cortisone-induced growth arrest. Experimental treatment consisted of subcutaneous injections of cortisone acetate in a dose of 2.5 mg/rat/day for 4 days, beginning at 29 to 30 days of age in Buffalo rats, or 5 mg/rat/day for 4 or 5 days, beginning at 39 to 41 days of age in Long-Evans rats. Groups of hypophysectomized rats were studied in parallel in one experiment. The sulfate uptake in the controls declined linearly with increasing age in both the in vitro and the in vivo studies. Hypophysectomy resulted in a constant low level of sulfate uptake in vitro. At the end of cortisone treatment, the in vitro sulfate uptake was approximately midway between that of the hypophysectomized rats and that of controls; at 7 days recovery, it was at the control level; at 14 days it showed an additional rise above the control value; from 14 days to 35 days it declined parallel with but above the sulfate uptake of controls. The in vivo sulfate uptake was depressed by cortisone treatment. During recovery it approximately control values at recovery day 21. In succeeding recovery periods in vivo sulfate uptake remained at control levels. Serum somatomedin activity was significantly reduced during cortisone treatment; it returned to the control level by 21 days of recovery. The incubation of the cartilage of controls and cortisone-treated rats at 14 days of recovery with and without the presence of normal rat serum, cortisone recovery serum, or hypophysectomy serum resulted in significantly higher sulfate uptake in the cortisone-treated rat cartilage in each medium. These sera did not differ significantly in their stimulation of sulfate uptake in either cortisone recovery cartilage or control cartilage. Both treated and control cartilage had greater sulfate uptake with larger doses of serum added to the medium. The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery. It is concluded that the increased in vitro sulfation after 14 days of recovery in cortisone-treated rats signifies a persistent alteration in cartilage metabolism. Normal in vivo sulfate uptake during that time may be the result of humoral controls. A mechanism other than the impairment of somatomedin production is probably involved in the failure of catch-up growth after glucocorticoid treatment in the rat.
在可的松诱导生长停滞期间及之后,测定了雄性大鼠体外和体内肋软骨对硫酸盐的摄取以及通过生物测定法测定的血清生长调节素活性。实验处理包括从布法罗大鼠29至30日龄开始,以2.5mg/大鼠/天的剂量皮下注射醋酸可的松,持续4天;或从Long-Evans大鼠39至41日龄开始,以5mg/大鼠/天的剂量皮下注射醋酸可的松,持续4或5天。在一个实验中,同时对垂体切除的大鼠组进行了平行研究。在体外和体内研究中,对照组的硫酸盐摄取均随年龄增长呈线性下降。垂体切除导致体外硫酸盐摄取持续处于低水平。在可的松治疗结束时,体外硫酸盐摄取约为垂体切除大鼠和对照组摄取量的中间值;在恢复7天时,其恢复到对照水平;在14天时,其显示出高于对照值的额外升高;从14天到35天,其与对照组的硫酸盐摄取平行下降,但高于对照组。可的松治疗使体内硫酸盐摄取降低。在恢复期间,其在恢复第21天时大致达到对照值。在随后的恢复阶段,体内硫酸盐摄取保持在对照水平。在可的松治疗期间,血清生长调节素活性显著降低;在恢复21天时恢复到对照水平。在恢复14天时,将对照组和可的松处理组大鼠的软骨分别在有或无正常大鼠血清、可的松恢复血清或垂体切除血清存在的情况下进行孵育,结果发现在每种培养基中,可的松处理组大鼠软骨的硫酸盐摄取均显著更高。这些血清在刺激可的松恢复软骨或对照软骨的硫酸盐摄取方面没有显著差异。向培养基中添加更大剂量的血清时,处理组和对照组软骨的硫酸盐摄取均增加。在治疗和早期恢复期间,剂量反应曲线平行;但在后期恢复期间,可的松处理组大鼠软骨的剂量反应曲线斜率大于对照组。结论是,可的松处理组大鼠恢复14天后体外硫酸化增加表明软骨代谢存在持续改变。在此期间体内正常的硫酸盐摄取可能是体液控制的结果。大鼠糖皮质激素治疗后追赶生长失败可能涉及除生长调节素产生受损之外的其他机制。