Etude expérimentale d'un nouveau sulfamide hypoglycémiant particulièrement actif,le HB 419 ou glibenclamide

Résumé Les auteurs ont montré chez la souris que le HB 419 administré chroniquement, stimule le développement des îlots de Langerhans et des cellules bêta. Ce produit est donc doué de l'action bêtacytotrophe. Chez le chien normal, l'administration pendant 4 mois de HB 419 a pour effets d'abaisser la glycémie à jeun ainsi que l'ensemble de la courbe de la glycémie nycthémérale.- L'expérimentation effectuée montre que sous l'influence de l'administration prolongée de HB 419, la quantité d'insuline endogène synthétisée et sécrétée en plus de la sécrétion normale est considérable.

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Experimental study on glibenclamide (HB 419), a new particularly action hypoglycaemic sulphonamide

Summary The authors have demonstrated that HB 419 chronically administered in the mouse, stimulated the development of the islets of Langerhans and particularly that of the beta cells. This substance is thus endowed with a beta cytotrophic action. — In the normal dog, HB 419 administered over a four-month period resulted in a decreased fasting glycaemia, as well as a decrease of the entire nyctohemeral glycaemia curve. The experiments carried out showed that under the influence of prolonged HB 419 administration, the amount of endogenous insulin synthesized and secreted over and above the normal secretory level, was considerable.

Le HB 419 ou glibenclamide portait initialement le nom de glybenzcyclamide. La dénomination commune internationale qui vient d'être définitivement adoptée est glibenclamide.     

早期血性脑脊液引流在颅内动脉瘤破裂介入治疗后的应用

目的:探讨颅内破裂动脉瘤血管内介入栓塞术后行早期血性脑脊液引流的临床效果。方法:本研究对2007年1月—2016年7月江苏大学附属澳洋医院神经外科收治的40例颅内动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,a SAH)患者在血管内介入栓塞术后早期接受腰椎穿刺引流和脑室持续外引流以引流血性脑脊液的治疗结果进行回顾性分析。结果:40例患者中,颅内动脉瘤破裂后2~7 d并发脑血管痉挛12例(30.0%),经对症治疗后病情缓解;出院后1~2个月,3例(7.5%)患者出现脑积水;术后1个月时,改良Rankin量表分级结果显示,37例(1级)为恢复良好,2例(2级)为轻度残疾,1例(6级)为预后不良(家属放弃治疗后,因肺部感染而死亡)。至随访结束,39例患者中,37例(94.9%)患者治愈或好转;2例(5.1%)患者智力下降,但未发生偏瘫、失语和肢体功能障碍等严重的后遗症。结论:颅内动脉瘤破裂出血后早期血管内介入栓塞治疗后行腰椎穿刺引流和脑室持续外引流以释放血性脑脊液,可以显著降低患者的并发症发生率,缩短恢复时间,是一种操作简便、安全而廉价的有效治疗方法。     

CT辅助下立体定向穿刺引流术治疗基底节区脑出血的疗效分析

目的探讨CT辅助下立体定向穿刺引流术治疗老年高血压基底节区脑出血的疗效及其并发症。方法将发病24 h内的80例老年高血压脑出血患者分为穿刺引流术组和对照组。两组患者分别采用CT辅助下立体定向穿刺引流术和药物保守治疗;观察比较两组患者的住院治疗时间、并发症、治疗后的神经功能恢复,以及治疗前、后的神经功能评分。结果引流术组患者的并发症发生率为12.5%,对照组则为32.5%。引流术组的住院时间(17.6 d)、最终NIHSS评分(3.28分)和总有效率(92.5%)均明显优于对照组(24.6 d,4.00分和77.5%)。结论 CT辅助下立体定向穿刺引流术治疗基底节区脑出血创伤小,可以明显减少各种并发症,缩短患者的住院时间减少花费。与保守治疗相比,能促进患者神经功能的早期恢复。     

钻颅引流辅助尿激酶纤溶治疗高血压脑出血的临床效果

目的研究小孔钻颅血肿抽吸引流辅助尿激酶纤溶治疗高血压脑出血的临床效果。方法回顾性分析103例经小孔钻颅血肿抽吸引流辅助尿激酶纤溶治疗的高血压脑出血患者的临床资料,并与内科保守治疗的患者进行比较。观察、比较治疗后患者的血肿清除率/d、住院时间、病死率与预后及生存质量。结果手术治疗组的死亡率明显低于对照组;手术治疗组的血肿清除/吸收时间为(7±2)d、平均住院时间(15±5)d,保守治疗组的血肿清除/吸收时间为(18±5)d、平均住院时间(21±7)d;手术治疗组均明显短于保守治疗组(均P0.05)。结论钻颅引流辅助尿激酶纤溶治疗高血压脑出血的效果优于内科保守治疗。     

Effect of glibenclamide on insulin release at moderate and high blood glucose levels in normal man

Insulin release occurs in two phases; sulphonylurea derivatives may have different potencies in stimulating first- and second-phase insulin release. We studied the effect of glibenclamide on insulin secretion at submaximally and maximally stimulating blood glucose levels with a primed hyperglycaemic glucose clamp. Twelve healthy male subjects, age (mean ± SEM) 22.5 ± 0.5 years, body mass index (BMI) 21.7 ± 0.6 kg m^?2, were studied in a randomized, double-blind study design. Glibenclamide 10 mg or placebo was taken before a 4-h hyperglycaemic clamp (blood glucose 8 mmol L^?1 during the first 2 h and 32 mmol L^?1 during the next 2 h). During hyperglycaemic clamp at 8 mmol L^?1, the areas under the Δinsulin curve (AUC_Δinsulin , mean ± SEM) from 0 to 10 min (first phase) were not different: 1007 ± 235 vs. 1059 ± 261 pmol L^?1 × 10 min (with and without glibenclamide, P = 0.81). However, glibenclamide led to a significantly larger increase in AUC_Δinsulin from 30 to 120 min (second phase): 16 087 ± 4489 vs. 7107 ± 1533 pmol L^?1 × 90 min (with and without glibenclamide respectively, P < 0.03). The same was true for AUC_ΔC-peptide: no difference from 0 to 10 min but a significantly higher AUC_ΔC-peptide from 30 to 120 min on the glibenclamide day (P < 0.01). The M/I ratio (mean glucose infusion rate divided by mean plasma insulin concentration) from 60 to 120 min, a measure of insulin sensitivity, did not change: 0.26 ± 0.05 vs. 0.22 ± 0.03 μmol kg^?1 min^?1 pmol L^?1 (with and without glibenclamide, P = 0.64). During hyperglycaemic clamp at 32 mmol L^?1, the AUC_Δinsulin from 120 to 130 min (first phase) was not different on both study days: 2411 ± 640 vs. 3193 ± 866 pmol L^?1 × 10 min (with and without glibenclamide, P = 0.29). AUC_Δinsulin from 150 to 240 min (second phase) also showed no difference: 59 623 ± 8735 vs. 77389 ± 15161 pmol L^?1 × 90 min (with and without glibenclamide, P = 0.24). AUC_ΔC-peptide from 120 to 130 min and from 150 to 240 min were slightly lower on the glibenclamide study day (both P < 0.04). The M/I ratio from 180 to 240 min did not change: 0.24 ± 0.04 vs. 0.30 ± 0.07 μmol kg^?1 min^?1 pmol L^?1 (with and without glibenclamide, P = 0.25). In conclusion, glibenclamide increases second-phase insulin secretion only at a submaximally stimulating blood glucose level without enhancement of first-phase insulin release and has no additive effect on insulin secretion at maximally stimulating blood glucose levels. Glibenclamide did not change insulin sensitivity in this acute experiment.