Significance of acid amyloglucosidase in sulphonylurea-induced insulin release

Summary The effect of exogenous acid amyloglucosidase on sulphonylurea-induced insulin release was investigated in mice and rats. 1. Pretreatment of mice with acid amyloglucosidase enhanced insulin release induced by the different sulphonylurea derivatives, carbutamide, tolbutamide, glibenclamide, and glibornuride. 2. A dose-response relationship between glibenclamide-induced insulin response and amyloglucosidase dosage covering a 64-fold concentration range was established in mice. 3. Pretreatment of the animals with other macromolecules of similar physiological or chemical properties to acid amyloglucosidase such as-amylase,-glucuronidase and albumin did not influence glibenlamide-induced insulin release. 4. The effect of acid amyloglucosidase pretreatment on insulin release induced by different agents known to affect the islet-cell adenylate cyclase-cyclic AMP system such as secretin, L-isopropylnoradrenaline (L-IPNA), arginine, glibenclamide and 3-isobutyl-1-methylxanthine (IBMX) was tested. It was observed that in animals pretreated with acid amyloglucosidase, insulin release was enhanced when stimulated by glibenclamide, a phosphodiesterase inhibitor, but it was similarly enhanced by arginine, a phosphodiesterase activator. Insulin release induced by secretin, L-IPNA, and IBMX was unaffected. 5. Acid amyloglucosidase pretreatment in rats enhanced plasma immunoreactive insulin levels following glibenclamide injection not only in the peripheral veins but also in the portal vein. 6. Mice fasted for 24 hrs displayed a markedly depressed insulin response to tolbutamide injection. Pretreatment of the fasted animals with acid amyloglucosidase could restore the tolbutamide-induced insulin release to the same level as that recorded in a group of freely fed mice. It is suggested that acid amyloglucosidase plays an important role in insulin secretion induced by sulphonylureas. Most evidence suggests that this effect is exerted within the B-cell although an additional effect on the liver cannot be ruled out.     

阻塞性睡眠呼吸暂停低通气综合征与糖代谢紊乱

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是一常见病，其心脑血管疾病的发病率及病死率也明显增高，但其机制并不十分清楚。阻塞性睡眠呼吸事件可导致许多急性的病理生理改变如间断低氧、严重睡眠片段、急性血压升高、交感神经系统激活、胸内压改变及心输出量降低等，反复而长期的上述改变最终可导致高血压及心脑血管疾病，而睡眠呼吸暂停与糖代谢异常之间的独立关系也可能代表了另一条导致心血管疾病的途径。本文对OSAHS与糖代谢异常之间的关系、糖代谢异常的可能中间机制及治疗OSAHS本身对糖代谢异常的影响等进行了深入阐述。     

内镜下氩离子凝固术治疗Barrett食管的临床研究

目的探讨内镜下氩离子凝固术（APC）联合抑酸治疗对Barrett食管的临床疗效。方法对32例病理证实伴有肠上皮化生的Barrett食管，在内镜下以APC完全毁损化生黏膜，并予以口服奥美拉唑40mg／d抑酸治疗。从末次治疗开始进行为期12个月的内镜随访监测，每次内镜检查时对再生的鳞状上皮进行间隔1cm的四象限活检，对可疑病灶进行针对性的活检。结果32例患者共接受61次APC治疗，31例（96．9％）达到完全的鳞状上皮再生，1例（3．1％）在再生的鳞状上皮间混有岛状的柱状上皮；除1例出现食管轻度狭窄外，无其他并发症的出现。12个月后，共有4例出现内镜下可见的复发，另活检发现d例内镜下无异常患者的再生鳞状上皮下有柱状上皮残留。结论BE的内镜下APC联合抑酸治疗安全有效，能使鳞状上皮替代BE黏膜，但仍有一定比例的复发和残留。     

糖耐量减低与心血管疾病及阿卡波糖作用

Impaired glucose tolerance(IGT) is a clinical state between normal and abnormal glucose metabolism with increased risk of cardiovascular disease. Its mechanism mainly related to insulin resistance, oxidative stress ,blood hypercoagulability, inflammatory response ,as well as related lipotoxieity. α-glucosidase inhibitor acarbose is safe and effective to reduce postprandial hyperglycemia, and has been approved for the treatment of patients with IGT. A growing number of studies have shown that acarbose also has cardiovascular benefit.     

Plasma lidocaine concentrations after local anesthesia of the groin for cardiac catheterization.

This study aimed to investigate serum lidocaine concentrations after subcutaneous infiltration of the groin for cardiac catheterization. One hundred twenty-six patients for planned heart catheterization received five different dosages (5-25 ml) of lidocaine 2% for local anesthesia of the groin in a randomized manner. All of them received an arterial sheath and 13 received both an arterial sheath and a venous sheath for right heart catheterization. Blood samples were taken before as well as 15, 30, and 120 min after subcutaneous application of the drug. Although in 33 patients with an arterial sheath (no venous sheath) excessive doses of lidocaine 2% (20-25 ml) were used, neither symptoms of intoxication nor toxic plasma levels were observed. However, in patients receiving an additional venous sheath, toxic plasma levels were obtained in a third of the cases. One of them showed symptoms of intoxication.     

Effect of misoprostol (PGE1) on glucose metabolism in type-2-diabetic and control subjects

In vitro and in vivo studies have demonstrated that prostaglandins of the E series enhance muscle glucose uptake. We examined the effect of acute misoprostol (PGE1) administration on whole body insulin-mediated glucose disposal, as well as the major intracellular pathways of glucose metabolism in type 2 diabetic (n = 10) and non-diabetic (n = 4) subjects. Each subject received two 240-min euglycaemic insulin (40 mU/m²/min) clamp studies with tritiated glucose and indirect calorimetry. During one of the insulin clamp studies, 200 µg of misoprostol was ingested at 90 and 150 min after the start of the insulin infusion. Insulin-mediated total body glucose disposal, glycolysis, glycogenesis and glucose oxidation were similar during the insulin clamp studies performed without and with misoprostol in both the diabetic and non-diabetic groups. These results demonstrate that the acute administration of misoprostol does not enhance insulin-mediated glucose disposal in either type-2-diabetic or non-diabetic subjects.     

急性脑血管病血糖水平与预后的临床分析

目的 :探讨急性脑血管病患者血糖水平与预后的关系。方法 :根据患者入院时的空腹血糖水平分为非高血糖组和高血糖组 ,分别对其预后进行临床分析。结果 :高血糖组的病死率明显高于非高血糖组 (45 .83%vs 12 .31% ,P <0 .0 1) ;死亡组的血糖均值也显著高于存活组 (8.6 1±1.0 2mmol/Lvs 6 .5 4± 1.15mmol/L ,P <0 .0 5 )。结论 :急性脑血管病患者发病早期血糖水平对判断病情 ,估计预后都具有一定的参考价值。     

Blood glucose regulation using closed- and open-loop insulin delivery systems

Summary Glucose was infused into anaesthetized dogs before and after pancreatectomy. In the diabetics blood glucose was regulated first by closed-loop and then by open-loop insulin delivery schemes. Insulin requirements for the latter were determined by resolving the former into a sequence of 3 different infusion rates: during the baseline and recovery periods, basal insulin was delivered at 0.37±0.02 mU/kg/min, while during the 60 min glucose infusion (10 mg/kg/min) there was an 8 min infusion at 4.96±0.37 mU/kg/min and a 52 min component at 1.85±0.08 mU/kg/min. With the open-loop method under these highly standardized conditions glycaemia was similar to normal controls but IRI levels were significantly higher, 13.5 vs 8.0 U/ml (p<0.05) in the baseline and recovery periods and 74 vs 25 U/ml (p<0.05) during the glucose infusion. It was concluded that: constant normogly-caemia can be maintained in the basal state by a constant rate of peripheral insulin delivery but at rates resulting in peripheral hyperinsulinaemia; the glycaemic response to glucose infusion can be normalized by a two component waveform of insulin delivery; and the closed-loop method can serve as a useful guide in determining insulin requirements.     

Blood glucose regulation using an open-loop insulin delivery system in pancreatectomized dogs given glucose infusions

Summary This study characterizes the glycaemic and insulin responses of a group of 5 anaesthetized dogs to a portal glucose infusion of 10 mg/kg/min before and after pancreatectomy. Insulin was administered intraportally to the pancreatectomized dogs according to a simple preprogrammed waveform composed of a constant basal rate of 0.35±0.02 mU/kg/min which was increased to 2.00mU/kg/min at the time of the 60 minute glucose challenge. When this square waveform was applied the glycaemic response was similar to that seen in the normal controls in the baseline and challenge periods. Blood glucose concentration differed significantly (p<0.05) only from 20 to 100 minutes after the end of the challenge when it was higher by 20±1 mg/dl. Insulin levels were not significantly different from controls. It may be concluded that normoglycaemia and normoinsulinaemia can be maintained by a simple constant rate of portal insulin delivery while the blood glucose response to a glucose infusion can be ostensibly normalized without hyperinsulinaemia simply by enhancing insulin delivery during the challenge. The feasibility of this approach implies that with further development of the preprogrammed waveforms and with a greater understanding of their characteristics portable insulin delivery systems may be realized which accomodate more physiological challenges. The portal route for insulin delivery may however be necessary if peripheral hyperinsulinism is inappropriate.