电场刺激对正常和糖尿病大鼠胰腺胰岛素和胰高血糖素分泌的影响。

Adeghate E, Ponery A S, Wahab A

Dept of Human Anatomy, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain.

Horm Metab Res. 2001 May;33(5):281-9. doi: 10.1055/s-2001-15284.

The effect of electrical field stimulation (EFS) on insulin (INS) and glucagon (GLU) secretion from normal and diabetic rat pancreas is poorly understood. In our study, EFS (5-20Hz, 50 V amplitude and 1.0 ms pulse width), when applied alone, resulted in a significant (p<0.05) increase in INS secretion from the pancreas of both normal and diabetic rats. Atropine (10(-5) M) did not inhibit the EFS (5 Hz)-evoked INS secretion in normal pancreas and failed to alter the effect of EFS (10-20 Hz) on INS secretion from the pancreas of both normal and diabetic rats. Propranolol (Prop) inhibited INS secretion to below basal level in the presence of EFS (5 Hz) but not at EFS (10- 20 Hz). Tetrodotoxin (TTX) also significantly (p = 0.002) inhibited INS secretion from normal pancreas in the presence of EFS (5-20 Hz). The decrease in insulin secretion observed when pancreatic tissue fragments were incubated in Prop and TTX in the presence of EFS was reversed by yohimbine (10(-5) M). In contrast, TTX did not significantly modify INS secretion from diabetic pancreas in the presence of EFS. EFS (5-20 Hz) significantly (p<0.05) increased GLU release from normal and diabetic rat pancreas when applied alone. Neither atropine, Prop nor TTX significantly modified GLU release from the pancreas of either normal or diabetic rats. This suggests that GLU secretion may be controlled through a different pathway. The EFS-evoked INS and GLU secretion is probably executed via different mechanisms. These mechanisms include 1) activation of cholinergic nerves by EFS; 2) EFS of alpha- and beta-adrenergic nerves; 3) activation of non-adrenergic non-cholinergic pathway by EFS; 4) EFS-induced depolarization and subsequent action potential in pancreatic endocrine cells and 5) electroporosity caused by EFS-induced membrane permeability. All of these effects may be summative. In conclusion, EFS (5-20 Hz), when applied alone, can evoke significant increases in INS and GLU secretion from the pancreas of both normal and diabetic rats. Insulin secretion is controlled via alpha-2 adrenergic (inhibition) and beta-adrenergic (stimulation) receptors. Glucagon secretion is enhanced by alpha2 adrenergic stimulation.

电场刺激（EFS）对正常和糖尿病大鼠胰腺胰岛素（INS）和胰高血糖素（GLU）分泌的影响尚不清楚。在我们的研究中，单独施加EFS（5 - 20Hz，振幅50V，脉冲宽度1.0ms）会使正常和糖尿病大鼠胰腺的INS分泌显著增加（p<0.05）。阿托品（10(-5) M）不抑制正常胰腺中EFS（5Hz）诱发的INS分泌，也不能改变EFS（10 - 20Hz）对正常和糖尿病大鼠胰腺INS分泌的影响。普萘洛尔（Prop）在EFS（5Hz）存在时将INS分泌抑制至基础水平以下，但在EFS（10 - 20Hz）时则不然。河豚毒素（TTX）在EFS（5 - 20Hz）存在时也显著（p = 0.002）抑制正常胰腺的INS分泌。当胰腺组织碎片在EFS存在下于Prop和TTX中孵育时观察到的胰岛素分泌减少可被育亨宾（10(-5) M）逆转。相反，在EFS存在时，TTX对糖尿病胰腺的INS分泌没有显著影响。单独施加EFS（5 - 20Hz）时，可使正常和糖尿病大鼠胰腺的GLU释放显著增加（p<0.05）。阿托品、Prop和TTX均未显著改变正常或糖尿病大鼠胰腺的GLU释放。这表明GLU分泌可能通过不同途径控制。EFS诱发的INS和GLU分泌可能通过不同机制执行。这些机制包括：1）EFS激活胆碱能神经；2）EFS作用于α和β肾上腺素能神经；3）EFS激活非肾上腺素能非胆碱能途径；4）EFS诱导胰腺内分泌细胞去极化及随后的动作电位；5）EFS诱导的膜通透性改变导致的电穿孔。所有这些效应可能是累加的。总之，单独施加EFS（5 - 20Hz）可使正常和糖尿病大鼠胰腺的INS和GLU分泌显著增加。胰岛素分泌通过α2肾上腺素能（抑制）和β肾上腺素能（刺激）受体控制。胰高血糖素分泌通过α2肾上腺素能刺激增强。