PubMed日本語 - ストレプトゾトシン-糖尿病患者ラットで十二指腸重炭酸塩分泌を促進することの一酸化窒素シンターゼ抑制薬の不履行。―QLifePro医療翻訳医療翻訳 QLifePro



Failure of the nitric oxide synthase inhibitor to stimulate duodenal bicarbonate secretion in streptozotocin-diabetic rats.

Published date


Failure of the nitric oxide synthase inhibitor to stimulate duodenal bicarbonate secretion in streptozotocin-diabetic rats.


Published date


Life Sci. 1997; 60; 1505-14;


K Takehara, K Tashima, S Kato, K Takeuchi


Department of Pharmacology & Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Japan.


We examined the HCO(3)- stimulatory effects of L-NAME (N(G)-nitro-L-arginine methyl ester) in the proximal duodenum of streptozotocin (STZ)-induced diabetic rats and compared with those of 16,16-dimethyl prostaglandin E2 (dmPGE2) and vagal electrical stimulation. Male SD rats were given STZ (70 mg/kg) i.p., and the experiments were done using 1 approximately 6 week STZ-diabetic rats with blood glucose levels of >300 mg/dl. Under urethane anesthesia the HCO(3)- secretion was measured in the proximal duodenal loop using a pH-stat method and by adding 10 mM HCl. Hyperglycemic conditions appeared 1 week after STZ treatment and remained during 6 week-test period. The duodenal HCO(3)- secretory response to L-NAME was significantly decreased in STZ-diabetic rats; the degree of reduction was dependent on the duration of diabetes, and the stimulatory effect disappeared completely in rats after 5 approximately 6 weeks of diabetes. Intravenous administration of L-NAME markedly increased arterial blood pressure with significant decrease in heart rate in normal rats, whereas in STZ-diabetic rats this agent caused only pressor response without any effect on heart rate. STZ-diabetic rats also secreted significantly less amount of HCO(3)- from the duodenum in response to dmPGE2 and vagal electrical stimulation after 5 approximately 6 weeks of diabetes. These all changes observed in STZ-diabetic rats were significantly reversed by daily injection of insulin. These results suggest that 1) L-NAME failed to stimulate duodenal HCO(3)- secretion in STZ-diabetic rats, and 2) impairment of the duodenal HCO(3)- secretory ability in STZ-diabetic conditions is due to both vagal-dependent neuronal dysfunction and decreased sensitivity of the secreting cell.


我々は、HCO(3) ― ストレプトゾトシン(STZ)-によって誘発された糖尿病患者ラットの近位十二指腸の、そして、16,16-ジメチル・プロスタグランジンE2(dmPGE2)と迷走神経の電気刺激のそれらと比較してL-NAME(N(G)-ニトロ-L-アルギニン・メチル・エステル)の刺激性の効果 ― を調べた。
STZ-糖尿病患者ラットも、有意により少ない量のHCO(3)を分泌した ― dmPGE2に応答する十二指腸と5約6週の糖尿病の後の迷走神経の電気刺激から。
これらの結果はそれを暗示する1)、L-NAMEは十二指腸HCO(3) ― STZ-糖尿病患者ラットと2の分泌 ― を刺激するのに失敗した)十二指腸HCO(3)の機能障害-STZ糖尿病性条件の才能が迷走神経の従属するニューロン機能不全と隠している細胞の減少した感受性に予定である分泌腺。

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