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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Miwa A, Takeuchi A, Fukata Y, Izumi H, Izawa T, Ogawa N

Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd, Gunma, Japan.

Gen Pharmacol. 1994 Oct;25(6):1171-8. doi: 10.1016/0306-3623(94)90134-1.

In the present study, we examined the vasospasmolytic effect of KRN2391 on rhythmic contractions of porcine coronary artery caused by 3,4-diaminopyridine (3,4-DAP) compared with cromakalim and nitroglycerin. 2. KRN2391 at 10(-7) showed a tendency to prolong the cycle length and at 10(-6) M completely eliminated rhythmic contractions in all preparations. The elimination by 10(-6) M KRN2391 was antagonized by either oxyhemoglobin (10(-5) M) or glibenclamide (3 x 10(-6)) although not completely. 3. Cromakalim at 10(-5) M and nitroglycerin at 10(-7) M completely eliminated 3,4-DAP-induced rythmic contractions in all preparations. The elimination by cromakalim and nitroglycerin was completely antagonized by glibenclamide and oxyhemoglobin, respectively. 4. The present study suggests that the vasospasmolytic effect of KRN2391 on 3,4-DAP-induced rhythmic contractions is based on its nitrate action and K channel opening action.

在本研究中，我们将KRN2391与克罗卡林和硝酸甘油相比较，研究了其对3,4-二氨基吡啶（3,4-DAP）引起的猪冠状动脉节律性收缩的血管解痉作用。2. 10⁻⁷ 的KRN2391有延长周期长度的趋势，而10⁻⁶ M的KRN2391能完全消除所有标本中的节律性收缩。10⁻⁶ M的KRN2391所致的这种消除作用，虽未被完全拮抗，但可被氧合血红蛋白（10⁻⁵ M）或格列本脲（3×10⁻⁶）拮抗。3. 10⁻⁵ M的克罗卡林和10⁻⁷ M的硝酸甘油能完全消除所有标本中3,4-DAP诱导的节律性收缩。克罗卡林和硝酸甘油所致的这种消除作用，分别被格列本脲和氧合血红蛋白完全拮抗。4. 本研究提示，KRN2391对3,4-DAP诱导的节律性收缩的血管解痉作用基于其硝酸盐作用和钾通道开放作用。

Miwa A, Takeuchi A, Fukata Y, Izumi H, Izawa T, Ogawa N

Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd, Gunma, Japan.

Gen Pharmacol. 1994 Oct;25(6):1171-8. doi: 10.1016/0306-3623(94)90134-1.

In the present study, we examined the vasospasmolytic effect of KRN2391 on rhythmic contractions of porcine coronary artery caused by 3,4-diaminopyridine (3,4-DAP) compared with cromakalim and nitroglycerin. 2. KRN2391 at 10(-7) showed a tendency to prolong the cycle length and at 10(-6) M completely eliminated rhythmic contractions in all preparations. The elimination by 10(-6) M KRN2391 was antagonized by either oxyhemoglobin (10(-5) M) or glibenclamide (3 x 10(-6)) although not completely. 3. Cromakalim at 10(-5) M and nitroglycerin at 10(-7) M completely eliminated 3,4-DAP-induced rythmic contractions in all preparations. The elimination by cromakalim and nitroglycerin was completely antagonized by glibenclamide and oxyhemoglobin, respectively. 4. The present study suggests that the vasospasmolytic effect of KRN2391 on 3,4-DAP-induced rhythmic contractions is based on its nitrate action and K channel opening action.

在本研究中，我们将KRN2391与克罗卡林和硝酸甘油相比较，研究了其对3,4-二氨基吡啶（3,4-DAP）引起的猪冠状动脉节律性收缩的血管解痉作用。2. 10⁻⁷ 的KRN2391有延长周期长度的趋势，而10⁻⁶ M的KRN2391能完全消除所有标本中的节律性收缩。10⁻⁶ M的KRN2391所致的这种消除作用，虽未被完全拮抗，但可被氧合血红蛋白（10⁻⁵ M）或格列本脲（3×10⁻⁶）拮抗。3. 10⁻⁵ M的克罗卡林和10⁻⁷ M的硝酸甘油能完全消除所有标本中3,4-DAP诱导的节律性收缩。克罗卡林和硝酸甘油所致的这种消除作用，分别被格列本脲和氧合血红蛋白完全拮抗。4. 本研究提示，KRN2391对3,4-DAP诱导的节律性收缩的血管解痉作用基于其硝酸盐作用和钾通道开放作用。