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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

Dorigo P, Fraccarollo D, Gaion R M, Santostasi G, Borea P A, Floreani M, Mosti L, Maragno I

Department of Pharmacology, University of Padova, Largo, Italy.

Gen Pharmacol. 1997 May;28(5):781-8. doi: 10.1016/s0306-3623(96)00271-6.

Two new milrinone analogs, 3-acetyl-6-phenyl-2(1H)-pyridone (SF 348) and 3-acetyl-7-methyl-7,8-dihydro-2,5(1H, 6H) quinolinone (SF 349), increase the contractile activity of spontaneously beating and electrically driven atria isolated from reserpine-treated guinea-pigs. 2. Propranolol 0.1 microM drastically inhibits the contractile effect of SF 348, whereas that of SF 349 is unaffected. Preincubation of the atria with adenosine-deaminase suppresses the cardiac activity of SF 349, but does not affect that of SF 348. 3. SF 349 competitively antagonizes the negative inotropic effect induced by N6-(R-phenylisopropyl)-adenosine (R-PIA) and displaces N6-cyclohexyl[3H]-adenosine (3H-CHA) from its binding sites to A1 receptors in the guinea-pig heart. 4. The positive inotropic effect of SF 348 is largely sustained by activation of beta-adrenoceptors, whereas SF 349 acts by displacing endogenous adenosine from its inhibitory (A1) receptors in the atria.

两种新型米力农类似物，3-乙酰基-6-苯基-2(1H)-吡啶酮（SF 348）和3-乙酰基-7-甲基-7,8-二氢-2,5(1H,6H)喹啉酮（SF 349），可增强从利血平处理的豚鼠分离出的自发搏动和电驱动心房的收缩活性。2. 0.1微摩尔的普萘洛尔可显著抑制SF 348的收缩作用，而SF 349的收缩作用不受影响。用腺苷脱氨酶预孵育心房可抑制SF 349的心脏活性，但不影响SF 348的活性。3. SF 349竞争性拮抗N6-(R-苯异丙基)-腺苷（R-PIA）诱导的负性肌力作用，并将N6-环己基[3H]-腺苷（3H-CHA）从其在豚鼠心脏A1受体的结合位点上置换下来。4. SF 348的正性肌力作用很大程度上是由β-肾上腺素能受体的激活维持的，而SF 349的作用是通过将内源性腺苷从心房中的抑制性（A1）受体上置换下来实现的。

Dorigo P, Fraccarollo D, Gaion R M, Santostasi G, Borea P A, Floreani M, Mosti L, Maragno I

Department of Pharmacology, University of Padova, Largo, Italy.

Gen Pharmacol. 1997 May;28(5):781-8. doi: 10.1016/s0306-3623(96)00271-6.

Two new milrinone analogs, 3-acetyl-6-phenyl-2(1H)-pyridone (SF 348) and 3-acetyl-7-methyl-7,8-dihydro-2,5(1H, 6H) quinolinone (SF 349), increase the contractile activity of spontaneously beating and electrically driven atria isolated from reserpine-treated guinea-pigs. 2. Propranolol 0.1 microM drastically inhibits the contractile effect of SF 348, whereas that of SF 349 is unaffected. Preincubation of the atria with adenosine-deaminase suppresses the cardiac activity of SF 349, but does not affect that of SF 348. 3. SF 349 competitively antagonizes the negative inotropic effect induced by N6-(R-phenylisopropyl)-adenosine (R-PIA) and displaces N6-cyclohexyl[3H]-adenosine (3H-CHA) from its binding sites to A1 receptors in the guinea-pig heart. 4. The positive inotropic effect of SF 348 is largely sustained by activation of beta-adrenoceptors, whereas SF 349 acts by displacing endogenous adenosine from its inhibitory (A1) receptors in the atria.

两种新型米力农类似物，3-乙酰基-6-苯基-2(1H)-吡啶酮（SF 348）和3-乙酰基-7-甲基-7,8-二氢-2,5(1H,6H)喹啉酮（SF 349），可增强从利血平处理的豚鼠分离出的自发搏动和电驱动心房的收缩活性。2. 0.1微摩尔的普萘洛尔可显著抑制SF 348的收缩作用，而SF 349的收缩作用不受影响。用腺苷脱氨酶预孵育心房可抑制SF 349的心脏活性，但不影响SF 348的活性。3. SF 349竞争性拮抗N6-(R-苯异丙基)-腺苷（R-PIA）诱导的负性肌力作用，并将N6-环己基[3H]-腺苷（3H-CHA）从其在豚鼠心脏A1受体的结合位点上置换下来。4. SF 348的正性肌力作用很大程度上是由β-肾上腺素能受体的激活维持的，而SF 349的作用是通过将内源性腺苷从心房中的抑制性（A1）受体上置换下来实现的。