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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

Wilson A N, Broadley K J

School of Biological Sciences/Frances Harrison College of Healthcare, University of Surrey, Guildford, England.

Gen Pharmacol. 1994 Mar;25(2):345-54. doi: 10.1016/0306-3623(94)90065-5.

The role of adenosine in the control of coronary vessel tone was studied using two guinea-pig hearts in series. Vasodilatory mediator(s) released by the donor heart were assayed by the recipient heart. 2. Adenosine deaminase reduced the activity of vasodilatory mediator(s) released by histamine and isoprenaline by 58.0 +/- 14.4% and 80.5 +/- 5.9% respectively; responses to exogenous adenosine were abolished. 3. Adenosine deaminase added to the donor perfusate supplying the recipient heart caused a significant increase in basal perfusion pressure. 4. Our results suggest adenosine is not the sole mediator of vasodilation in stressed hearts and additionally unstressed hearts appear to release a basal vasodilatory level of adenosine.

使用两个串联的豚鼠心脏研究了腺苷在控制冠状血管张力中的作用。供体心脏释放的血管舒张介质由受体心脏进行测定。2. 腺苷脱氨酶使组胺和异丙肾上腺素释放的血管舒张介质活性分别降低了58.0±14.4%和80.5±5.9%；对外源性腺苷的反应被消除。3. 添加到供应受体心脏的供体灌注液中的腺苷脱氨酶导致基础灌注压力显著升高。4. 我们的结果表明，腺苷不是应激心脏血管舒张的唯一介质，此外，未应激的心脏似乎也释放基础水平的血管舒张性腺苷。

Wilson A N, Broadley K J

School of Biological Sciences/Frances Harrison College of Healthcare, University of Surrey, Guildford, England.

Gen Pharmacol. 1994 Mar;25(2):345-54. doi: 10.1016/0306-3623(94)90065-5.

The role of adenosine in the control of coronary vessel tone was studied using two guinea-pig hearts in series. Vasodilatory mediator(s) released by the donor heart were assayed by the recipient heart. 2. Adenosine deaminase reduced the activity of vasodilatory mediator(s) released by histamine and isoprenaline by 58.0 +/- 14.4% and 80.5 +/- 5.9% respectively; responses to exogenous adenosine were abolished. 3. Adenosine deaminase added to the donor perfusate supplying the recipient heart caused a significant increase in basal perfusion pressure. 4. Our results suggest adenosine is not the sole mediator of vasodilation in stressed hearts and additionally unstressed hearts appear to release a basal vasodilatory level of adenosine.

使用两个串联的豚鼠心脏研究了腺苷在控制冠状血管张力中的作用。供体心脏释放的血管舒张介质由受体心脏进行测定。2. 腺苷脱氨酶使组胺和异丙肾上腺素释放的血管舒张介质活性分别降低了58.0±14.4%和80.5±5.9%；对外源性腺苷的反应被消除。3. 添加到供应受体心脏的供体灌注液中的腺苷脱氨酶导致基础灌注压力显著升高。4. 我们的结果表明，腺苷不是应激心脏血管舒张的唯一介质，此外，未应激的心脏似乎也释放基础水平的血管舒张性腺苷。