Interaction between adenosine and inotropic interventions in guinea pig atria.
Interaction between adenosine and inotropic interventions in guinea pig atria.
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腺苷和正性肌力干预对豚鼠心房的相互作用。
DOI：
10.1152/ajpheart.1983.245.3.h475
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
DobsonJr,JG
中科院分区：
文献类型：
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作者：
DobsonJr,JG
用离体豚鼠心房刺激进行等距收缩，以确定腺苷浓度是否对峰值收缩力、力发展率和松弛率没有直接抑制作用，能够影响这些收缩参数的升高，这些参数是由预负荷增加、配对电刺激、收缩频率增加、和儿茶酚胺刺激K+去极化和非去极化心房肌。腺苷对通过增加预负荷或配对电刺激而增强的收缩参数没有影响。核苷降低了异丙肾上腺素刺激引起的收缩参数的增加、收缩频率的增加和异丙肾上腺素引起的心房去极化收缩。所有腺苷的还原都被茶碱（一种腺苷的拮抗剂）所抑制。阿托品（一种毒蕈碱拮抗剂）或心得安（一种β -肾上腺素能阻滞剂）不能阻止因收缩频率增加而引起的收缩参数升高的腺苷减少。这些结果表明，在不产生直接负性肌力反应的浓度下，腺苷能够减弱儿茶酚胺刺激引起的收缩力升高、收缩频率增加和儿茶酚胺诱导的心房去极化收缩。然而，收缩频率增加引起的收缩反应的腺苷减少似乎与儿茶酚胺无关。
Isolated guinea pig atria stimulated to contract isometrically were used to determine whether adenosine at a concentration that does not cause a direct depressant effect on peak contractile force, rate of force development, and rate of relaxation was capable of influencing the elevation in these contractile parameters caused by an increase in preload, paired electrical stimulation, an increase in contraction frequency, and catecholamine stimulation in K+-depolarized and nondepolarized atrial muscle. Adenosine had no effect on the contractile parameters that were enhanced by an increase in preload or paired electrical stimulation. The nucleoside reduced the increases in the contractile parameters produced by isoproterenol stimulation, an increase in contraction frequency, and isoproterenol-induced contractions in depolarized atria. All adenosine reductions were inhibited by theophylline, an antagonist of adenosine actions. The adenosine reduction of the elevated contractile parameters caused by increasing contraction frequency was not prevented by atropine (a muscarinic antagonist) or propranolol (a beta-adrenergic blocking agent). These results suggest that adenosine at a concentration that does not produce direct negative inotropic responses is capable of attenuating the elevation in contractility elicited by catecholamine stimulation, an increase in contraction frequency, and catecholamine-induced contractions in depolarized atria. However, the reduction by adenosine of the contractile responses elicited by an increase in contraction frequency appears to be independent of catecholamines.