Ungerer M, Richardt G
Medizinische Klinik II, Medizinische Universität zu Lübeck.
Z Kardiol. 1996;85 Suppl 6:171-5.
Adenosine exerts most of its cardiac effects via direct interaction with sympathetic neurotransmission: Release of norepinephrine is inhibited in presynaptic neurons, and catecholamine-induced activation of adenylyl cyclase is inhibited in postsynaptic effector cells. While presynaptic effects fade rapidly during ischemia, postsynaptic antagonism to catecholamines remains an important protective element during sustained ischemia.
去甲肾上腺素的释放在突触前神经元中受到抑制,并且儿茶酚胺诱导的腺苷酸环化酶激活在突触后效应细胞中受到抑制。虽然突触前效应在缺血期间迅速消退,但在持续缺血期间,对儿茶酚胺的突触后拮抗作用仍然是一个重要的保护因素。