Horn E M, Bilezikian J P
Columbia Univeristy College of Physicians and Surgeons, Department of Medicine, New York, NY 10032.
Circulation. 1990 Aug;82(2 Suppl):I26-34.
Congestive heart failure is associated with blunted cardiac adrenergic responsiveness, clinically manifested by diminished chronotropic, inotropic, and lusitropic responses to beta-adrenergic stimulation. Recent advances in our understanding of the multiple components of the beta-adrenergic receptor complex and of the mechanisms by which these components interact with each other have led to insights beyond the mere evaluation of beta-receptors to account for adrenergic hyporesponsiveness in congestive heart failure. In addition to a reduction in beta-adrenergic receptors, the failing heart appears to show key abnormalities in the guanine nucleotide-binding proteins that link the beta-receptor to its biochemical effector. A reduction in the stimulatory protein and in the extent to which the stimulatory protein is linked to the beta-receptor are demonstrable in peripheral circulating lymphocytes and in cardiac tissue. These abnormalities are at least partially reversible.
充血性心力衰竭与心脏肾上腺素能反应迟钝有关，临床表现为对β-肾上腺素能刺激的变时性、变力性和舒张性反应减弱。我们对β-肾上腺素能受体复合物的多个组成部分以及这些组成部分相互作用机制的理解取得了新进展，这使我们不仅能评估β受体，还能深入了解充血性心力衰竭中肾上腺素能反应低下的原因。除了β-肾上腺素能受体减少外，衰竭心脏似乎还在将β受体与其生化效应器相连的鸟嘌呤核苷酸结合蛋白中表现出关键异常。在外周循环淋巴细胞和心脏组织中可证实刺激蛋白减少以及刺激蛋白与β受体的连接程度降低。这些异常至少部分是可逆的。
