ALPHA-ADRENOCEPTORS AND ALPHA-ADRENOCEPTOR-MEDIATED POSITIVE INOTROPIC EFFECTS IN FAILING HUMAN MYOCARDIUM
ALPHA-ADRENOCEPTORS AND ALPHA-ADRENOCEPTOR-MEDIATED POSITIVE INOTROPIC EFFECTS IN FAILING HUMAN MYOCARDIUM
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DOI：
10.1097/00005344-198809000-00015
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发表时间：
1988-09-01
影响因子：
3
通讯作者：
ERDMANN, E
中科院分区：
文献类型：
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作者：
BOHM, M;DIET, F;ERDMANN, E
实验旨在研究纽约心脏协会(NYHA)中度心力衰竭(NYHA)II-III级和重度心力衰竭(NYHA IV)患者的心脏[α]-肾上腺素能受体和α-肾上腺素能受体介导的正性肌力作用。中、重度心力衰竭患者心脏α受体数目较少，但相似(NYHA II-III级：6.7+/-0.8fmol/mg蛋白，3 H-哌唑嗪结合，n=12；NYHA IV级：7.4+/-0.9fmol/mg蛋白，3 H-哌唑嗪结合，n=9；NS)。相应地，[α]-肾上腺素受体介导的正性肌力作用(心得安存在时的苯肾上腺素)在两组中没有显著差异。在相同的心脏中，测量了[β]-肾上腺素能受体的数量。严重心力衰竭患者的[β]-肾上腺素能受体数量显著减少(NYHA分级：22.0+/-1.5fmol/mg蛋白~3H-CGp 12177结合，n=12；NYHA分级IV：11.9+/-0.8fmol/mg蛋白~3H-CGp 12177结合，n=9；p<；0.05)。NYHA分级为IV级时，异丙肾上腺素的正性肌力作用明显减弱，而钙离子的正性肌力作用在两组中相似。总之，在严重衰竭的心肌中，心脏[β]-肾上腺素能受体和[β]-肾上腺素能受体介导的正性变力作用减弱。心脏[α]-肾上腺素能受体及其刺激所产生的正性变力作用不变。因此，人类心脏显然不会因交感神经刺激增加或[α]-肾上腺素能受体代偿性增加而下调。由于心脏[α]-肾上腺素能受体没有减少，而是[α]-肾上腺素能受体占肾上腺素能受体总数的比例增加，它们可能有助于在严重心力衰竭时维持心脏的收缩能力，在严重心力衰竭中，[β]-肾上腺素能受体介导的反应受到影响。
Experiments were designed to characterize cardiac [alpha]-adrenoceptors and the a-adrenoceptor-mediated positive inotropic effects in human myocardial tissue from patients with moderate New York Heart Association (NYHA) class II-III and severe (NYHA class IV) heart failure. The number of cardiac a-adrenoceptors was low but similar in moderate and severe heart failure (NYHA class II-III: 6.7+/-0.8 fmol/mg protein 3H-prazosin bound, n= 12; NYHA class IV: 7.4+/-0.9 fmol/mg protein 3H-prazosin bound, n= 9; NS). Correspondingly, the [alpha]-adrenoceptor-mediated positive inotropic effect (phenylephrine in the presence of propranolol) did not significantly differ in both groups. In the same hearts, the number of [beta]-adrenoceptors was measured. The number of [beta]-adrenoceptors was significantly reduced in severe heart failure (NYHA class II-III: 22.0+/-1.5 fmol/mg protein 3H-CGP 12177 bound, n= 12; NYHA class IV: 11.9+/-0.8 fmol/mg protein 3H-CGP 12177 bound, n= 9; p< 0.05). The positive inotropic effect of isoprenaline was significantly reduced in NYHA class IV. The positive inotropic effect of Ca2+ was similar in both groups. In conclusion, cardiac [beta]-adrenoceptors and the [beta]-adrenoceptor-mediated positive inotropic effects were reduced in severely failing myocardium. Cardiac [alpha]-adrenoceptors and the positive inotropic effect resulting from their stimulation is unchanged. Therefore, down regulation in response to increased sympathetic stimulation or a compensatory increase of [alpha]-adrenoceptors does obviously not occur in the human heart. Because there is no reduction of cardiac [alpha]-adrenoceptors but an increased ratio of [alpha]-adrenoceptors to the total amount of adrenoceptors, they might serve to contribute to the maintenance of cardiac contractility in severe heart failure, in which [beta]-adrenoceptor-mediated responses are compromised.