Hu K, Gaudron P, Bahner U, Palkovits M, Ertl G
Department of Medicine, Würzburg University, Germany.
Am J Physiol. 1996 Jan;270(1 Pt 2):H312-6. doi: 10.1152/ajpheart.1996.270.1.H312.
We measured immunoreactive atrial natriuretic peptide (ANP) in 18 selected, microdissected brain areas. Rats were studied 8 wk after coronary ligation or sham operation or as nonoperated control animals. In separate animals, hemodynamic and plasma parameters were measured. Rats with myocardial infarction had marked elevated right atrial and left ventricular end-diastolic pressure (2.6 +/- 0.6 and 16.2 +/- 3.1 mmHg, respectively; n = 15) vs. sham-operated rats (1.3 +/- 1.0 and 5.5 +/- 1.2 mmHg, n = 14; P < 0.05) and depressed maximal rate of pressure development (9,613 +/- 980 vs. 15,600 +/- 2,027 mmHg/s; P < 0.05) but similar arterial pressure (126 +/- 4 vs. 124 +/- 3 mmHg; P > 0.05). After myocardial infarction (n = 10), plasma ANP, renin activity, and angiotensin (ANG) II were elevated (53.1 +/- 16.2 pg/ml, 10.7 +/- 2.5 ng ANG I ml-1 h-1, and 219.6 +/- 11.0 fmol/ml, respectively) vs. sham rats (12.0 +/- 2.2 pg/ml, 5.7 +/- 0.7 ng ANG I ml-1, h-1, and 142.9 +/- 9.4 fmol/ml; n = 10; P < 0.05), whereas vasopressin and aldosterone levels remained unchanged among groups. In rats with myocardial infarction, a substantial decrease of ANP was found in the medial preoptic nucleus, the supraoptic nucleus, the subfornical organ, the paraventricular nucleus, and the locus ceruleus. These nuclei are involved in electrolyte, and fluid homeostasis, blood pressure regulation, and modulation of neuroendocrine systems. The mechanism of this reduction and the consequences for systemic adaption or decompensation remain unclear. However, the data suggest that myocardial infarction and chronic left ventricular dysfunction may induce changes of a neurotransmitter in brain.
我们在18个选定的经显微切割的脑区测量了免疫反应性心房利钠肽（ANP）。对冠状动脉结扎术后8周的大鼠、假手术大鼠或未手术的对照动物进行了研究。在另外的动物中，测量了血流动力学和血浆参数。与假手术大鼠相比，心肌梗死大鼠的右心房和左心室舒张末期压力显著升高（分别为2.6±0.6和16.2±3.1 mmHg；n = 15），而假手术大鼠分别为1.3±1.0和5.5±1.2 mmHg，n = 14；P < 0.05），压力最大上升速率降低（9,613±980对15,600±2,027 mmHg/s；P < 0.05），但动脉血压相似（126±4对124±3 mmHg；P > 0.05）。心肌梗死后（n = 10），与假手术大鼠（分别为12.0±2.2 pg/ml、5.7±0.7 ng血管紧张素I ml-1 h-1和142.9±9.4 fmol/ml；n = 10；P < 0.05）相比，血浆ANP、肾素活性和血管紧张素（ANG）II升高（分别为53.1±16.2 pg/ml、10.7±2.5 ng血管紧张素I ml-1 h-1和219.6±11.0 fmol/ml），而各实验组间血管加压素和醛固酮水平保持不变。在心肌梗死大鼠中，视前内侧核、视上核、穹窿下器官、室旁核和蓝斑中的ANP显著减少。这些核参与电解质和液体平衡、血压调节以及神经内分泌系统的调节。这种减少的机制以及对全身适应或失代偿的影响尚不清楚。然而，数据表明心肌梗死和慢性左心室功能障碍可能会引起大脑中神经递质的变化。
