EFFECTS OF CHRONIC PROGRESSIVE MYOCARDIAL HYPERTROPHY ON INDEXES OF CARDIAC AUTONOMIC INNERVATION
EFFECTS OF CHRONIC PROGRESSIVE MYOCARDIAL HYPERTROPHY ON INDEXES OF CARDIAC AUTONOMIC INNERVATION
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DOI：
10.1161/01.res.61.1.55
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发表时间：
1987-07-01
影响因子：
20.1
通讯作者：
SCHMID, PG
中科院分区：
文献类型：
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作者：
LINDPAINTNER, K;LUND, DD;SCHMID, PG
心脏肥大的发展与心脏自主神经支配的显著变化有关。显著和持续地降低心肌儿茶酚胺储存以及酪氨酸羟化酶和多巴胺β-受体的活性，羟化酶在急性诱导的心室肥大模型中已有报道。相反，胆碱乙酰转移酶的活性，副交感神经功能的标志物，在急性右心室肥大的发展过程中表现出短暂的增加。这些变化的潜在生理重要性促使我们研究一种临床上更相关的缓慢进行性心室肥大模型。在断奶豚鼠的肺动脉周围应用一个松散的带导致与生长相关的进行性右心室压力超负荷。在9周和18周时，捆绑动物的右心室重量与体重的比率显著地和进行性地增加（0.92 ± 0.95）。0.05和1.31 .+-。0.11 mg/g，p < 0.01）与假手术对照组（0.55 ± 0.01）相比，0.02和0.59 ±。0.01 mg/g），但在27周时没有显示进一步的增加（1.41 ± 0.01mg/g）。0.10 mg/g）。酪氨酸羟化酶和多巴胺β-受体的活性羟化酶在所有实验组中保持不变，而在18周和27周时，捆绑动物的右心室去甲肾上腺素含量显示持续和进行性增加（2.45 ± 0.05）。0.11和3.40 .+-。0.19μ g/右心室）相对于对照组（1.80 ± 0.05 μ g/右心室）的差异。0.13和2.40 .+-。0.22μ g/右心室，p < 0.01）。在18周时，带状动物中胆碱乙酰转移酶的活性显著升高（32.6 ± 0.01）。2.7 nmol/hr/右心室），但在27周时恢复到基线（22.8 ± 0.001）。1.4 nmol/hr/右心室）。我们的结论是，压力超负荷的时间过程是一个重要的变量，影响交感神经指数在肥厚的心脏。因此，与急性诱导的右心室肥大相反，如果严重的心脏肥大以生理性的、渐进的方式发展，交感神经支配的标记物可能会在严重的心脏肥大中保留下来。另一方面，心脏副交感神经标记物的短暂增加似乎是急性或慢性进行性压力超负荷引起的心肌肥大发展的共同特征。我们的观察结果表明，交感神经副交感神经的相互作用可能会有所不同，在慢性进行性心肌肥厚的发展过程中，这些相互作用可能会有所不同，在慢性进行性和急性心室肥大。
The development of cardiac hypertrophy is associated with marked changes in cardiac autonomic innervation. Significant and sustained reductions of myocardial catecholamine stores and activities of tyrosine hydroxylase and dopamine .beta.-hydroxylase have been reported in models of acutely induced ventricular hypertrophy. Conversely, activity of choline acetyltransferase, a marker of parasympathetic nervous function, shows transient increases during the development of acute right ventricular hypertrophy. The potential physiological importance of these changes prompted us to examine a clinically more relevant model of slowly progressive ventricular hypertrophy. Application of a loose band around the pulmonary artery of weanling guinea pigs resulted in a growth-related progressive right ventricular pressure overload. Right ventricular weight-to-body-weight ratio was increased significantly and progressively at 9 and 18 weeks in banded animals (0.92 .+-. 0.05 and 1.31 .+-. 0.11 mg/g, respectively, p < 0.01) compared with sham-operated controls (0.55 .+-. 0.02 and 0.59 .+-. 0.01 mg/g, respectively) but showed no further gain at 27 weeks (1.41 .+-. 0.10 mg/g). Activities of tyrosine hydroxylase and dopamine .beta.-hydroxylase remained unchanged in all experiment groups, while right ventricular contents of norepinephrine in banded animals at 18 and 27 weeks exhibited sustained and progressive increases (2.45 .+-. 0.11 and 3.40 .+-. 0.19 .mu.g/right ventricle, respectively) over controls (1.80 .+-. 0.13 and 2.40 .+-. 0.22 .mu.g/right ventricle, respectively, p < 0.01). The activity of choline acetyltransferase was markedly elevated in banded animals at 18 weeks (32.6 .+-. 2.7 nmol/hr/right ventricle) but returned to baseline by 27 weeks (22.8 .+-. 1.4 nmol/hr/right ventricle). We conclude that the time course of pressure overload is an important variable influencing sympathetic neural indexes in the hypertrophied heart. Thus, in contrast to acutely induced right ventricular hypertrophy, markers of sympathetic innervation may be preserved in severe cardiac hypertrophy provided it develops in a physiological, gradual fashion. On the other hand, transient increases of the cardiac parasympathetic marker appear to be a common feature of the development of myocardial hypertrophy produced by either acute or chronic progressive pressure overload. Our observations suggest that sympathetic-parasympathetic interactions may vary during the development of chronic progressive cardiac hypertrophy and that these interactions may differ in chronic progressive and acute ventricular hypertrophy.