Vogt M, Jacob R, Noma K, Onegi B, Rupp H
Physiologisches Institut II, Universität Tübingen, F.R.G.
Basic Res Cardiol. 1987;82 Suppl 2:161-72. doi: 10.1007/978-3-662-11289-2_16.
The significance of various factors for the development of structural dilatation in the chronically pressure-loaded and failing heart were evaluated. The investigations were performed on male rats with renal (Goldblatt II) and spontaneous (Aoki-Okamoto) hypertension at different stages of haemodynamic overload. Two groups of SHR were submitted to intermittent feeding (SHR IF); one group received additionally the beta-blocking agent atenolol (50 mg/kg b.w.; SHR IF + beta Bl.). Haemodynamic measurements were carried out under open chest conditions. Myosin isoenzyme pattern, hydroxyproline concentration and circulating blood volume were determined. Transformation to slower myocardium per se, induced by IF, did not lead to significant change in ventricular configuration. After additional blockade of beta-adrenergic receptors there were indications of unfavourable development of left ventricular configuration. Inhibition of hypertrophic mass increase due to curtailed adrenergic stimulation could be an influential factor in the development of dilatation. Further investigations, however, are required to establish the relationship between the adrenergic system, on the one hand, and degree of hypertrophy as well as structural dilatation of the ventricle, on the other hand. The established marked increase in hydroxyproline concentration of the dilated ventricle of SHR in congestive failure is consistent with the assumption of a causal link between the degree of fibrosis and structural dilatation. Observations on rats with aorto-caval shunt and Goldblatt II rats with eccentric hypertrophy and corresponding increase in filling potential or circulating blood volume indicate a correlation between the latter and ventricular size. Thus, we assume that curtailed protein synthesis, fibrosis and regulatory processes related to water and electrolyte balance, but not myocardial transformation per se, play a role in the development of structural dilatation. The relative contribution of each factor, however, may depend on the experimental model that is used.
评估了各种因素对慢性压力负荷和衰竭心脏结构扩张发展的意义。研究在处于血流动力学过载不同阶段的雄性肾性（Goldblatt II型）和自发性（青木冈本型）高血压大鼠身上进行。两组自发性高血压大鼠接受间歇性喂养（自发性高血压大鼠间歇性喂养组）；一组额外给予β受体阻滞剂阿替洛尔（50毫克/千克体重；自发性高血压大鼠间歇性喂养组 + β受体阻滞剂）。在开胸条件下进行血流动力学测量。测定肌球蛋白同工酶模式、羟脯氨酸浓度和循环血容量。由间歇性喂养诱导的向较慢心肌的转变本身并未导致心室构型的显著变化。在额外阻断β肾上腺素能受体后，有迹象表明左心室构型发展不利。由于肾上腺素能刺激减少而抑制肥厚性质量增加可能是扩张发展的一个影响因素。然而，需要进一步研究来确定一方面肾上腺素能系统与另一方面心室肥厚程度以及结构扩张之间的关系。在充血性心力衰竭中，已确定的自发性高血压大鼠扩张心室中羟脯氨酸浓度的显著增加与纤维化程度和结构扩张之间存在因果关系的假设一致。对主动脉 - 腔静脉分流大鼠和具有离心性肥厚以及相应充盈潜能或循环血容量增加的Goldblatt II型大鼠的观察表明，后者与心室大小之间存在相关性。因此，我们假设蛋白质合成减少、纤维化以及与水和电解质平衡相关的调节过程，而非心肌转变本身，在结构扩张的发展中起作用。然而，每个因素的相对贡献可能取决于所使用的实验模型。
