Effects of genetic hypertension and nutritional anaemia on ventricular remodelling and myocardial damage in rats.
Effects of genetic hypertension and nutritional anaemia on ventricular remodelling and myocardial damage in rats.
复制标题
遗传性高血压和营养性贫血对大鼠心室重构和心肌损伤的影响。
DOI：
10.1093/cvr/27.7.1316
复制
发表时间：
1993
影响因子：
10.8
通讯作者：
Anversa,P
中科院分区：
文献类型：
--
作者：
Olivetti,G;Quaini,F;Lagrasta,C;Ricci,R;Tosini,P;Capasso,JM;Anversa,P
目的：为了确定自发性高血压大鼠（SHR）生命早期心脏功能和结构是否发生改变，以及增加容量负荷是否会影响心肌生长和血流动力学性能，将SHR暴露于缺铁和缺铜饮食12周（SHR-A），并与未经治疗的SHR和Wistar京都对照组（WKY）进行比较。结果：SHR的收缩动脉压升高，而营养性贫血则阻止了血压的升高在 SHR-A 中。在SHR-A中，所采用的饮食会引起严重的低色素性小细胞性贫血，血液粘度显着降低，心脏容量负荷增加。仅由遗传决定的高血压就会导致左心室重量增加 16%，左心室收缩峰值压 (LVPSP) 和 +dP/dt 增加。贫血叠加导致左心室重量扩大 43%，LVSPP 和 +dP/dt 降低，左心室舒张末压升高。 SHR 出现室壁增厚和心室容积保留，而 SHR-A 的心室扩张程度超过了室壁增厚的程度。然而，遗传性高血压伴随着心肌组织损伤，这可以通过添加营养性贫血来完全预防。此外，SHR 中毛细血管容积减少，SHR-A 中毛细血管容积增加。结论：尽管毛细血管管腔容积增加且结构损伤有限，但基因决定的高血压与贫血相结合导致偏心心室肥厚和心功能不全。心血管研究1993；27：1316-1325
Objective:In order to determine whether alterations in cardiac function and structure occur early in life in spontaneously hypertensive rats (SHR) and whether the addition of a volume load would affect myocardial growth and haemodynamic performance, SHR were exposed to an iron and copper deficient diet for 12 weeks (SHR-A) and compared with untreated SHR and Wistar Kyoto controls (WKY).Results:Systolic arterial blood pressure increased in SHR, whereas nutritional anaemia prevented the rise of blood pressure in SHR-A. The diet employed provoked a severe hypochromic microcytic anaemia with a marked reduction in blood viscosity and increased volume load on the heart in SHR-A. Genetically determined hypertension alone induced a 16% increase in left ventricular weight and an increase in left ventricular peak systolic pressure (LVPSP) and +dP/ dt. The superimposition of anaemia resulted in a 43% expansion in left ventricular weight with a decrease in LVPSP and +dP/dt, and an increase in left ventricular end diastolic pressure. Wall thickening and a preservation of chamber volume occurred in SHR, while SHR-A had a degree of ventricular dilatation which exceeded the extent of wall thickening. However, genetic hypertension was accompanied by myocardial tissue injury which was fully prevented by the addition of nutritional anaemia. Moreover, the capillary volume was decreased in SHR and increased in SHR-A.Conclusions:Genetically determined hypertension in combination with anaemia results in eccentric ventricular hypertrophy and cardiac dysfunction in spite of an increase in capillary luminal volume and limited structural damage.Cardiovascular Research1993;27:1316-1325