EFFECTS OF GENETIC-HYPERTENSION AND NUTRITIONAL ANEMIA ON VENTRICULARREMODELING AND MYOCARDIAL DAMAGE IN RATS

Objective: In order to determine whether alterations in cardiac functi on and structure occur early in life in spontaneously hypertensive rat s (SHR) and whether the addition of a volume load would affect myocard ial growth and haemodynamic performance, SHR were exposed to an iron a nd copper deficient diet for 12 weeks (SHR-A) and compared with untrea ted SHR and Wistar Kyoto controls (WKY). Results: Systolic arterial bl ood pressure increased in SHR, whereas nutritional anaemia prevented t he rise of blood pressure in SHR-A. The diet employed provoked a sever e hypochromic microcytic anaemia with a marked reduction in blood visc osity and increased volume load on the heart in SHR-A. Genetically det ermined hypertension alone induced a 16% increase in left ventricular weight and an increase in left ventricular peak systolic pressure (LVP SP) and +dP/dt. The superimposition of anaemia resulted in a 43% expan sion in left ventricular weight with a decrease in LVPSP and +dP/dt, a nd an increase in left ventricular end diastolic pressure. Wall thicke ning and a preservation of chamber volume occurred in SHR, while SHR-A had a degree of ventricular dilatation which exceeded the extent of w all thickening. However, genetic hypertension was accompanied by myoca rdial tissue injury which was fully prevented by the addition of nutri tional anaemia. Moreover, the capillary volume was decreased in SHR an d increased in SHR-A. Conclusions: Genetically determined hypertension in combination with anaemia results in eccentric ventricular hypertro phy and cardiac dysfunction in spite of an increase in capillary lumin al volume and limited structural damage.