Vectorcardiographical and pathological approach to the relationship between cardiac hypertrophy and coronary arteriosclerosis in spontaneously hypertensive rats (SHR).
To study the pathophysiology and the pathogenesis of hypertensive cardiac diseases such as cardiac hypertrophy and ischemic heart diseases, and to determine the relationship between these cardiopathies, spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) were used as models. Vectorcardiography was applied to the rat according to orthogonal Takayasu lead system and "vectorcardiography for small animals" with a good reproducibility was established. Characteristic vectorcardiogram (VCG) was obtained from 5-month-old SHR, compared with normotensive Wistar-Kyoto rats (WK). Left superior (posterior) deviation of QRS vector usually with ST-T changes was recognized as LVH (Left Ventricular Hypertrophy) pattern of SHR and such corresponded to the pathological findings of the increased heart weight and the increased weight and thickness of the left ventricular wall, and also to the high blood pressure. Macroscopical morphological features of the heart were also studied. Chest roentgenography showed and increased cardiothoracic ratio (CTR) and the protrusion of the left ventricular portion in the posteroanterior cardiac silhouette of SHR. The horizontal view of the chest, cross-sectioned by the apparatus of whole body autoradiography, PMV-cryomicrotome 450 MP, indicated the left anterior orientation of the interventricular septum in rats, as is the case in humans, and the clockwise rotation of the left ventricular cavity in SHR, compared with WK. The coronary arterial wall thickening with narrowed lumen was noted even in the prehypertensive 1-month-old SHR. Such correlated well with the wall thickening of the left ventricle. From these vectorcardiographical and morphological studies on SHR and SHRSP, genetic hypertension was ascertained to be significant not only for cardiac hypertrophy but for the coronary arterial wall thickening, both of which may also enhance the myocardial lesions in SHR, particularly in SHRSP.
D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009929:Organ Size; D051381:Rats; D014672:Vectorcardiography