Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats.

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a rightward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at normotensive' or 'hypertensive' levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.