Rj. Tomanek et al., CORONARY BLOOD-FLOW IN SENESCENT RATS WITH LATE-ONSET HYPERTENSION, The American journal of physiology, 264(6), 1993, pp. 1854-1860
We tested the hypothesis that the imposition of hypertension late in l
ife would markedly limit maximal myocardial perfusion (MP). Young adul
t (8 mo) and senescent (24 mo) Fischer 344 rats were studied 3 mo afte
r one-kidney, figure-8 renal wrap hypertension (RH) was induced. Sham-
operated rats served as controls (Con). Regional MP was determined wit
h radioactive microspheres in conscious rats before and during maximal
coronary vasodilation with infusion of dipyridamole. Systolic arteria
l pressure (SAP) was significantly elevated in both RH age groups duri
ng weeks 2-6 following surgery and then fell to normotensive levels. A
fter 3 mo SAP (mmHg) was significantly lower in the senescent RH rats
(125 +/- 5) compared with their controls (147 +/- 3). In senescent RH
rats left ventricular (LV) end-diastolic pressure increased fivefold.
LV mass increased with age but not with treatment. LV minimal coronary
vascular resistance (MCVR, mmHg . ml-1 . min . 100 g) increased signi
ficantly both with age and treatment (8 mo: Con = 0.07 +/- 0.01, RH =
0.14 +/- 0.01; 24 mo: Con = 0.11 +/- 0.01, RH 0.17 +/- 0.02). Treatmen
t affected similar changes in the right ventricular MCVR. LV endocardi
al-to-epicardial perfusion ratio during rest was lower in the senescen
t groups but was not altered by hypertension. These data indicate that
1) both aging and this model of hypertension compromise maximal coron
ary perfusion and reserve in Fischer 344 rats, and 2) aging is associa
ted with an increase in coronary vascular resistance in both ventricle
s at rest and in a relative reduction in maximal endocardial perfusion
in the left ventricle.