ENERGY GENERATION IN HYPERTROPHIED POSTISCHEMIC MYOCARDIUM FEASIBILITY OF PROLONGED INOTROPIC STIMULATION WITH DOPAMINE IN HYPERTROPHIED REPERFUSED LEFT-VENTRICLES
Hm. Hoffmeister et al., ENERGY GENERATION IN HYPERTROPHIED POSTISCHEMIC MYOCARDIUM FEASIBILITY OF PROLONGED INOTROPIC STIMULATION WITH DOPAMINE IN HYPERTROPHIED REPERFUSED LEFT-VENTRICLES, Basic research in cardiology, 93(3), 1998, pp. 201-208
Background Non-hypertrophied reversibly injured postischemic myocardiu
m can be stimulated for a prolonged period without detrimental effects
. Since no data on hypertrophied myocardium are available, our aim was
to examine the effects of a prolonged postischemic positive inotropic
stimulation on moderately hypertrophied left ventricles. Methods Usin
g a Langendorff-type isovolumically contracting isolated heart model,
moderately hypertrophied (+50 % of ventricular mass) hearts from spont
aneously hypertensive rats (SHR) were investigated and compared to dat
a from non-hypertrophied hearts of normotensive rats. A 30 minutes no-
flow ischemia was performed, and in the postischemic period dopamine w
as continuously administered for 20 minutes in order to stimulate the
postischemic hearts to the control level of function. Data were compar
ed to postischemic hearts without stimulation and to non-ischemic cont
rols. After 50 minutes of reperfusion and cessation of the catecholami
ne steady state function, maximum contractile response, and high energ
y phosphates were determined. Results 30 minutes ischemia followed by
50 minutes reperfusion caused a significant reduction in developed LVP
to 77.8 +/- 4.2 % in SHR. Dp/dtmax was reduced to 67.0 +/- 2.3 %. Aft
er cessation of dopamine stimulation developed LVP was 64.3 +/- 3.5 %
and dp/ dtmax 69.3 +/- 3.7 % in SHR. The double product was identicall
y reduced in all postischemic groups. The con tractile reserve was com
parable in stimulated and non-stimulated postischemic SHR hearts. In h
ypertrophied myocardium, ATP was reduced to 1.1 +/- 0.1 mu mol/gww (no
n-ischemic controls 2.5 +/- 0.3 mu mol/gww) in unstimulated and to 1.0
+/- 0.1 mu mol/gww in stimulated postischemic hearts. Comparably the
ischemia-induced reduction in ATP in non-hypertrophied myocardium was
1.3 mu mol/gww. Similar results were obtained for ADP and AMP. Creatin
e phosphate levels were normal in stimulated and non-stimulated postis
chemic myocardium of hypertrophied and nonhypertrophied hearts. Conclu
sion These results indicate that prolonged stimulation of stunned hype
rtrophied myocardium is feasible without detrimental effects on postst
imulation contractile function. The energy generating apparatus is cap
able to deliver sufficient energy during stimulation of stunned hypert
rophied hearts.