F. Randsbaek et al., Captopril improves oxygen and glucose extraction in pig hearts during reperfusion after cold cardioplegic storage, SC CARDIOVA, 34(2), 2000, pp. 201-208
The purpose of this study was to evaluate the haemodynamic and metabolic ef
fects of captopril during reperfusion of Pig hearts following 360 min globa
l hypothermic cardioplegia and storage (HCS). The hearts were perfused with
one litre of cold crystalloid cardioplegia (Bretschneider solution no. 3),
excised and stored in saline at 4 degrees C for 360 min. The hearts were t
hen reperfused with blood in a modified Langendorff model for 60 min. Left
ventricular function, myocardial blood flow, and arteriovenous differences
in oxygen, glucose and lactate were monitored intraoperatively and during r
eperfusion. Two groups of hearts were studied. Group I (captopril treated,
n = 9): the pigs were pre-medicated with increasing oral doses of captopril
for 3 weeks (12.5 mg-150 mg daily) and an intravenous dose (25 mg) upon ar
rival at the laboratory. Captopril was added to the cardioplegia (1000 mu g
/l) and to the reperfusion media (1000 mu g/l). Group II (controls, n = 8):
the pigs were given no premedication, captopril-free cardioplegia and the
hearts were reperfused with captopril-free blood. Captopril increased myoca
rdial oxygen and glucose extraction during reperfusion (p < 0.05 for both)
while lactate remained unchanged after 360 min HCS. Treatments with captopr
il increased developed left ventricular pressure (DLVP) and relaxation (-dP
/dtmax) during reperfusion (p < 0.05 for both), while contractility (+dP/dt
max) was unchanged. Heart rate was reduced in captopril- treated hearts (p
< 0.05) while myocardial blood flow (MBF) was similar in the two groups. Ca
ptopril administration prior to and during HCS and postcardioplegic reperfu
sion improves oxygen and glucose extraction in large spontaneously beating
porcine hearts during reperfusion. The underlying mechanisms seem to involv
e metabolic modulation, since myocardial uptake of oxygen and glucose was i
ncreased in the absence of changes in myocardial blood flow.