title: Captopril improves oxygen and glucose extraction in pig hearts during reperfusion after cold cardioplegic storage.
abstract: The purpose of this study was to evaluate the haemodynamic and metabolic effects of captopril during reperfusion of pig hearts following 360 min global 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 then 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 reperfusion. 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 arrival at the laboratory. Captopril was added to the cardioplegia (1000 microg/l) and to the reperfusion media (1000 microg/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 myocardial oxygen and glucose extraction during reperfusion (p < 0.05 for both) while lactate remained unchanged after 360 min HCS. Treatments with captopril increased developed left ventricular pressure (DLVP) and relaxation (-dP/dtmax) during reperfusion (p < 0.05 for both), while contractility (+dP/dtmax) was unchanged. Heart rate was reduced in captopril-treated hearts (p < 0.05) while myocardial blood flow (MBF) was similar in the two groups. Captopril administration prior to and during HCS and postcardioplegic reperfusion improves oxygen and glucose extraction in large spontaneously beating porcine hearts during reperfusion. The underlying mechanisms seem to involve metabolic modulation, since myocardial uptake of oxygen and glucose was increased in the absence of changes in myocardial blood flow.
authors.affiliation: Department of Cardiology, Aarhus University Hospital at Skejby, University of Aarhus, Denmark. skejfr@au.dk
authors.forename: F
authors.initials: F
authors.lastname: Randsbaek
authors.forename: H H
authors.initials: HH
authors.lastname: Kimose
authors.forename: S B
authors.initials: SB
authors.lastname: Hansen
authors.forename: B
authors.initials: B
authors.lastname: Jacobsen
authors.forename: H E
authors.initials: HE
authors.lastname: Bøtker
authors.forename: T T
authors.initials: TT
authors.lastname: Nielsen
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D002314:Cardioplegic Solutions; D003080:Cold Temperature; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006321:Heart / Q000187:drug effects*; D008297:Male; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D009926:Organ Preservation / Q000379:methods*; D010100:Oxygen / Q000378:metabolism*; D013552:Swine
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002314:Cardioplegic Solutions; D002216:Captopril; D005947:Glucose; D010100:Oxygen