,J hlol
Cell
Cardiol
24,
1237-1252
Energy Riccardo *Istituto
Zucchi*
(1992)
Metabolism
t, Gongyuan
in Myocardial
Stunning
Yu *, Simonetta Ronca-Testoniz, Giovanni Roncaf
Mario
Mariani*,
di Cardiologia, TScuola Superiore di Studi LJniversitari e Perfee,-ionamento S. .&ma. z Istituto di Chimica Biologica, LJniver.rit_y qf Piss, Piss. It& (Received 20 May 1991, accepted in revisedform
21 Mq
1992)
S. KONCA-TESTONI, M. MARIANI, G. RONCA. Energy Metabolism in Xiyorardial Stunning. Cardiolo~ (1992) 24, 1237-l 252. We investigated the rffect of rwrrsiblr ischcmia, leading to persistent contractile dysfunction (stunning). on myocardial enrrgy mrtabolism. The balance (II‘ energy metabolism is expressed by the phosphorylation state of cytosolic nuclrotidcs. This variable c.rnnrjt hr measured directly because of nucleotide compartmentation, but in the isolated heart it can bc estimated h) the release ofpurinr catabolites. We have previously shown that increased energy consumption or impaired txqq production cause purinr release to increase, while primary reduction in rnergy consumption has thr opposite t+l+ct. Isolated working rat hearts were rrperfused after 10 min of global ischcmia. measuring hrmod>:namic variables, tissue high energy phosphate compounds and purine r&ax. In post-ischcmicrccoverv. aorta flow and minute work dwrrased to 82+3% and 77+4% of control, adeninr nuclcotidc pool was rrduwd tq 4.6~mol/g dry wt, phosphocreatine to creatine ratio increased significantly and purinc r&ax decreaacd to -1-2 * 6% (PC 0.0 1 ). ‘The rate of purine salvage, as cvaluatrd by thr incorporation of cxogrnous ‘H-adwosinr and “(l:-hypoxanthinr into tissue nuclcotides, was much lower than nrt purinc relcasc. and way unchanged afictischrmia and reperfusion. The adeninr nurleotidc pool could he deplvtrd to the same cxtcnt ds in thv ,runncd m)ocardium by prolon,ged [60min) aerobic perfusion. In this group the hrmodynamic varialh ww unchanged and purinc release averaged 87 f 9 o/o ofcontrol (P= NS!. In other experiments prolonged pCrlusion was wmbinrd with preload reduction in order to drrrcase energy demand. This protoc~~l reprvducrd the &&I~ of ischc,mia~reperfusic,n: aortic flow and minute work averaged 79 f 4°K and 73 f 9 5% of ~vntrol. ad~~nirw nurlcotidc drpletion was 4.4 @mol/g dry wt and purine release decreased to 38 Z& :)F”/;, ~P
Cell
Cardiol
24,
1237-1252
Energy Riccardo *Istituto
Zucchi*
(1992)
Metabolism
t, Gongyuan
in Myocardial
Stunning
Yu *, Simonetta Ronca-Testoniz, Giovanni Roncaf
Mario
Mariani*,
di Cardiologia, TScuola Superiore di Studi LJniversitari e Perfee,-ionamento S. .&ma. z Istituto di Chimica Biologica, LJniver.rit_y qf Piss, Piss. It& (Received 20 May 1991, accepted in revisedform
21 Mq
1992)
S. KONCA-TESTONI, M. MARIANI, G. RONCA. Energy Metabolism in Xiyorardial Stunning. Cardiolo~ (1992) 24, 1237-l 252. We investigated the rffect of rwrrsiblr ischcmia, leading to persistent contractile dysfunction (stunning). on myocardial enrrgy mrtabolism. The balance (II‘ energy metabolism is expressed by the phosphorylation state of cytosolic nuclrotidcs. This variable c.rnnrjt hr measured directly because of nucleotide compartmentation, but in the isolated heart it can bc estimated h) the release ofpurinr catabolites. We have previously shown that increased energy consumption or impaired txqq production cause purinr release to increase, while primary reduction in rnergy consumption has thr opposite t+l+ct. Isolated working rat hearts were rrperfused after 10 min of global ischcmia. measuring hrmod>:namic variables, tissue high energy phosphate compounds and purine r&ax. In post-ischcmicrccoverv. aorta flow and minute work dwrrased to 82+3% and 77+4% of control, adeninr nuclcotidc pool was rrduwd tq 4.6~mol/g dry wt, phosphocreatine to creatine ratio increased significantly and purinc r&ax decreaacd to -1-2 * 6% (PC 0.0 1 ). ‘The rate of purine salvage, as cvaluatrd by thr incorporation of cxogrnous ‘H-adwosinr and “(l:-hypoxanthinr into tissue nuclcotides, was much lower than nrt purinc relcasc. and way unchanged afictischrmia and reperfusion. The adeninr nurleotidc pool could he deplvtrd to the same cxtcnt ds in thv ,runncd m)ocardium by prolon,ged [60min) aerobic perfusion. In this group the hrmodynamic varialh ww unchanged and purinc release averaged 87 f 9 o/o ofcontrol (P= NS!. In other experiments prolonged pCrlusion was wmbinrd with preload reduction in order to drrrcase energy demand. This protoc~~l reprvducrd the &&I~ of ischc,mia~reperfusic,n: aortic flow and minute work averaged 79 f 4°K and 73 f 9 5% of ~vntrol. ad~~nirw nurlcotidc drpletion was 4.4 @mol/g dry wt and purine release decreased to 38 Z& :)F”/;, ~P
