The role of phosphocreatine and ATP in contraction of normal and ischemic heart.
The effect of cellular creatine (Cr) and adenine nucleotides (AdN) deficiency on cardiac work, ATP turnover rate and flux through creatine kinase (CK) has been investigated. Depletion of 60-65% of total heart AdN by 2-deoxyglucose treatment in the presence of pyruvate and subsequent washout resulted in only 25% decrease in contractile activity and phosphocreatine level. Substitution of 80-90% of heart Cr (and PCr) by guanidinopropionic acid (GP) by feeding of rats with 1% GP diet reduced maximal values of cardiac work, ATP turnover and flux through CK by 40-50% and elevated end diastolic pressure and index of diastolic stiffness. Hearts depleted of AdN or glycogen showed better post-ischemic recovery of mechanical function that can be attributed to restriction of accumulation of ischemic catabolytes (lactate, H+, Pi). These data imply that in myocardium PCr is an essential high energy phosphate and contractile function stays unchanged at significantly reduced ATP levels.
USSR Cardiology Research Centre, Acad. Med. Sci. USSR, Moscow.
V V
VV
Kupriyanov
V L
VL
Lakomkin
Steinschneider AYa
N A
NA
Novikova
Severina MYu
V I
VI
Kapelko
V A
VA
Saks
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D066298:In Vitro Techniques; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010725:Phosphocreatine / Q000378:metabolism*; D051381:Rats
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D003402:Creatine Kinase