The effects of global ischemia and reperfusion on compensated hypertrophied rat hearts.
Abdominal aorta constriction was performed in 10-week-old Lewis rats (Aoband). Ten weeks later the hearts were isolated and attached to a non-recirculating perfusion apparatus. The hearts could eject against a diastolic aortic pressure of either 60 or 100 mmHg. The functional recovery was compared with that of hearts of sham-operated (Sham) rats. After 45 min of global ischemia, Sham hearts regained cardiac output up to 75% and 70% of the pre-ischemic levels at 60 and 100 mmHg, respectively. At 60 mmHg Aoband hearts showed a minor recovery of ejection function. However, at 100 mmHg the recovery of Aoband hearts was completely comparable with that of Sham hearts. At 60 mmHg but not at 100 mmHg, the pre-ischemic and post-ischemic coronary flow was lower in Aoband than in Sham hearts (P less than or equal to 0.05). During the initial reperfusion phase Sham hearts, perfused at 60 mmHg, released more degradation products of adenine nucleotides and lactate dehydrogenase (LDH) than Aoband hearts (P less than or equal to 0.05), while the Aoband hearts lost more degradation products and LDH than the Sham hearts later during the reperfusion phase (P less than or equal to 0.05). In the groups perfused at 60 mmHg, higher tissue levels of ATP were found in Sham than in Aoband hearts at the end of the reperfusion period (P less than or equal to 0.05). However, at 100 mmHg comparable levels were found in the Sham and Aoband hearts. It is concluded that the height of the coronary perfusion pressure is of critical importance for the post-ischemic functional recovery of the compensated hypertrophied heart. At sufficiently high perfusion pressure levels, the functional and biochemical recovery of the hypertrophied heart is at least as good as in the non-hypertrophied heart. However, in the hypertrophied heart a coronary perfusion pressure which is too low leads to relative underperfusion during the initial reperfusion period which is associated with severely depressed cardiac performance and delayed wash-out of metabolites and intracellular enzymes.
Snoeckx
L H
LH
Department of Physiology, Cardiovascular Research Institute Maastricht, University of Limburg, The Netherlands.
van der Vusse
G J
GJ
Coumans
W A
WA
Reneman
R S
RS
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D003402:Creatine Kinase / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew
D000227:Adenine Nucleotides; D006003:Glycogen; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase