-transparent.png){kind=logo}
Hypothermia protects ischemic tissues by reducing ATP utilization and accumulation of harmful metabolites. However, it also reduces ATP production, which might cause deterioration in the energy supply/demand ratio. Modulation of energy supply/demand according to temperature has not been previously studied in detail. In this study, isolated, perfused rabbit hearts (n = 60) were used to determine the effects of various temperatures on myocardial energy metabolism and function during cardioplegic arrest. Ischemia was induced by crystalloid cardioplegic solution at 4, 18, 30, and 34 degrees C for 120 min, respectively. At each temperature, the hearts were divided into a glucose-treated group which contained 22 mM glucose in cardioplegic solution as the only substrate and a control group which contained 22 mM mannitol to keep same osmolarity. Following 15 min reperfusion, recovery of left ventricular developed pressure (DP), +/- dP/dtmax, and the product of heart rate and DP were significantly higher in 30, 18, and 4 degrees C groups than those in 34 degrees C control group. The functional recovery was also significantly higher in the 34 degrees C glucose-treated group than that in the 34 degrees C control group, but there was no difference between those groups at 30 degrees C and the temperature below 30 degrees C. Myocardial ATP concentration was significantly lower in 34 degrees C control group than those in other groups. There is a close relationship between myocardial ATP concentration and functional recovery (R2 = 0.90). The accumulations of lactate and CO2 were significantly higher at 34 degrees C in glucose-treated group than those in the control group. However, there was no significant difference between these two groups at 30 degrees C and the temperature below 30 degrees C. These results indicate that under these study conditions: (1) a marked decrease in energy supply/demand occurs above 30 degrees C, implying that a temperature threshold exists; and (2) this can be ameliorated by provision of glucose as substrate in cardioplegia solution.
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
February 1989,
Journal of molecular and cellular cardiology,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
October 1977,
Thoraxchirurgie, vaskulare Chirurgie,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
January 1976,
Basic research in cardiology,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
November 1963,
Thoraxchirurgie und vaskulare Chirurgie,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
January 1973,
Archiv fur experimentelle Veterinarmedizin,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
April 2002,
Molecular and cellular biochemistry,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
August 2000,
The Annals of thoracic surgery,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
March 2005,
International heart journal,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
November 1991,
The Journal of thoracic and cardiovascular surgery,
X H Ning, and
C S Xu, and
Y C Song, and
K F Childs, and
Y Xiao, and
S F Bolling, and
F M Lupinetti, and
M A Portman
March 1998,
The American journal of physiology,
