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Eighteen dogs underwent transmural left ventricular biopsies for adenosine triphosphate and suturing of the noncoronary cusp, creating valvular aortic stenosis. Three months after aortic stenosis and the subsequent development of left ventricular hypertrophy, animals underwent repeat transmural left ventricular biopsies followed by total myocardial ischemia at 37 degrees C. Left ventricular tissue samples for adenosine triphosphate and lactate levels were determined at 15-minute intervals and compared with 15 control animals. No significant difference between subendocardial and subepicardial adenosine triphosphate levels was found between left ventricular samples taken before left ventricular hypertrophy and 3 months after left ventricular hypertrophy. Significant differences in adenosine triphosphate utilization occurred between subendocardial and subepicardial layers in control and left ventricular hypertrophy myocardium, however. The gradient between the subendocardium and the subepicardium was significantly increased by left ventricular hypertrophy (p less than 0.05). Significant differences also occurred within the same layer when left ventricular hypertrophy and control groups were compared. During total ischemia, lactate concentration was significantly greater within the subendocardium than within the subepicardium in left ventricular hypertrophy. The onset of ischemic contracture was 48.2 +/- 2.1 minutes in left ventricular hypertrophy versus 62.3 +/- 1.8 minutes in control hearts (p less than 0.01). Subendocardial intramyocardial pressure increased significantly earlier than subepicardial in both left ventricular hypertrophy and control hearts. Adenosine triphosphate was used, and lactate accumulated more rapidly in animals with a more pronounced hemodynamic gradient. These data show that after left ventricular hypertrophy, adenosine triphosphate stores in the subendocardium and the subepicardium are unchanged from control values, yet the rates of adenosine triphosphate utilization and lactate accumulation during total ischemia are significantly increased. Furthermore, the subendocardial to subepicardial gradient of adenosine triphosphate utilization during ischemia found in normal hearts is markedly increased by left ventricular hypertrophy.
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1990,
Journal of molecular and cellular cardiology,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1993,
Cardiology,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1999,
Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1991,
Journal of the Association for Academic Minority Physicians : the official publication of the Association for Academic Minority Physicians,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
October 1977,
Journal of molecular and cellular cardiology,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1968,
Pflugers Archiv fur die gesamte Physiologie des Menschen und der Tiere,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1967,
Pflugers Archiv fur die gesamte Physiologie des Menschen und der Tiere,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1975,
Recent advances in studies on cardiac structure and metabolism,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
March 1995,
Circulation,
M R Bladergroen, and
H Takei, and
T D Christopher, and
R G Cummings, and
S M Blanchard, and
J E Lowe
January 1981,
Journal of electrocardiology,
