Our previous work indicates that myocardial ischemia could be the mechanism responsible for the left ventricular (LV) dysfunction that frequently develops after massive sympathetic nervous system (SNS) activation. In this study, coronary blood flow (CBF) and
myocardial ATP, creatine phosphate, and lactate concentrations
were measured after massively activating the SNS of anesthetized
rabbits with an intracisternal injection of veratrine. CBF was
measured at time 0 (baseline), and at 2, 10, and 20 min after
SNS activation in one group, and at 0, 45, 90, and 150 min in
a second group. Myocardial ATP, creatine phosphate, and lactate
were measured at 0, 2, 10, 20, 90, and 150 min in separate groups
of rabbits.
SNS activation caused LV dysfunction in 
60% of the rabbits. SNS-related increases in CBF kept pace with the increases
in myocardial energy demand as determined from the systolic
pressure-heart rate product. The subendocardial-to-subepicardial
blood flow ratio did not change significantly. Myocardial creatine
phosphate concentration was depressed 2 min after SNS activation
and remained depressed for at least 20 min.
ATP fell continuously and was significantly lower than baseline by 20 min. Tissue lactate concentration was elevated at this time. Jennifer M. Smith and Charles F. Pilati,1 Department of Physiology, Northeastern Ohio University College of Medicine, Rootstown, Ohio 44272
Experimental Biology and Medicine 227:125-132 (2002)
© 2002 Society for Experimental Biology and Medicine