Submitted on February 25, 2006
Accepted on February 16, 2007
CONTRIBUTION OF ANAEROBIC METABOLISM TO REACTIVE HYPEREMIA IN SKELETAL MUSCLE
Andras Toth1, Miklos Pal2, Marcos Intaglietta3, and Paul C Johnson4*
1 Department of Human Physiology, Semmelweis University, Budapest, Hungary
2 Human Physiology, Semmelweis University, Budapest, Hungary
3 Department of Bioengineering, University of California, San Diego, La Jolla, California, United States
4 Department of Bioengineering, University of California, San Diego, La Jolla, California, United States; Department of Physiology, University of Arizona, Tucson, Arizona, United States
* To whom correspondence should be addressed. E-mail: pjohnson{at}bioeng.ucsd.edu.
Elevated blood flow (reactive hyperemia) is seen in many organs after a period of blood flow stoppage. This hyperemia is often considered to be due in part to a shift to anaerobic metabolism during tissue hypoxia. The aim of this study was to obtain more definitive information on the relation between the hyperemia and anaerobic changes. For this purpose we measured NADH fluorescence at localized tissue areas in cat sartorius muscle during and following blood flow stoppage of 5 to 300 s. In parallel studies, red blood cell velocity was measured in venules. Tissue NADH fluorescence rose significantly with occlusions of 45 s or greater and reached a maximum at about 180 s. Arterial occlusions of up to 45 s duration induced successively greater peak values of the hyperemic response with little change in duration. Occlusions longer than 45 s increased the duration of elevated RBC velocity but not the peak value except at 300 s where a significantly higher peak and shorter duration was seen. With flow occlusions of 45 to 300 s both the time integral of increased NADH fluorescence and of reduced fluorescence following occlusion release showed a high degree of correlation with the additional hyperemia. We conclude that in this muscle anaerobic vasodilator metabolites are responsible for the increase in reactive hyperemia with arterial occlusions longer than 45 s. Since the durations of post-occlusion hyperemia and reduced fluorescence are substantially different, we speculate that vasodilator metabolite removal may be due to washout by the blood stream rather than metabolic uptake.
