Relationship between brachial artery blood flow and total [hemoglobin+myoglobin] during post-occlusive reactive
Christopher M Bopp1, Dana K Townsend2, Steve Warren3
1Department of Kinesiology, The Pennsylvania State University, State College, PA 16803, USA; Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66503, USA.
The associations between macrovascular and microvascular responses reported previously during post-occlusive reactive hyperemia have been inconsistent. The purpose of this study was therefore to determine the temporal relationship between the reactive hyperemic responses within a conduit artery and the downstream microvessels. Conduit artery blood flow was measured in the brachial artery with pulsed Doppler ultrasound. A potential analog of microvascular flow, changes in skeletal muscle total[hemoglobin+myoglobin] (T[Hb+Mb]), was assessed with near-infrared spectroscopy (NIRS). We found a high degree of correlation between these two measures (r=0.91). Cross-correlation analysis revealed two distinct response patterns. In 10 of our 15 subjects there was time displacement between peak brachial artery blood flow (BABF) and T[Hb+Mb] responses; in the remaining 5 the peaks were coincident. Granger causality testing suggested that reactive hyperemia in the macrovessel determined hyperemia in the downstream microvessels in all 15 study subjects. Time constants for the on (τ1) and off (τ2) kinetics of each response were calculated; our initial hypothesis was that τ1 and τ2 for T[Hb+Mb] would correlate with τ1 and τ2 for BABF, respectively. However, only for τ2 was this observed (r=0.52; p<0.05). No similar relationship was observed for τ1. Adipose tissue thickness did not influence either time constant for T[Hb+Mb]. Taken together, our results show that the temporal characteristics of the hyperemic response in the conduit artery are qualitatively reflected in the downstream microvasculature, but mechanisms for quantitative differences remain to be identified.
The associations between macrovascular and microvascular responses reported previously during post-occlusive reactive hyperemia have been inconsistent. The purpose of this study was therefore to determine the temporal relationship between the reactive hyperemic responses within a conduit artery and the downstream microvessels. Conduit artery blood flow was measured in the brachial artery with pulsed Doppler ultrasound. A potential analog of microvascular flow, changes in skeletal muscle total[hemoglobin+myoglobin] (T[Hb+Mb]), was assessed with near-infrared spectroscopy (NIRS). We found a high degree of correlation between these two measures (r=0.91). Cross-correlation analysis revealed two distinct response patterns. In 10 of our 15 subjects there was time displacement between peak brachial artery blood flow (BABF) and T[Hb+Mb] responses; in the remaining 5 the peaks were coincident. Granger causality testing suggested that reactive hyperemia in the macrovessel determined hyperemia in the downstream microvessels in all 15 study subjects. Time constants for the on (τ1) and off (τ2) kinetics of each response were calculated; our initial hypothesis was that τ1 and τ2 for T[Hb+Mb] would correlate with τ1 and τ2 for BABF, respectively. However, only for τ2 was this observed (r=0.52; p<0.05). No similar relationship was observed for τ1. Adipose tissue thickness did not influence either time constant for T[Hb+Mb]. Taken together, our results show that the temporal characteristics of the hyperemic response in the conduit artery are qualitatively reflected in the downstream microvasculature, but mechanisms for quantitative differences remain to be identified.
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