Suppression of the reactive hyperemic response in the forearm due to local hand cooling

Forearm blood flow (FBF) was measured by electrical impedance plethysmography in order to identify the influence of local cooling of the contralateral hand after 3 min of arterial occlusion. Ten volunteers (six females, four males) were randomly assigned to the following three experimental conditions on separate days: a) 6 min of local hand cooling (5-7 degrees C); b) 3 min of arterial occlusion of the forearm; and c) combined arterial occlusion and local cooling.

All subjects experienced the typical pressor response during 6 min of hand cooling as evidenced by the significant increase (p < and = 0.05) in heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP). The FBF responses demonstrated an immediate increase (p < and = 0.05) within the first 30 s of hand submersion and then progressively declined over the next 5 min. The forearm vascular resistance (FVR = MAP/FBF) made an initial drop during the first 30 s of cooling and then gradually rose to reach peak levels between 5-6 min of cooling. With respect to the hyperemic response, FBF significantly increased (p < and = 0.05) from baseline (mean +/- SEM; 1.09 +/- 0.18 ml x 100 ml-1.min-1) and achieved peak levels (6.75 +/- 0.64 ml x 100 ml-1.min-1) within the initial 30 s of the post-occlusion period. Thereafter, FBF declined rapidly by 30-60 s (1.67 +/- 0.29 ml x 100 ml-1.min-1) and 60-90 s (1.26 +/- 0.33 ml x 100 ml-1.min-1) of the post-occlusion period.

When the reactive hyperemic response was coupled with hand cooling, FBF increased above baseline values and reached peak levels during the initial 30 s of the post-occlusion period. However, the magnitude of the hyperemic response was significantly lower in the cold condition compared to the hyperemia alone (3.20 +/- 0.42 vs 6.75 +/- 0.64 ml x 100 ml-1.min-1; p < and = 0.05). Clearly, the overall sympathetic response to local cooling had an overriding effect on the factors that promote peripheral vasodilation following brief periods (3 min) of arterial occlusion.