Ischemic and pressure-induced hyperemia

A comparison

Marc S. Rendell, Joana M. Wells

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Objective: There is reason to question whether hyperemia after pressure occlusion is caused solely by local ischemia. This study quantitatively compared the response to the two forms of occlusion on the finger. Design: Blood flow was measured by laser Doppler continuously before, during, and for 40 minutes after a 2-minute occlusion of flow at the finger dorsum and at the plantar surface of the finger tip (finger pulp), which has a much higher arteriolar density than the dorsum. Occlusion to the same low level was carded out either with a cuff at the base of the finger or by direct pressure of the laser Doppler probe head. Comparison experiments were performed with the probe head heated to 44°C to elicit maximal local vasodilation. Setting: Outpatient clinic. Participants: Eleven healthy volunteers. Main Outcome Measures: Magnitude and duration of skin blood flow after occlusion. Results: Cuff occlusion at the base of the finger produced a typical, short-lived hyperemic response at both finger dorsum and finger pulp. The peak level at finger dorsum was 17.6 ± 1.4mL/min/100g, approximately a twofold increase over the baseline flow level. The duration of the hyperemic response was 3.6 ± 0.8 minutes. The baseline flow at the finger pulp was three times greater than at the finger dorsum, and peak flow after occlusion was also three times higher (44.3 ± 2.6 mL/min/100g). The duration of hyperemia at finger pulp was 4.2 ± 0.9 minutes. After pressure occlusion at the finger dorsum the hyperemic peak was higher (26.7 ± 4.2 mL/min/100g;p <.05) and the duration of hyperemia was four times longer (16.9 ± 2.3 minutes; p <.01) than after cuff occlusion. At the finger pulp, the pressure-induced hyperemic peak was also greater than the peak after cuff occlusion (56.3 ± 1.7mL/min/100g; p <.05), with a longer duration than after cuff occlusion (11.1 ± 1.1min; p <.01). Thermal stimulation significantly reduced the differences between cuff- and pressure-induced occlusion. There was a slow increase in flow over the 40-minute monitoring period. The maximal flow reached was approximately 100mL/min/100g at both finger dorsum and finger pulp. At both sites, however, the maximal flow level was attained more rapidly than the control condition without prior occlusion. Conclusions: These results confirmed that the pressure-induced hyperemic response is greater and of longer duration than that produced by flow ischemia alone. Thermal stimulation essentially abolishes the differences, suggesting that there is a common mechanism of vasodilatation. The mechanistic differences between pressure-induced an ischemic hyperemia remain to be determined.

Original languageEnglish
Pages (from-to)1451-1455
Number of pages5
JournalArchives of Physical Medicine and Rehabilitation
Volume79
Issue number11
StatePublished - Nov 1998

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Hyperemia
Fingers
Pressure
Vasodilation
Lasers
Ischemia
Hot Temperature
Head
Ambulatory Care Facilities

All Science Journal Classification (ASJC) codes

  • Rehabilitation

Cite this

Ischemic and pressure-induced hyperemia : A comparison. / Rendell, Marc S.; Wells, Joana M.

In: Archives of Physical Medicine and Rehabilitation, Vol. 79, No. 11, 11.1998, p. 1451-1455.

Research output: Contribution to journalArticle

Rendell, Marc S. ; Wells, Joana M. / Ischemic and pressure-induced hyperemia : A comparison. In: Archives of Physical Medicine and Rehabilitation. 1998 ; Vol. 79, No. 11. pp. 1451-1455.
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abstract = "Objective: There is reason to question whether hyperemia after pressure occlusion is caused solely by local ischemia. This study quantitatively compared the response to the two forms of occlusion on the finger. Design: Blood flow was measured by laser Doppler continuously before, during, and for 40 minutes after a 2-minute occlusion of flow at the finger dorsum and at the plantar surface of the finger tip (finger pulp), which has a much higher arteriolar density than the dorsum. Occlusion to the same low level was carded out either with a cuff at the base of the finger or by direct pressure of the laser Doppler probe head. Comparison experiments were performed with the probe head heated to 44°C to elicit maximal local vasodilation. Setting: Outpatient clinic. Participants: Eleven healthy volunteers. Main Outcome Measures: Magnitude and duration of skin blood flow after occlusion. Results: Cuff occlusion at the base of the finger produced a typical, short-lived hyperemic response at both finger dorsum and finger pulp. The peak level at finger dorsum was 17.6 ± 1.4mL/min/100g, approximately a twofold increase over the baseline flow level. The duration of the hyperemic response was 3.6 ± 0.8 minutes. The baseline flow at the finger pulp was three times greater than at the finger dorsum, and peak flow after occlusion was also three times higher (44.3 ± 2.6 mL/min/100g). The duration of hyperemia at finger pulp was 4.2 ± 0.9 minutes. After pressure occlusion at the finger dorsum the hyperemic peak was higher (26.7 ± 4.2 mL/min/100g;p <.05) and the duration of hyperemia was four times longer (16.9 ± 2.3 minutes; p <.01) than after cuff occlusion. At the finger pulp, the pressure-induced hyperemic peak was also greater than the peak after cuff occlusion (56.3 ± 1.7mL/min/100g; p <.05), with a longer duration than after cuff occlusion (11.1 ± 1.1min; p <.01). Thermal stimulation significantly reduced the differences between cuff- and pressure-induced occlusion. There was a slow increase in flow over the 40-minute monitoring period. The maximal flow reached was approximately 100mL/min/100g at both finger dorsum and finger pulp. At both sites, however, the maximal flow level was attained more rapidly than the control condition without prior occlusion. Conclusions: These results confirmed that the pressure-induced hyperemic response is greater and of longer duration than that produced by flow ischemia alone. Thermal stimulation essentially abolishes the differences, suggesting that there is a common mechanism of vasodilatation. The mechanistic differences between pressure-induced an ischemic hyperemia remain to be determined.",
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