Nitric oxide synthase inhibition does not alter the reactive hyperemic response in the cutaneous circulation

Brett J. Wong, Brad W. Wilkins, Lacy Marie Alexander, Christopher T. Minson

Research output: Contribution to journalArticle

112 Citations (Scopus)

Abstract

Reactive hyperemia is the sudden rise in blood flow after release of an arterial occlusion. Currently, the mechanisms mediating this response in the cutaneous circulation are poorly understood. The purpose of this study was to 1) characterize the reactive hyperemic response in the cutaneous circulation and 2) determine the contribution of nitric oxide (NO) to reactive hyperemia. Using laser-Doppler flowmetry, we characterized reactive hyperemia after 3-, 5-, 10-, and 15-min arterial occlusions in 10 subjects. The total hyperemic response was calculated by taking the area under the curve (AUC) of the hyperemic response minus baseline skin blood flow (SkBF) {i.e., total hyperemic response = AUC - [baseline SkBF as %maximal cutaneous vascular conductance (CVCmax) x duration of hyperemic response in s]}. For the characterization protocol, the total hyperemic response significantly increased as the period of ischemia increased from 5 to 15 min (P < 0.05). However, the 3-min response was not significantly different from the 5-min response. In the NO contribution protocol, two microdialysis fibers were placed in the forearm skin of eight subjects. One site served as a control and was continuously perfused with Ringer solution. The second site was continuously perfused with 10 mM NG-nitro-L-arginine methyl ester (L-NAME) to inhibit NO synthase. CVC was calculated as flux/mean arterial pressure and normalized to maximal blood flow (28 mM sodium nitroprusside). The total hyperemic response in control sites was not significantly different from L-NAME sites after a 5-min occlusion (3,261 ± 890 vs. 2,907 ± 531% CVCmax·S). Similarly, total hyperemic responses in control sites were not different from L-NAME sites (9,155 ± 1,121 vs. 9,126 ± 1,088% CVCmax·S) after a 15-min arterial occlusion. These data suggest that NO does not directly mediate reactive hyperemia and that NO is not produced in response to an increase in shear stress in the cutaneous circulation.

Original languageEnglish (US)
Pages (from-to)504-510
Number of pages7
JournalJournal of Applied Physiology
Volume95
Issue number2
DOIs
StatePublished - Aug 1 2003

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Nitric Oxide Synthase
NG-Nitroarginine Methyl Ester
Hyperemia
Skin
Nitric Oxide
Area Under Curve
Laser-Doppler Flowmetry
Microdialysis
Nitroprusside
Forearm
Blood Vessels
Arterial Pressure
Ischemia

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Nitric oxide synthase inhibition does not alter the reactive hyperemic response in the cutaneous circulation",
abstract = "Reactive hyperemia is the sudden rise in blood flow after release of an arterial occlusion. Currently, the mechanisms mediating this response in the cutaneous circulation are poorly understood. The purpose of this study was to 1) characterize the reactive hyperemic response in the cutaneous circulation and 2) determine the contribution of nitric oxide (NO) to reactive hyperemia. Using laser-Doppler flowmetry, we characterized reactive hyperemia after 3-, 5-, 10-, and 15-min arterial occlusions in 10 subjects. The total hyperemic response was calculated by taking the area under the curve (AUC) of the hyperemic response minus baseline skin blood flow (SkBF) {i.e., total hyperemic response = AUC - [baseline SkBF as {\%}maximal cutaneous vascular conductance (CVCmax) x duration of hyperemic response in s]}. For the characterization protocol, the total hyperemic response significantly increased as the period of ischemia increased from 5 to 15 min (P < 0.05). However, the 3-min response was not significantly different from the 5-min response. In the NO contribution protocol, two microdialysis fibers were placed in the forearm skin of eight subjects. One site served as a control and was continuously perfused with Ringer solution. The second site was continuously perfused with 10 mM NG-nitro-L-arginine methyl ester (L-NAME) to inhibit NO synthase. CVC was calculated as flux/mean arterial pressure and normalized to maximal blood flow (28 mM sodium nitroprusside). The total hyperemic response in control sites was not significantly different from L-NAME sites after a 5-min occlusion (3,261 ± 890 vs. 2,907 ± 531{\%} CVCmax·S). Similarly, total hyperemic responses in control sites were not different from L-NAME sites (9,155 ± 1,121 vs. 9,126 ± 1,088{\%} CVCmax·S) after a 15-min arterial occlusion. These data suggest that NO does not directly mediate reactive hyperemia and that NO is not produced in response to an increase in shear stress in the cutaneous circulation.",
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Nitric oxide synthase inhibition does not alter the reactive hyperemic response in the cutaneous circulation. / Wong, Brett J.; Wilkins, Brad W.; Alexander, Lacy Marie; Minson, Christopher T.

In: Journal of Applied Physiology, Vol. 95, No. 2, 01.08.2003, p. 504-510.

Research output: Contribution to journalArticle

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N2 - Reactive hyperemia is the sudden rise in blood flow after release of an arterial occlusion. Currently, the mechanisms mediating this response in the cutaneous circulation are poorly understood. The purpose of this study was to 1) characterize the reactive hyperemic response in the cutaneous circulation and 2) determine the contribution of nitric oxide (NO) to reactive hyperemia. Using laser-Doppler flowmetry, we characterized reactive hyperemia after 3-, 5-, 10-, and 15-min arterial occlusions in 10 subjects. The total hyperemic response was calculated by taking the area under the curve (AUC) of the hyperemic response minus baseline skin blood flow (SkBF) {i.e., total hyperemic response = AUC - [baseline SkBF as %maximal cutaneous vascular conductance (CVCmax) x duration of hyperemic response in s]}. For the characterization protocol, the total hyperemic response significantly increased as the period of ischemia increased from 5 to 15 min (P < 0.05). However, the 3-min response was not significantly different from the 5-min response. In the NO contribution protocol, two microdialysis fibers were placed in the forearm skin of eight subjects. One site served as a control and was continuously perfused with Ringer solution. The second site was continuously perfused with 10 mM NG-nitro-L-arginine methyl ester (L-NAME) to inhibit NO synthase. CVC was calculated as flux/mean arterial pressure and normalized to maximal blood flow (28 mM sodium nitroprusside). The total hyperemic response in control sites was not significantly different from L-NAME sites after a 5-min occlusion (3,261 ± 890 vs. 2,907 ± 531% CVCmax·S). Similarly, total hyperemic responses in control sites were not different from L-NAME sites (9,155 ± 1,121 vs. 9,126 ± 1,088% CVCmax·S) after a 15-min arterial occlusion. These data suggest that NO does not directly mediate reactive hyperemia and that NO is not produced in response to an increase in shear stress in the cutaneous circulation.

AB - Reactive hyperemia is the sudden rise in blood flow after release of an arterial occlusion. Currently, the mechanisms mediating this response in the cutaneous circulation are poorly understood. The purpose of this study was to 1) characterize the reactive hyperemic response in the cutaneous circulation and 2) determine the contribution of nitric oxide (NO) to reactive hyperemia. Using laser-Doppler flowmetry, we characterized reactive hyperemia after 3-, 5-, 10-, and 15-min arterial occlusions in 10 subjects. The total hyperemic response was calculated by taking the area under the curve (AUC) of the hyperemic response minus baseline skin blood flow (SkBF) {i.e., total hyperemic response = AUC - [baseline SkBF as %maximal cutaneous vascular conductance (CVCmax) x duration of hyperemic response in s]}. For the characterization protocol, the total hyperemic response significantly increased as the period of ischemia increased from 5 to 15 min (P < 0.05). However, the 3-min response was not significantly different from the 5-min response. In the NO contribution protocol, two microdialysis fibers were placed in the forearm skin of eight subjects. One site served as a control and was continuously perfused with Ringer solution. The second site was continuously perfused with 10 mM NG-nitro-L-arginine methyl ester (L-NAME) to inhibit NO synthase. CVC was calculated as flux/mean arterial pressure and normalized to maximal blood flow (28 mM sodium nitroprusside). The total hyperemic response in control sites was not significantly different from L-NAME sites after a 5-min occlusion (3,261 ± 890 vs. 2,907 ± 531% CVCmax·S). Similarly, total hyperemic responses in control sites were not different from L-NAME sites (9,155 ± 1,121 vs. 9,126 ± 1,088% CVCmax·S) after a 15-min arterial occlusion. These data suggest that NO does not directly mediate reactive hyperemia and that NO is not produced in response to an increase in shear stress in the cutaneous circulation.

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