Metabolic forearm vasodilation is enhanced following Bier block with phentolamine

Raman Moradkhan, Patrick McQuillan, Cynthia Hogeman, Andrea Leuenberger, Latoya Linton-Frazier, Urs A. Leuenberger

Research output: Contribution to journalArticle

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Abstract

The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O2 fraction = 0.1) before and after regional sympathetic blockade with the α-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with α-receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 ± 0.05 vs. 1.03 ± 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 ± 0.14 vs. 0.53 ± 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 ± 75 vs. 826 ± 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 ± 66 vs. 661 ± 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 ± 0.06 vs. 1.16 ± 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 ± 0.16 vs. 0.87 ± 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O2 saturation = 77 ± 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.

Original languageEnglish (US)
Pages (from-to)H2289-H2295
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume293
Issue number4
DOIs
StatePublished - Oct 1 2007

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Phentolamine
Forearm
Vasodilation
Ischemia
Doppler Ultrasonography
Hyperemia
Vasoconstrictor Agents
Vasodilator Agents
Blood Vessels
Arterial Pressure
Skeletal Muscle
Control Groups
Skin
Hypoxia

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Moradkhan, Raman ; McQuillan, Patrick ; Hogeman, Cynthia ; Leuenberger, Andrea ; Linton-Frazier, Latoya ; Leuenberger, Urs A. / Metabolic forearm vasodilation is enhanced following Bier block with phentolamine. In: American Journal of Physiology - Heart and Circulatory Physiology. 2007 ; Vol. 293, No. 4. pp. H2289-H2295.
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abstract = "The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O2 fraction = 0.1) before and after regional sympathetic blockade with the α-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with α-receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 ± 0.05 vs. 1.03 ± 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 ± 0.14 vs. 0.53 ± 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 ± 75 vs. 826 ± 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 ± 66 vs. 661 ± 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 ± 0.06 vs. 1.16 ± 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 ± 0.16 vs. 0.87 ± 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O2 saturation = 77 ± 1{\%}) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.",
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Metabolic forearm vasodilation is enhanced following Bier block with phentolamine. / Moradkhan, Raman; McQuillan, Patrick; Hogeman, Cynthia; Leuenberger, Andrea; Linton-Frazier, Latoya; Leuenberger, Urs A.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 293, No. 4, 01.10.2007, p. H2289-H2295.

Research output: Contribution to journalArticle

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T1 - Metabolic forearm vasodilation is enhanced following Bier block with phentolamine

AU - Moradkhan, Raman

AU - McQuillan, Patrick

AU - Hogeman, Cynthia

AU - Leuenberger, Andrea

AU - Linton-Frazier, Latoya

AU - Leuenberger, Urs A.

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N2 - The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O2 fraction = 0.1) before and after regional sympathetic blockade with the α-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with α-receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 ± 0.05 vs. 1.03 ± 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 ± 0.14 vs. 0.53 ± 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 ± 75 vs. 826 ± 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 ± 66 vs. 661 ± 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 ± 0.06 vs. 1.16 ± 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 ± 0.16 vs. 0.87 ± 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O2 saturation = 77 ± 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.

AB - The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O2 fraction = 0.1) before and after regional sympathetic blockade with the α-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with α-receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 ± 0.05 vs. 1.03 ± 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 ± 0.14 vs. 0.53 ± 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 ± 75 vs. 826 ± 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 ± 66 vs. 661 ± 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 ± 0.06 vs. 1.16 ± 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 ± 0.16 vs. 0.87 ± 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O2 saturation = 77 ± 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.

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