What question did this study set out to answer?

To determine whether shear-dependent venular nitric oxide production alters tone in adjacent arterioles and whether this pathway contributes to functional arteriolar dilation in contracting muscle.

August 1, 1996AJP Heart and Circulatory Physiology

Shear-dependent release of venular nitric oxide: effect on arteriolar tone in rat striated muscle

Q: What is the clinical evidence from this study?

Study design: Other. Intervention: Occlusion of one branch of an arcade venular bifurcation. Primary outcome: Arteriolar dilation.

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Key result

Shear-dependent increases in venular NO release dilated nearby arterioles by an average of 30% in resting muscle, but this mechanism did not contribute to sustained dilation during muscle contraction.

Population

Anesthetized rats (spinotrapezius muscle model)

Comparison

Occlusion of one branch of an arcade venular… vs Unoccluded state and absence of NO synthase…

Design

Preclinical

Authors

MBMatthew A. BoegeholdUniversity of Georgia

Discussion

Member takes

Implication

Venular-arteriolar NO signaling operates in resting muscle; leaves open its role in exercise hyperemia and human translation.

Key Points

To determine whether shear-dependent venular nitric oxide production alters tone in adjacent arterioles and whether this pathway contributes to functional arteriolar dilation in contracting muscle.
Assessed resting and contracting spinotrapezius muscle in anesthetized rats by occluding a branch of an arcade venular bifurcation with divergent flow to alter wall shear rate.
Quantified flow, shear rates, and paired arteriolar diameters before and after treatment with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine.
Venular branch occlusion increased parallel branch flow by an average of 99% and wall shear rate by 72%, inducing a 30% average dilation in paired arcade arterioles after 10–30 seconds that correlated with the shear rate rise.
Muscle contraction elicited a 73% to 97% dilation of arcade arterioles and increased arcade venular shear rate by 48% to 83%.
Inhibition with NG-monomethyl-L-arginine substantially attenuated arteriolar dilation induced by elevated venular shear rate in resting muscle, but produced no effect on arteriolar dilation in contracting muscle.

Structured PICO

Population

Anesthetized rats (spinotrapezius muscle model)

Intervention

Occlusion of one branch of an arcade venular bifurcation to increase shear rate, and administration of NO synthase inhibitor NG-monomethyl-L-arginine

Comparator

Unoccluded state and absence of NO synthase inhibitor

Outcome

Arteriolar dilation and venular shear ratesurrogate

Shear-dependent venular NO release dilates nearby arterioles in resting muscle but does not significantly contribute to sustained dilation during functional hyperemia in contracting muscle.

Cite This Study

Matthew A. Boegehold (1996) studied this question. Occlusion of one branch of an arcade venular bifurcation was evaluated on Arteriolar dilation. Shear-dependent increases in venular NO release dilated nearby arterioles by an average of 30% in resting muscle, but this mechanism did not contribute to sustained dilation during muscle contraction.

synapsesocial.com/papers/6a9a217edefad88af8fb479b https://doi.org/10.1152/ajpheart.1996.271.2.h387

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Shear-dependent release of venular nitric oxide: effect on arteriolar tone in rat striated muscle

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Shear-dependent release of venular nitric oxide: effect on arteriolar tone in rat striated muscle

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider