reactive hyperemia


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hyperemia

 [hi″per-e´me-ah]
an excess of blood in a part; called also engorgement. adj., adj hypere´mic.
active hyperemia (arterial hyperemia) that due to local or general relaxation of arterioles.
leptomeningeal hyperemia congestion of the pia-arachnoid.
passive hyperemia that due to obstruction of flow of blood from the area.
reactive hyperemia that due to increase in blood flow after its temporary interruption.
venous hyperemia passive hyperemia.

re·ac·tive hy·per·e·mi·a

hyperemia following the arrest and subsequent restoration of the blood supply to a part.

re·ac·tive hy·per·e·mi·a

(rē-ak'tiv hī'pĕr-ē'mē-ă)
Excess blood following the arrest and subsequent restoration of the blood supply to a part.

hyperemia

an excess of blood in a part.

active hyperemia, arterial hyperemia
that due to local or general relaxation of arterioles.
leptomeningeal hyperemia
congestion of the pia-arachnoid.
passive hyperemia
that due to obstruction to flow of blood from the area.
pulpal hyperemia
hyperemia of the tooth pulp.
reactive hyperemia
that due to increase in blood flow after its temporary interruption.
venous hyperemia
passive hyperemia.
References in periodicals archive ?
Postocclusive reactive hyperemia and thermal response in the skin microcirculation of subjects with spinal cord injury.
Amongst 18 % patients of 2nd group during conducting of test for reactive hyperemia it was registered the paradoxical vasoconstrictive reaction, indicating a more expressed endothelial dysfunction.
The primary outcome of interest for this pilot study was comparing the 6 week change in brachial artery vasodilator response to reactive hyperemia between the folic acid and placebo groups.
The noninvasive test, reactive hyperemia peripheral arterial tonometry (RH-PAT), measures how the volume of a fingertip changes as blood flows through it.
Forearm blood flow was measured during reactive hyperemia and reflected endothelium-dependent vasodilation.
Subsequently, peak flux (PF; in volts) was assessed during reactive hyperemia following a 3-min arterial occlusion induced by inflating a cuff around the arm to 200 mmHg.
The researchers found that the effects of HAGE on FMD and reactive hyperemia were entirely prevented by benfotiamine.
Endothelium-dependent and independent dilations were expressed as the percentage change in the brachial artery diameter from baseline to following reactive hyperemia and to following sublingual nitrate administration.

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