A sphygmomanometer cuff is inflated above systolic pressure on a volunteer's arm for three minutes and then rapidly deflated. Forearm blood flow measured immediately after release is found to be several times greater than the resting value. This response is called reactive hyperemia, and its principal mediators are:
- A Reflex increase in sympathetic cholinergic vasodilator fibers
- B Increased circulating epinephrine acting on beta-2 receptors
- C Baroreceptor-driven reduction in systemic vascular resistance
- D Accumulated local metabolites and myogenic relaxation of arterioles distal to the occlusion ✓
Explanation
During arterial occlusion, metabolites such as adenosine, CO2, potassium and lactate accumulate, and arterioles relax myogenically because transmural stretch is absent. On release, these local mechanisms produce a flow debt repayment that exceeds control flow. The response persists in denervated limbs, which excludes neural explanations in options A and C, and circulating catecholamines contribute little to this purely local phenomenon.
Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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