title: The effect of vasoactive agents on post-pressure hyperemia.
abstract: The cutaneous hyperemic response following the release of direct pressure occlusion lasts much longer than the short-term hyperemia that occurs after proximal arterial occlusion. Post-pressure hyperemia may be an important mechanism to prevent pressure induced injury to the skin. The role of vasoactive mediators in modulating post-pressure hyperemia is unknown. In an effort to better understand this phenomenon, we performed an initial study using microdialysis infusion to measure the effect of several known mediators of vascular response on post-pressure hyperemia. A vise clamp was used to apply direct occlusive pressure to a laser Doppler sensor on the skin surface overlying the microdialysis fiber. Skin blood flow was measured continuously pre, during and post-occlusion while infusing the vasoactive substance or control phosphate buffer. Angiotensin II, Calcitonin gene related peptide and histamine had minimal effect on post pressure blood flow. Conversely, prostaglandin E1, prostaglandin E2, and L-NAME diminished the early phase of the post-occlusion hyperemic response. Perhaps the most profound effect we observed was the decrease in post-occlusive blood flow due to administration of epinephrine, dopamine and prostaglandin F2alpha. In contrast, adenosine and caffeine augmented blood flow post occlusion. In this initial survey study, we have demonstrated differential effects of various vascular mediators on the post-pressure hyperemic phenomenon. Our findings may lead to the development of agents to prevent pressure sores by augmenting the skin blood flow response to locally applied pressure.
authors: Creighton Diabetes Center, 601 North 30th Street, Omaha, NE 68131, USA.
authors: Anne
authors: A
authors: Belzowzki
authors: Dale
authors: D
authors: Bergren
authors: Alexandra
authors: A
authors: Brugler
authors: Brandon G
authors: BG
authors: Hillman
authors: Kyle C
authors: KC
authors: Hillman
authors: Shane R
authors: SR
authors: Hillman
authors: Brandon
authors: B
authors: Kuss
authors: Binh T
authors: BT
authors: Ngo
authors: Thomas
authors: T
authors: Pisarri
authors: Marc S
authors: MS
authors: Rendell
authors: Shaun L
authors: SL
authors: Thompson
authors: Scott A
authors: SA
authors: Turner
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000527:Alprostadil / Q000378:metabolism; D000818:Animals; D019540:Area Under Curve; D062186:Arterial Pressure; D002021:Buffers; D002110:Caffeine / Q000494:pharmacology; D015232:Dinoprostone / Q000378:metabolism; D004298:Dopamine / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D006801:Humans; D006940:Hyperemia / Q000188:drug therapy* / Q000378:metabolism; D017551:Microdialysis; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D010710:Phosphates / Q000737:chemistry; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology; D012867:Skin / Q000098:blood supply; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D002021:Buffers; D010710:Phosphates; D014662:Vasoconstrictor Agents; D002110:Caffeine; D000527:Alprostadil; D000241:Adenosine; D015232:Dinoprostone; D019331:NG-Nitroarginine Methyl Ester; D004298:Dopamine; D004837:Epinephrine