TY - JOUR

T1 - Blood flow autoregulation in pedicled flaps

AU - Bonde, Christian T

AU - Holstein-Rathlou, Niels-Henrik

AU - Elberg, Jens J

N1 - Keywords: Animals; Calcium Channel Blockers; Calcium Channels; Constriction, Pathologic; Homeostasis; Microcirculation; Nimodipine; Papaverine; Regional Blood Flow; Surgical Flaps; Sus scrofa; Vasodilator Agents

PY - 2009

Y1 - 2009

N2 - INTRODUCTION: Clinical work on the blood perfusion in skin and muscle flaps has suggested that some degree of blood flow autoregulation exists in such flaps. An autoregulatory mechanism would enable the flap to protect itself from changes in the perfusion pressure. The purpose of the present study was to evaluate if, and to what extent, a tissue flap could compensate a reduction in blood flow due to an acute constriction of the feed artery. Further, we wanted to examine the possible role of smooth muscle L-type calcium channels in the autoregulatory mechanism by pharmacological intervention with the L-type calcium channel blocker nimodipine and the vasodilator papaverine. MATERIAL AND METHODS: Pedicled flaps were raised in pigs. Flow in the pedicle was reduced by constriction of the feed artery (n=34). A transit time flow probe measured the effect on blood flow continuously. Following this, three different protocols were followed: (1) Time control (n=10): the procedure described above was repeated in the same flap to determine whether autoregulatory efficiency changed over time. (2) Nimodipine infusion (n=13): continuous intra-arterial infusion of nimodipine (0.2mg/ml, 0.5 ml/min) started when the flow had returned to the initial value. After stabilisation, the flow was reduced. When the flow had been stable for at least 5 min, the constriction was removed. (3) Nimodipine and papaverine (n=8): the infusion of nimodipine was followed by an intra-arterial bolus of papaverine (10mg). After stabilisation, the flow in the pedicle was reduced and the flow was recorded. RESULTS: The flaps showed a strong autoregulatory response with complete compensation for flow reductions of up to 70-80%. Infusion of nimodipine caused a 28+/-10% increase in blood flow and removed the autoregulation. Papaverine caused a further increase in blood flow by 61+/-19%. The time control experiments proved that the experimental procedure was reproducible and stable over time. CONCLUSIONS: A tissue flap can nearly completely compensate for repeated flow reductions of up to 70-80%. This is due to a decrease in the peripheral resistance, mediated by a local intrinsic mechanism. Nimodipine (a blocker of L-type voltage-activated calcium channels) abolishes the autoregulation, but a significant vasodilatory reserve exists, as an additional injection of papaverine (a smooth muscle relaxant) results in a further increase in the blood flow. This strongly suggests a direct role for voltage-activated calcium channels in the autoregulatory process.

AB - INTRODUCTION: Clinical work on the blood perfusion in skin and muscle flaps has suggested that some degree of blood flow autoregulation exists in such flaps. An autoregulatory mechanism would enable the flap to protect itself from changes in the perfusion pressure. The purpose of the present study was to evaluate if, and to what extent, a tissue flap could compensate a reduction in blood flow due to an acute constriction of the feed artery. Further, we wanted to examine the possible role of smooth muscle L-type calcium channels in the autoregulatory mechanism by pharmacological intervention with the L-type calcium channel blocker nimodipine and the vasodilator papaverine. MATERIAL AND METHODS: Pedicled flaps were raised in pigs. Flow in the pedicle was reduced by constriction of the feed artery (n=34). A transit time flow probe measured the effect on blood flow continuously. Following this, three different protocols were followed: (1) Time control (n=10): the procedure described above was repeated in the same flap to determine whether autoregulatory efficiency changed over time. (2) Nimodipine infusion (n=13): continuous intra-arterial infusion of nimodipine (0.2mg/ml, 0.5 ml/min) started when the flow had returned to the initial value. After stabilisation, the flow was reduced. When the flow had been stable for at least 5 min, the constriction was removed. (3) Nimodipine and papaverine (n=8): the infusion of nimodipine was followed by an intra-arterial bolus of papaverine (10mg). After stabilisation, the flow in the pedicle was reduced and the flow was recorded. RESULTS: The flaps showed a strong autoregulatory response with complete compensation for flow reductions of up to 70-80%. Infusion of nimodipine caused a 28+/-10% increase in blood flow and removed the autoregulation. Papaverine caused a further increase in blood flow by 61+/-19%. The time control experiments proved that the experimental procedure was reproducible and stable over time. CONCLUSIONS: A tissue flap can nearly completely compensate for repeated flow reductions of up to 70-80%. This is due to a decrease in the peripheral resistance, mediated by a local intrinsic mechanism. Nimodipine (a blocker of L-type voltage-activated calcium channels) abolishes the autoregulation, but a significant vasodilatory reserve exists, as an additional injection of papaverine (a smooth muscle relaxant) results in a further increase in the blood flow. This strongly suggests a direct role for voltage-activated calcium channels in the autoregulatory process.

U2 - 10.1016/j.bjps.2008.07.039

DO - 10.1016/j.bjps.2008.07.039

M3 - Journal article

C2 - 19223259

VL - 62

SP - 1671

EP - 1676

JO - Journal of Plastic, Reconstructive & Aesthetic Surgery (Print Edition)

JF - Journal of Plastic, Reconstructive & Aesthetic Surgery (Print Edition)

SN - 1748-6815

IS - 12

ER -