J Reconstr Microsurg 2001; 17(7): 535-544
DOI: 10.1055/s-2001-17756
Copyright © 2001 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Circulatory Changes After Prolonged Ischemia in the Epigastric Flap

Florian Fitzal1 , Daniela Valentini1 , Rainer Mittermayr1 , Artur Worseg2 , Ing Harald Gasser1 , Heinz Redl1
  • 1Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria
  • 2Ludwig Boltzmann Institute for Endoscopic Soft Tissue Surgery, Vienna, Austria
Further Information

Publication History

Publication Date:
12 October 2001 (online)

ABSTRACT

The circulation system seems to have early encounters with pathophysiologic processes during ischemia and reperfusion, such as overproduction of oxygen radicals, nitric oxide depletion, and leukocyte plugging. The aim of this study was to determine the superficial perfusion and vessel distribution of the epigastric flap with a laser Doppler Imaging (LDI) system during ischemia/reperfusion, and to observe the clinical outcomes 7 days after reperfusion in a separate set of animals. An epigastric flap from male Sprague-Dawley rats (320 to 380 g) was used to assess perfusion in sham animals (n=6) or in 12 hr-ischemia animals (12 hr of ischemia and 3 hr of reperfusion, n = 10) with the LDI system. In a separate experiment, flap size, flap failure index, and histologic sections of the flap from sham animals (n=6) and 12-hr ischemia animals (n=6) were evaluated 7 days after reperfusion. Evaluation of the vessel distribution demonstrated a diffuse picture of flap perfusion after clamp release. Moreover, in the distal portion of the flap, circulation stopped immediately, resulting in a significantly decreased perfusion in the 12-hr ischemia animals during reperfusion, when compared with pre-surgical values (100 percent) or sham animals (77 ± 26.5 vs. 108 ± 9.6 percent PU). On day 7, the flaps of animals after ischemia and reperfusion showed significant shrinkage, an increase in flap failure index, as well as necrosis, edema, and leukocyte infiltration. Based on the findings, the authors propose that, after prolonged ischemia, the circulation becomes diffuse, and ``no-reflow'' occurs in the distal portions of the myocutaneous flap during reperfusion. Perfused areas, assessed with the LDI early during reperfusion, might still become necrotic after several days. In the authors' flap model, edema formation and leukocyte infiltration seem to be related more to ischemia reperfusion damage than to thrombus formation.

REFERENCES

  • 1 Glicksman A, Ferder M, Casale P. 1457 years of microsurgical experience.  Plast Reconstr Surg . 1997;  100 355
  • 2 Khouri R K, Shaw W W. Reconstruction of the lower extremity with microvascular free flaps: a 10-year experience with 304 consecutive cases.  J Trauma . 1989;  29 1086
  • 3 Kasabian A K, Colen S R, Shaw W W, Pachter H L. The role of microvascular free flaps in salvaging below-knee amputation stumps: a review of 22 cases.  J Trauma . 1991;  31 495
  • 4 Freischlag J A, Hanna D. Superoxide anion release after ischemia and reperfusion.  J Surg Res . 1991;  50 565
  • 5 Reimer K A, Jennings R B, Tatum A H. Pathobiology of acute myocardial ischemia: metabolic, functional and ultrastructural studies.  Am J Cardiol . 1983;  52 72A
  • 6 Strock P E, Majno G. Microvascular changes in acutely ischemic rat muscle.  Surg Gynecol Obstet . 1969;  129 1213
  • 7 Gidlof A, Lewis D H. The relation of post-ischemic reperfusion impairment to the severity of ischemia in the tibialis anterior muscle of the rat.  Int J Microcirc . 1990;  9 187
  • 8 Smith A R, van Alphen B, Faithfull N S, Fennema N. Limb preservation in replantation surgery.  Plast Reconstr Surg . 1985;  75 227
  • 9 Carden D L, Granger D N. Pathophysiology of ischemia-reperfusion injury.  J Pathol . 2000;  190 255
  • 10 Kubes P, Suzuki M, Granger D N. Nitric oxide: an endogenous modulator of leukocyte adhesion.  Proc Natl Acad Sci USA . 1991;  88 4651
  • 11 Kubes P, Kurose I, Granger D N. NO donors prevent integrin-induced leukocyte adhesion but not P-selectin-induced rolling in postischemic venules.  Am J Physiol . 1994;  267 H931
  • 12 Kurose I, Wolf R, Granger D N. Modulation of ischemia/ reperfusion-induced microvascular dysfunction by nitric oxide.  Circ Res . 1994;  74 376
  • 13 Granger D N, Hollwarth M E, Parks D A. Ischemia reperfusion injury: role of oxygen derived free radicals.  Acta Physiol Scand [Suppl] . 1986;  548 47
  • 14 Bulkley G B. The role of oxygen free radicals in human disease processes.  Surgery . 1983;  94 407
  • 15 McCord J M. Oxygen-derived free radicals in postischemic tissue injury.  New Engl J Med . 1985;  312 159
  • 16 Lindsay T, Walker P, Mickle D, Romaschin A D. Measurement of hydroxy conjugated dienes after ischemia/reperfusion in canine skeletal muscle.  Am J Physiol . 1988;  254 H578
  • 17 Crake T, Poole-Wilson P. Evidence that calcium influx on reoxygenation is not due to cell membrane disruption in isolated rabbit heart.  J Mol Cell Cardiol . 1986;  18 31
  • 18 Punch J, Rees R, Cashmer B. Xanthin oxidase: its role in the no-reflow phenomenon.  Surgery . 1992;  111 169
  • 19 Chait L A, May J M, O'Brian B M, Hurley J V. The effects of perfusion of various solutions on the no-reflow phenomenon in experimental free flaps.  Plast Reconstr Surg . 1978;  61 421
  • 20 May J W, Chait L A, O'Brien B M, Hurley J V. The no-reflow phenomenon in experimental free flaps.  Plast Reconstr Surg . 1978;  61 256
  • 21 Frick A F, Baumhauer A, Baumeister R GH, Wiebecke B. Experimentelle Untersuchungen zum No-Reflow-Phänomen unter Prostacyclin.  Handchir Mikrochir Plast Chir . 1993;  25 296
  • 22 Feng L J, Berger B E, Lysz T W, Shaw W W. Vasoactive prostaglandines in the impending no-reflow state: evidence for a primary disturbance in microvascular tone.  Plast Reconstr Surg . 1988;  81 755
  • 23 Rosen H M, Slivjak M J, McBrearty F X. Preischemic flap washout and its effect on the no-reflow phenomenon.  Plast Reconstr Surg . 1985;  76 737
  • 24 Arnold F, He C F, Jia C Y, Cherry G W. Perfusion imaging of skin island flap blood flow by scanning laser-Doppler technique.  Br J Plast Surg . 1995;  48 280
  • 25 Menger M D, Rücker M, Vollmar B. Capillary dysfunction in striated muscle ischemia/reperfusion: on the mechanisms of capillary ``no-reflow''.  Shock . 1997;  8 2
  • 26 Hickey M J, Hurley J V, Morrison W A. Temporal and spatial relationship between no-reflow phenomenon and postischemic necrosis in skeletal muscle.  Am J Physiol . 1996;  271 H1277
  • 27 Majno G, Ames A, Chiang J, Wright R L. No reflow after cerebral ischaemia.  Lancet . 1967;  2 569
  • 28 Fernando B, Young V L, Logan S E. Miniature implantable laser Doppler probe monitoring of free tissue transfer.  Ann Plast Surg . 1988;  20 434
  • 29 Engler R. Consequences of activation and adenosine-mediated inhibition of granulocytes during myocardial ischemia.  Federation Proc . 1987;  46 2407
  • 30 Allen D M, Chen L, Seaber A V, Urbaniak J R. Pathophysiology and related studies of the no reflow phenomenon on skeletal muscle.  Clin Orthop . 1995;  314 122
  • 31 Schmid-Schönbein G W. Capillary plugging by granulocytes and the no-reflow phenomenon in the microcirculation.  Federation Proc . 1987;  46 2397
  • 32 Marzella L, Jesudass R R, Manson P N. Functional and structural evaluation of the vasculature of skin flaps after ischemia and reperfusion.  Plast Reconstr Surg . 1987;  81 742
  • 33 Gidlöf A, Lewis D H, Hammersen F. The effect of prolonged total ischemia on the ultrastructure of human skeletal muscle capillaries: a morphometric analysis.  Int J Microcirc Clin Exp . 1987;  7 67
  • 34 Rücker M, Vollmar B, Menger M D. Association of capillary diameter response and nutritive perfusion failure postischemic striated muscle.  Adv Exp Med Biol . 1997;  428 305-310
  • 35 Jerome S N, Akimitsu T, Korthuis R J. Leukocyte adhesion, edema, and development of postischemic capillary no-reflow.  Am J Physiol . 1994;  167 H1329
  • 36 Jerome S N, Doré M, Paulson J C. P-selectin and ICAM-1-dependent adherence reactions: role in the genesis of postischemic no-reflow.  Am J Physiol . 1994;  266 H1316
  • 37 Jerome S N, Smith W, Korthuis R J. CD18-dependent adherence reactions play an important role in the development of the no-reflow phenomenon.  Am J Physiol . 1993;  264 H479
  • 38 Messina L M. In vivo assessment of acute microvascular injury after reperfusion of ischemic tibialis anterior muscle of the hamster.  J Surg Res . 1990;  48 615
  • 39 Barroso-Aranda J, Schmid-Schoenbein G W, Zweifach B W, Engler R L. Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock.  Circ Res . 1988;  63 437
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