Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels

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Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels. / Hauge, E M; Balling, E; Hartmund, T; Hjortdal, V E.

In: Plastic and Reconstructive Surgery, Vol. 99, No. 3, 03.1997, p. 825-33.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Hauge, EM, Balling, E, Hartmund, T & Hjortdal, VE 1997, 'Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels', Plastic and Reconstructive Surgery, vol. 99, no. 3, pp. 825-33. https://doi.org/10.1097/00006534-199703000-00032

APA

Hauge, E. M., Balling, E., Hartmund, T., & Hjortdal, V. E. (1997). Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels. Plastic and Reconstructive Surgery, 99(3), 825-33. https://doi.org/10.1097/00006534-199703000-00032

Vancouver

Hauge EM, Balling E, Hartmund T, Hjortdal VE. Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels. Plastic and Reconstructive Surgery. 1997 Mar;99(3):825-33. https://doi.org/10.1097/00006534-199703000-00032

Author

Hauge, E M ; Balling, E ; Hartmund, T ; Hjortdal, V E. / Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels. In: Plastic and Reconstructive Surgery. 1997 ; Vol. 99, No. 3. pp. 825-33.

Bibtex

@article{489263f4d87247f797da904323c508c5,
title = "Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels",
abstract = "Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.",
keywords = "Adenosine Triphosphate/metabolism, Animals, Arteries/physiopathology, Glucose-6-Phosphate/metabolism, Graft Survival/physiology, Rectus Abdominis/metabolism, Reperfusion Injury/etiology, Surgical Flaps/blood supply, Swine, Time Factors, Veins/physiopathology",
author = "Hauge, {E M} and E Balling and T Hartmund and Hjortdal, {V E}",
year = "1997",
month = mar,
doi = "10.1097/00006534-199703000-00032",
language = "English",
volume = "99",
pages = "825--33",
journal = "Plastic and Reconstructive Surgery",
issn = "0032-1052",
publisher = "Lippincott Williams & Wilkins",
number = "3",

}

RIS

TY - JOUR

T1 - Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels

AU - Hauge, E M

AU - Balling, E

AU - Hartmund, T

AU - Hjortdal, V E

PY - 1997/3

Y1 - 1997/3

N2 - Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.

AB - Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.

KW - Adenosine Triphosphate/metabolism

KW - Animals

KW - Arteries/physiopathology

KW - Glucose-6-Phosphate/metabolism

KW - Graft Survival/physiology

KW - Rectus Abdominis/metabolism

KW - Reperfusion Injury/etiology

KW - Surgical Flaps/blood supply

KW - Swine

KW - Time Factors

KW - Veins/physiopathology

U2 - 10.1097/00006534-199703000-00032

DO - 10.1097/00006534-199703000-00032

M3 - Journal article

C2 - 9047203

VL - 99

SP - 825

EP - 833

JO - Plastic and Reconstructive Surgery

JF - Plastic and Reconstructive Surgery

SN - 0032-1052

IS - 3

ER -

ID: 243522266