Changes in Endothelin-1, 6-Keto-PG-F1α, and TX-B2 in Random Pattern Flaps

Inoue, Hajime; Aihara, Masaki; Tomioka, Miyuki; Ishida, Hirotomo

doi:10.1097/00005344-199800001-00136

Cited by 7 publications

(8 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown a benefit of an ET-A-receptor antagonist in rats [5,15] and a nonselective combined ET-receptor antagonist in pigs [1]. However, no comparison with ET-B-receptor antagonists were preformed in those experiments.…”

Section: Discussionmentioning

confidence: 99%

“…Increased ET concentrations were found locally [4,[14][15][16][17] but not systemically [2,3] after surgical trauma inflicted by flap elevation. Therefore, the administration of ET-receptor antagonists might be ideal to improve local flap microcirculation by vasodilation without causing systemic hypotension, detrimental to the flap's perfusion pressure.…”

Section: Introductionmentioning

confidence: 88%

“…Therefore, the administration of ET-receptor antagonists might be ideal to improve local flap microcirculation by vasodilation without causing systemic hypotension, detrimental to the flap's perfusion pressure. ET-A-and combined ET-A-and ET-B-receptor antagonists proved to be beneficial in the prevention of ischemic tissue damage in acute [1] and chronic [5][6][7][8][9][10][11][12][13][14][15] experimental settings. However, no direct examination of the effect of ET-receptor blockade on the microvasculature and, hence, the microcirculation, i.e., the target of ETs, has been performed in these previous studies.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Selective blockade of endothelin-B receptor improves survival of critically perfused musculocutaneous flaps

Wettstein

Mörsdorf

Bächle

et al. 2007

Langenbecks Arch Surg

View full text Add to dashboard Cite

Background and aims Insufficient perfusion of distal flap areas, which may lead to partial necrosis, still represents a challenge in reconstructive surgery. In the process of microvascular and endothelial dysfunction, endothelins (ETs) and their receptors may play an important role. Therefore, the aim of the study was to investigate in a chronic in vivo model the effect of various ET-receptor antagonists in critically perfused flap tissue. Materials and methods A random pattern musculocutaneous flap was elevated in the back of 25 C57BL/6 mice and fixed into a dorsal skinfold chamber. Repetitive intravital fluorescence microscopy was performed over a 10-day observation period, assessing arteriolar diameter, arteriolar blood flow (aBF), functional capillary density (FCD), the area of tissue necrosis, and the development of newly formed blood vessels. ET-receptor blockers were administrated intraperitoneally 30 min before induction of ischemia, as well as daily during the subsequent 4-day period, including (1) BQ-123, a specific ET-A-receptor antagonist (ET-A=1 mg/kg), (2) BQ-788, a selective ET-B-receptor antagonist (ET-B=1 mg/kg), and (3) PD-142893, a nonselective ET-AB-receptor antagonist (ET-AB=0.5 mg/kg). Animals receiving saline only served as controls (n=7).Results Despite an increase in aBF during the 10-day observation period (day 1=1.92±0.29 nl/s; day 10=4.70±

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Selective blockade of endothelin-B receptor improves survival of critically perfused musculocutaneous flaps

Wettstein

Mörsdorf

Bächle

et al. 2007

Langenbecks Arch Surg

View full text Add to dashboard Cite

show abstract

“…11 Inoue et al showed that the administration of an ETA receptor antagonist, FR-139317, extended the survival length of the flap. 33 Wettstein et al showed that the administration of ET-B receptor antagonists is useful in the treatment of critically perfused flaps. 34 This study shows parallel results with the aforementioned studies.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Effect of Bosentan-Mediated Endothelin Receptor Blockade on Flap Survival in Rats: An Experimental Study

et al. 2016

View full text Add to dashboard Cite

Local skin flaps are important tools for performing plastic surgery. Skin flaps are used for closure of defects after tumor excision or in tissue losses after trauma. However, problems associated with these flaps are commonly encountered, particularly in areas of marginal necrosis. Bosentan is a vasodilator that exerts its effect through endothelin receptor blockade, and has been shown to prevent ischemic tissue damage. However, no reports have addressed the effect of bosentan on skin flaps. The aim of the study was to investigate the effects of bosentan, which may be applied clinically to promote survival of ischemic skin flaps. A modified McFarlane flap was elevated in the dorsum of 20 Albino Wistar rats with a width-to-length ratio of 3 to 10 cm, respectively, with the caudal base. Perioperatively, 0.9% of physiologic NaCl and injectable distilled water of identical volume were injected into rats in Group 1 (n = 10), and 5 mg/kg bosentan was injected intraperitoneally into rats in Group 2 (n = 10). All of the rats were followed up for 7 days postoperatively. The surviving parts of the flaps were measured at the end of day 7. Acute and chronic inflammation, amount of granulation tissue, fibroblast maturation, amount of collagen, and amounts of reepithelialization and neovascularization present in the ischemic zones of the distal parts of the flaps were evaluated histopathologically, and results were compared statistically. The mean flap survivals were 61.1% in Group 1 and 91.1% in Group 2; the percentage of the surviving flap area in Group 2 was higher than that in Group 1 (p < 0.005). In both groups, there was significantly less acute inflammation in the ischemic zones in Group 2 than in Group 1 (p < 0.005). No significant difference was found in the amounts of chronic inflammation and granulation tissue between the two groups (p > 0.005). Fibroblast maturation, amount of collagen, and amounts of reepithelialization and neovascularization investigated in Group 2 were statistically significantly higher than those in Group 1 (p < 0.005). We believe that bosentan may be used prophylactically to increase survival in risky skin flaps because it decreases ischemic necrosis distal to skin flaps, thus exerting favorable effects on flap survival.

show abstract

“…Surgical trauma may induce local vasospasm by stimulating the sympathetic nerve ending to release NE (30). The synthesis and release of endothelium-derived relaxing factors, such as prostacyclin and nitric oxide, may be reduced or the synthesis and release of endothelium-derived contracting factors, such as TxA 2 and ET-1, may be increased (2,3,7,9,13,18,22). Last but not least, reduced local blood flow due to vasospasm may also increase the thrombogenic nature of the suture lines of the vascular anastomosis.…”

mentioning

confidence: 99%

Amplification effect and mechanism of action of ET-1 in U-46619-induced vasoconstriction in pig skin

Pang

Huang

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The aim of this study was to investigate if a low concentration of endothelin-1 (ET-1; 8 x 10(-10) M) may amplify the skin vasoconstrictor effect of other vasoactive substances in the pathogenesis of skin vasospasm. Pig skin flaps (6 x 16 cm) were perfused with Krebs buffer equilibrated with 95% O(2) and 5% CO(2) at 37 degrees C and pH 7.4. Skin perfusion pressure measured by a pressure transducer and skin perfusion assessed by the dermofluorometry technique were used for assessment of skin vasoconstriction. We observed that ET-1 (8 x 10(-10) M) significantly amplified the concentration-dependent (10(-7)-10(-5) M) skin vasoconstrictor effect of norepinephrine. More importantly, we observed for the first time that this low concentration of ET-1 also amplified the concentration-dependent (10(-8)-10(-6) M) skin vasoconstrictor effect of the thromboxane A(2) mimetic U-46619, and this amplification effect of ET-1 was completely blocked by the protein kinase C (PKC) inhibitor chelerythrine (5 x 10(-6) M). Conversely, the PKC activator phorbol 12,13-dibutyrate (10(-7) M) amplified the vasoconstrictor effect of U-46619. Furthermore, the sensitivity of the skin vasculature to the vasoconstrictor effect of extracellular Ca(2+) in U-46619-induced skin vasoconstriction was significantly enhanced in the presence of 8 x 10(-10) M ET-1. Finally, the cyclooxygenase inhibitor indomethacin (5 x 10(-6) M) did not affect the amplification effect of ET-1 on U-46619-induced skin vasoconstriction. We conclude that a low concentration of ET-1 can amplify the skin vasoconstrictor effect of U-46619 independent of endogenous cyclooxygenase products, and the mechanism may involve activation of PKC and increase in sensitivity of the contractile apparatus to Ca(2+) in smooth muscle cells.

show abstract

Changes in Endothelin-1, 6-Keto-PG-F1α, and TX-B2 in Random Pattern Flaps

Cited by 7 publications

References 6 publications

Selective blockade of endothelin-B receptor improves survival of critically perfused musculocutaneous flaps

Selective blockade of endothelin-B receptor improves survival of critically perfused musculocutaneous flaps

Evaluation of the Effect of Bosentan-Mediated Endothelin Receptor Blockade on Flap Survival in Rats: An Experimental Study

Amplification effect and mechanism of action of ET-1 in U-46619-induced vasoconstriction in pig skin

Contact Info

Product

Resources

About