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Energy-based vessel sealing remains a common alternative to traditional mechanical ligation procedures, despite considerable uncertainty as to the origin and stability of vascular adhesion forces. Evidence of conformal changes in Collagen IA has fostered support of denatured collagen as the origin of tissue adhesion; experimental observation suggests that while pure collagen fails to adhere, remaining vascular constituents play a critical adhesive role. This study initiates a constitutive model of adhesion forces in thermal fusion by determining the effects of glycosaminoglycan (GAG) content on the bursting pressure of thermally sealed vessels. GAG content of porcine splenic arteries was progressively altered via pre-fusion treatment in Chondroitinase ABC (ChABC) for 0-5h at 1U/mL (n=10/gp.), followed by fusion with the ConMed ALTRUS® thermal fusion device and subsequent strength testing. Sulfated GAG (sGAG) concentrations as quantified by the Dimethylmethylene Blue (DMMB) assay were reduced in ChABC-treated vessels (5h) by 73.8 ± 4.2 % as compared with untreated tissue. Bursting pressures of ChABC-treated vessels (5h) were significantly greater than those of control vessels (800.33 ± 54.34 mmHg and 438.40 ± 51.81 mmHg respectively, p=2.0e-04). Histology enabled qualitative visualization of the treated arterial cross-section and of the bonding interface. The negative correlation between GAG content and arterial seal strengths suggests that by resisting water transport, arterial GAG presence may inhibit adhesive interactions between adjacent cellular tissue layers during energy-based vessel sealing. By elucidating the components which facilitate or inhibit adhesion in thermal vessel sealing, this study provides an important step towards understanding the chemistry underlying fusion and evaluating its potential for expansion to avascular tissues.
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