Clinical observations and physiological data supporting a vascular response as a mechanism of the novel wound-healing agent, OPAL A

Mitchell, G. K., Windeggar, T. and Russell, F. D. (2010). Clinical observations and physiological data supporting a vascular response as a mechanism of the novel wound-healing agent, OPAL A. In: Patricia A. Hebda, Wound Repair and Regeneration. Abstracts of: The 2nd Australasian Wound and Tissue Repair Society (AWTRS). Crossing the Boundaries. The 2nd Australasian Wound and Tissue Repair Society Annual Meeting. AWTRS 2010: Crossing the boundaries, Perth, WA, Australia, (A65-A65). 22-24 March 2010. doi:10.1111/j.1524-475X.2010.00600.x


Author Mitchell, G. K.
Windeggar, T.
Russell, F. D.
Title of paper Clinical observations and physiological data supporting a vascular response as a mechanism of the novel wound-healing agent, OPAL A
Conference name The 2nd Australasian Wound and Tissue Repair Society Annual Meeting. AWTRS 2010: Crossing the boundaries
Conference location Perth, WA, Australia
Conference dates 22-24 March 2010
Proceedings title Wound Repair and Regeneration. Abstracts of: The 2nd Australasian Wound and Tissue Repair Society (AWTRS). Crossing the Boundaries   Check publisher's open access policy
Journal name Wound Repair and Regeneration   Check publisher's open access policy
Place of Publication Malden, MA, U.S.A.
Publisher Blackwell Science
Publication Year 2010
DOI 10.1111/j.1524-475X.2010.00600.x
ISSN 1067-1927
1524-475X
Editor Patricia A. Hebda
Volume 18
Issue 4
Start page A65
End page A65
Total pages 1
Language eng
Formatted Abstract/Summary
OPAL A is paw paw pulp treated by a process involving heating and alkalinisation. The resultant filtrate is applied to wound surfaces and a 30% cream to the surrounding skin, daily. Preclinical data suggest effective wound resolution with this treatment regime in a range of wound types, in particular wounds where hypoperfusion at the arteriolar level contributes to the wound aetiology (eg diabetes, pressure ulcers, possibly arteriosclerosis). These findings indicate a possible vasodilator response to OPAL A. This paper will present clinical observational data suggesting the vasodilatory mechanism of action, and the physiological data supporting a potential mechanism of action.

We conclude that treatment of non-healing wounds with OPAL A increases local tissue perfusion, possibly due to vasodilation. OPAL A causes late onset oxidation of NA via a mechanism that is likely to involve enzyme activity and require the presence of metal ions. Although the oxidation of NA by OPAL A caused only a minor reduction in potency of NA in the thoracic aorta, a large conduit vessel, this might be expected to have an important impact on perfusion of the vascular bed if also observed in small diameter arterioles (not tested in this study).
© 2010 by the Wound Healing Society
Subjects 1103 Clinical Sciences
Q-Index Code EX
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Presented during Session IV: "Novel mechanisms of repair". Published as Abstract 28.

Document type: Conference Paper
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Created: Sun, 18 Jul 2010, 00:00:19 EST