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Clinical Observations and Physiological Data Supporting A Vascular Response as a Mechanism of the Novel Wound-Healing Agent, Opal A
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Clinical Observations and Physiological Data Supporting A Vascular Response as a Mechanism of the Novel Wound-Healing Agent, Opal A

G K Mitchell, Tanja Windegger and Fraser D Russell
Wound Repair and Regeneration, Vol.18(4), p.A65
Australasian Wound and Tissue Repair Society (AWTRS) Meeting, 2nd (Perth, Australia)
2010
DOI: https://doi.org/10.1111/j.1524-475X.2010.00600.x
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https://doi.org/10.1111/j.1524-475X.2010.00600.xView
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Abstract

Clinical Sciences vascular response Opal A wound healing
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 hypothesised that the observed response was caused by metabolism of noradrenaline (NA) by OPAL A, and we tested this by measuring the formation of oxidation products of NA at A490. OPAL A (10% solution) or NaHCO3 control was incubated with NA (2mM) for 3.7 h at 21 1C. OPAL A initially delayed the onset of oxidation b EOT1 h compared to control, but then gave rise to a markedly elevated oxidant response after 2-3.7 h incubation at 21 1C (A490 at 3.7 h; control, 0.37 ENQ 0.01; OPALA, 0.66 ENQ 0.03, n=6, Po0.0001). The oxidant response was attenuated by heat-treatment of OPAL A (100 1C, 10 min), abolished by incubation of the reaction mixture with DL-dithiothreitol (10mM), and delayed by a further 1.5 h by incubation with EDTA (1 mM). Pre-incubation of NA with OPAL A (3.7 h at 23 1C) caused only a small (o2 fold) decrease in potency of NA (8 nM-80 mM) for contraction of isolated rabbit thoracic aortic rings. 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).

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