Recent studies have demonstrated impaired skin hyperaemia to local injury in diabetes mellitus. In order to gain insight into the mechanisms of impaired hyperaemia, dose-response curves to intradermal substance P (25, 50, 100 pmol) and capsaicin (1.0, 2.5, 5.0 nmol) were examined before and after histamine blockade with chlorpheniramine, in 6 patients with uncomplicated Type 1 diabetes and 9 matched control subjects. Skin hyperaemia was measured indirectly as the peak laser Doppler flow in proximity to the area of hyperaemia. The response to the three doses of substance P was significantly lower in diabetic patients (0.37 +/- 0.12 (+/- SD), 0.51 +/- 0.12, 0.67 +/- 0.09 V) than in control subjects (0.57 +/- 0.15, 0.70 +/- 0.19, 0.84 +/- 0.21 V; p less than 0.01). In contrast there was no significant difference in skin hyperaemia to capsaicin between diabetic patients (0.41 +/- 0.07, 0.50 +/- 0.09, 0.59 +/- 0.09 V) and control subjects (0.41 +/- 0.06, 0.52 +/- 0.08, 0.63 +/- 0.07 V). Following chlorpheniramine, the response to capsaicin remained unaltered (0.39 +/- 0.07, 0.51 +/- 0.05, 0.60 +/- 0.07 in diabetic patients and 0.43 +/- 0.08, 0.50 +/- 0.10, 0.63 +/- 0.07 V in control subjects), but there was a significant reduction in hyperaemia to substance P in both patients (20.4 +/- 12.3% reduction, p less than 0.05) and control subjects (20.6 +/- 14.1% reduction, p less than 0.05). It is suggested that impaired skin hyperaemia may represent decreased vascular reactivity to locally released substance P from peripheral nerve fibres.
No takes yet. Share an insight, caveat, or question.
Boolell et al. (1990) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: