Areas Of Forearm Skin Research Articles

A comparison of the effects of bath additives on the barrier function of skin in normal volunteer subjects

BACKGROUND: Emollients form an occlusive layer on the skin surface, reducing transepidermal water loss (TEWL), thus providing a temporary restoration of barrier function in compromised skin. This study evaluated the ability of three bath additives to reduce TEWL from compromised skin. METHODS: The stratum corneum on areas of forearm skin was removed by the repeated application of D-Squame discs. After 1 hour, baseline measurements ( t = 0) of TEWL were recorded before each arm was immersed for 10 min in a warm waterbath containing one of four treatments. The arms were air-dried for 20 min and the TEWL measurements repeated. Three further TEWL measurements were made at 30-min intervals. Measurements were made using a Tewameter in a controlled atmosphere. RESULTS: There was little difference between the products in terms of changes in mean TEWL values. However, when expressed relative to t = 0 values, some differences became apparent. The mean values for sites treated with Balmandol were lower than the other sites at 60, 90 and 120 min. When analysed by using the summary statistic AUC (area under the curve), the difference between Balmandol ® and water and also Balmandol and Eucerin ® was statistically significant ( p < 0.05). CONCLUSION: These results would suggest that Balmandol has a greater effect on barrier function (as assessed by measurement of a reduction in TEWL values) than Eucerin.

Evidence that the human cutaneous venoarteriolar response is not mediated by adrenergic mechanisms.

The venoarteriolar response causes vasoconstriction to skin and muscle via local mechanisms secondary to venous congestion. The purpose of this project was to investigate whether this response occurs through alpha-adrenergic mechanisms. In supine individuals, forearm skin blood flow was monitored via laser-Doppler flowmetry over sites following local administration of terazosin (alpha(1)-antagonist), yohimbine (alpha(2)-antagonist), phentolamine (non-selective alpha-antagonist) and bretylium tosylate (inhibits neurotransmission of adrenergic nerves) via intradermal microdialysis or intradermal injection. In addition, skin blood flow was monitored over an area of forearm skin that was locally anaesthetized via application of EMLA (2.5 % lidocaine (lignocaine) and 2.5 % prilocaine) cream. Skin blood flow was also monitored over adjacent sites that received the vehicle for the specified drug. Each trial was performed on a minimum of seven subjects and on separate days. The venoarteriolar response was engaged by lowering the subject's arm from heart level such that the sites of skin blood flow measurement were 34 +/- 1 cm below the heart. The arm remained in this position for 2 min. Selective and non-selective alpha-adrenoceptor antagonism and presynaptic inhibition of adrenergic neurotransmission did not abolish the venoarteriolar response. However, local anaesthesia blocked the venoarteriolar response without altering alpha-adrenergic mediated vasoconstriction. These data suggest that the venoarteriolar response does not occur through adrenergic mechanisms as previously reported. Rather, the venoarteriolar response may due to myogenic mechanisms associated with changes in vascular pressure or is mediated by a non-adrenergic, but neurally mediated, local mechanism.