The influence of histamine and PGE2-induced hyperaemia and oedema on respiratory metabolism in normal human forearm skin

Abstract

Transcutaneous measurements of pO2 and pCO2 were made on the forearm skin after intradermal injection of histamine, PGE2, and saline. The mediators, used at concentrations which induce intense hyperaemia, did not modify the steady state tcpO2/pCO2 levels measured with a sensor head temperature of 44 degrees C when breathing air or hyperbaric (2ATA) oxygen. It was deduced that gas transport is unaffected by mediator-induced conditions in the skin. The rates of fall of tcpO2 and of rise of tcpCO2 after arresting the forearm circulation by cuff occlusion of the arm were significantly less at the histamine site than at the PGE2 and saline sites. The values over the PGE2 and saline injection sites were less than those over undisturbed skin. The dynamic tests of respiratory gas exchange indicate that the skin metabolic rate is reduced at all injection sites and the greatest effect was seen with histamine. Measurement of dermal thickness after saline injection has shown that the excess interstitial fluid persists at the time of maximal hyperaemia: this is further accentuated at the histamine site through active oedema formation. Accumulation of excess interstitial fluid (persistence of aqueous injection or oedema generated by the action of mediator) separates the tissue cells. The reduction in the number of cells per unit volume is sufficient to explain the observed reduction in oxygen consumption per unit volume of skin. It is concluded that the increased diffusional distances in mediator-induced oedema are unimportant for the respiration of otherwise normal tissues, but that oedema by reducing oxygen flux may contribute appreciably to the hypoxia of inflamed tissue infiltrated with metabolically active cells.

Dermal oedema assessed by high frequency ultrasound in venous leg ulcers

“…14 By increasing the distance between capillaries and target tissues, oedema may directly reduce oxygen and nutrient exchange and significantly impair skin metabolism. 10,12,36 Oedema could cause a rise in mechanical tissue tension and pressure, which ultimately causes tissue ischaemia, necrosis and ulceration. 13 Furthermore, in older people (patient ages: 53-75 years, median 62 in the present study) the skin is less elastic and less compliant, oedema cannot be easily accommodated and skin tension rises.…”

“…[6][7][8] So far, various theories have been developed to explain why oedema is associated with venous leg ulcers, and some studies have demonstrated that the oedema in the papillary dermis, a site of intensive metabolism in the skin, might be a more important mechanism underlying tissue injury and ulceration. [9][10][11][12][13][14][15][16] Because of this, new techniques to investigate the distribution of oedema in the skin are important.…”

A new device for assessing changes in skin viscoelasticity using indentation and optical measurement

“…Possibly, more common than the assessment of cardiac failure is the evaluation of the degree of hydration in a patient. A fast quantitative method of monitoring the fluid balance of a patient would be a useful tool in the hospital emergency room to help avoid the risks associated with intravenous rehydration of the dehydrated patient [previous work has shown that oedema due to over‐hydration can lead to venous eczema and ulceration, as the excess fluid increases the distance between tissue cells (41), reducing oxygen consumption (42, 43)]. The proposed device could fulfil this requirement by tracking changes in the viscoelastic properties in a particular patient over time.…”