A comparison of cutaneous vascular responses to transient pressure loading in smokers and nonsmokers.
Smoking has been recognized as a risk factor for pressure ulcer development. This study investigated the hypothesis that smoking causes alterations in cutaneous vascular perfusion, which may contribute to this increased risk. With the use of the laser Doppler fluximetry (LDF), the adaptive vasodilatory response to a transient pressure load at the sacrum was measured in nine healthy female smokers and their age, sex, body mass index (BMI), and menstrual cycle matched nonsmoker controls. In all subjects, removal of the pressure load resulted in a reactive hyperaemic response. The total hyperaemic response was approximately 45% smaller in smokers compared to nonsmoker controls. The reduction was due to a shortening of the duration of the response predominantly through an increase in the rate of recovery from peak, which was twice as fast in the smokers (2.4 +/- 1.7 AU x seconds) compared with the nonsmoking controls (1.1 +/- 0.9 AU x seconds) (p < 0.005). We conclude that changes in the vascular responsiveness can be measured objectively at skin sites at risk of pressure ulcers. We have also shown that vascular responsiveness is altered in light smokers compared to control subjects. These preliminary data open the way for further investigation into the risk factors associated with pressure ulcer development.
School of Nursing and Midwifery and School of Medicine, University of Southampton, Southampton, United Kingdom.
Miriam
M
Noble
David
D
Voegeli
Geraldine F
GF
Clough
D000328:Adult; D015992:Body Mass Index; D005260:Female; D006801:Humans; D017078:Laser-Doppler Flowmetry; D011312:Pressure; D011336:Probability; D012016:Reference Values; D012039:Regional Blood Flow / Q000502:physiology*; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D012867:Skin / Q000098:blood supply*; D012881:Skin Temperature; D012907:Smoking / Q000009:adverse effects*; D018709:Statistics, Nonparametric; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology