RESUMO
OBJECTIVE: The immune response to an inflammatory stimulus is balanced and orchestrated by stimulatory and inhibitory factors. After a thermal trauma, this balance is disturbed and an excessive immune reaction with increased production and release of proinflammatory cytokines results. The nicotine-stimulated anti-inflammatory reflex offsets this. The goal of this study was to verify that transdermal administration of nicotine downregulates proinflammatory cytokine release after burn trauma. METHODS: A 30% total body surface area full-thickness rat burn model was used in Sprague Dawley rats (n = 35, male). The experimental animals were divided into a control group, a burn trauma group, a burn trauma group with additional nicotine treatment, and a sham + nicotine group with 5 experimental animals per group. The last 2 groups received a transdermal nicotine administration of 1.75 mg. The concentrations of tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 were determined in homogenates of hearts, livers, and spleens 12 or 24 hours after burn trauma. RESULTS: Experimental burn trauma resulted in a significant increase in cytokine levels in hearts, livers, and spleens. Nicotine treatment led to a decrease of the effect of the burn trauma with significantly lower concentrations of tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 compared to the trauma group. CONCLUSIONS: This study confirms in a standardized burn model that stimulation of the nicotinic acetylcholine receptor is involved in the regulation of effectory molecules of the immune response. Looking at the results of our study, further experiments designed to explore and evaluate the potency and mechanisms of the immunomodulating effects of this receptor system are warranted.
RESUMO
INTRODUCTION: Salvage rates of free flaps have been reported to be inversely related to the time interval between the onset of ischaemia and its clinical recognition. Consecutively, monitoring of free flaps remains of major importance. The aim of this study was to analyse the correlation of postoperative free flap microcirculation and free flap skin temperature as a potential tool of postoperative flap monitoring. HYPOTHESIS: Free flap skin temperature correlates to free flap capillary microcirculation. METHODS: Fifty-four free flaps were prospectively monitored during the study. Postoperative flap monitoring was performed using a regular digital infrared surface thermometer (Medisana FTD, Germany) simultaneously to microcirculatory assessment using combined Laser-Doppler and photospectrometry (Oxygen-to-see, Lea Medizintechnik, Germany). RESULTS: Mean microcirculatory blood flow was 105±35 arbitrary units (AU). Mean temperature was 34.9±2.2 °C. We found a significant correlation between free flap temperature and free flap capillary blood flow (Pearson correlation r=0.48; p<0.001) and postcapillary venous filling pressure (r=-0.32; p=0.021) in 54 free flaps. A 1 °C less free flap temperature was associated with a decrease of the mean microcirculatory capillary blood flow by 37 relative units. CONCLUSION: Our study demonstrates free flap skin temperature related to capillary microcirculation. Our primary hypothesis was confirmed. We postulate an acute temperature drop of 3 °C at the centre of the skin island as indicative of arterial thrombosis, whereas a 1-2 °C uniform temperature drop of the flap is indicative of venous compromise. Consecutively, free flap skin temperature assessment might be a reliable and inexpensive adjunct monitoring method in plastic reconstructive surgery to improve patients' safety.
