Differences of bioelectrical impedance in the development and healing phase of pressure ulcers and erythema in mouse model.

Pressure ulcers (PUs) are economically burdensome medical conditions. Early changes in pressure ulcers are associated with erythema. In this study, bioelectrical impedance was used to measure the differences between PUs and blanchable erythema. We divided 21 ICR mice into three groups: control, 1000 mmHg-1h, and 1000 mmHg-6h. Healthy skin, blanchable erythema, and PUs were induced on the dorsal skin. The results indicated an immediate increase in impedance, resistance, and reactance values in the pressure group after release, followed by a subsequent decrease until two days after release. Compared with the control group, impedance and reactance significantly increased by 30.9% (p < 0.05) and 30.1% (p < 0.01), respectively, in the 6 h-loading group immediately after release. One and two days after release, the 1 h-loading and 6 h-loading groups exhibited significantly different degrees of decline. One day after release, impedance and resistance decreased by 30.2% (p < 0.05) and 19.8% (p < 0.05), respectively, in the 1 h-loading group; while impedance, resistance, and reactance decreased by 39.2% (p < 0.01), 26.8% (p < 0.01), and 45.7% (p < 0.05), respectively, in the 6 h-loading group. Two days after release, in the 1 h-loading group, impedance and resistance decreased by 28.3% (p < 0.05) and 21.7% (p < 0.05), respectively; while in the 6 h-loading group, impedance, resistance, and reactance decreased by 49.8% (p < 0.001), 34.2% (p < 0.001), and 59.8% (p < 0.01), respectively. One and two days after release the pressure group reductions were significantly greater than those in the control group. Additionally, we monitored changes during wound healing. Distinguishing early PUs from blanchable erythema by noninvasive bioelectrical impedance technology may have applications value in early assessment of PUs.

Inhibition by intrathecal prazosin but not yohimbine of fentanyl-induced muscular rigidity in the rat.

We evaluated the effect of intrathecally administered prazosin, alpha 1-adrenoceptor antagonist, or yohimbine, alpha 2-adrenoceptor antagonist, on fentanyl-induced muscular rigidity. Adult, male Sprague-Dawley rats were anesthetized with ketamine and were under mechanical ventilation. Fentanyl given intravenously (100 micrograms/kg) or microinjected into the bilateral locus coeruleus (LC) (2.5 microgram/50 nl) consistently evoked a significant increase in the electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle. This implied muscular rigidity was appreciably antagonized by prior intrathecal (10 microliters) administration of prazosin (5 or 10 nmol), but not equimolar dose of yohimbine. These results suggest that the spinal alpha 1-adrenoceptors in the coerulospinal noradrenergic pathway play a key role in fentanyl-induced muscular rigidity.