Patel S, Knapp C F, Donofrio J C, Salcido R
Center for Biomedical Engineering and the Department of Physical Medicine and Rehabilitation, University of Kentucky, Lexington 40536-0284, USA.
J Rehabil Res Dev. 1999 Jul;36(3):189-201.
The effect of varying local skin temperature on surface pressure-induced changes in skin perfusion and deformation was determined in hairless fuzzy rats (13.5+/-3 mo, 474+/-25 g). Skin surface pressure was applied by a computer-controlled plunger with corresponding skin deformation measured by a linear variable differential transformer while a laser Doppler flowmeter measured skin perfusion. In Protocol I, skin surface perfusion was measured without heating (control, T=28 degrees C), with heating (T=36 degrees C), for control (probe just touching skin, 3.7 mmHg), and at two different skin surface pressures, 18 mmHg and 73 mmHg. Heating caused perfusion to increase at control and 18 mmHg pressure, but not at 73 mmHg. In Protocol II, skin perfusion was measured with and without heating as in Protocol I, but this time skin surface pressure was increased from 3.7 to 62 mmHg in increments of 3.7 mmHg. For unheated skin, perfusion increased as skin surface pressure increased from 3.7 to 18 mmHg. Further increases in surface pressure caused a decrease in perfusion until zero perfusion was reached for pressures over 55 mmHg. Heating increased skin perfusion for surface pressures from 3.7 to 18 mmHg, but not for pressures greater than 18 mmHg. After the release of surface pressure, the reactive hyperemia peak of perfusion increased with heating. In Protocol III, where skin deformation (creep and relaxation) was measured during the application of 3.7 and 18 mmHg, heating caused the tissue to be stiffer, allowing less deformation. It was found that for surface pressures below 18 mmHg, increasing skin temperature significantly increased skin perfusion and tissue stiffness. The clinical significance of these findings may have relevance in evaluating temperature and pressure effects on skin blood flow and deformation as well as the efficacy of using temperature as a therapeutic modality in the treatment of pressure ulcers.
在无毛模糊大鼠（13.5±3个月，474±25克）中，测定了局部皮肤温度变化对表面压力引起的皮肤灌注和变形变化的影响。通过计算机控制的柱塞施加皮肤表面压力，用线性可变差动变压器测量相应的皮肤变形，同时用激光多普勒血流仪测量皮肤灌注。在方案I中，在不加热（对照，T = 28℃）、加热（T = 36℃）的情况下测量皮肤表面灌注，对照时（探头刚接触皮肤，3.7 mmHg），以及在两个不同的皮肤表面压力18 mmHg和73 mmHg下测量。加热使对照和18 mmHg压力下的灌注增加，但在73 mmHg时未增加。在方案II中，如方案I一样在有加热和无加热的情况下测量皮肤灌注，但这次皮肤表面压力以3.7 mmHg的增量从3.7增加到62 mmHg。对于未加热的皮肤，随着皮肤表面压力从3.7增加到18 mmHg，灌注增加。表面压力进一步增加导致灌注减少，直到压力超过55 mmHg时灌注降至零。加热使表面压力从3.7到18 mmHg时的皮肤灌注增加，但压力大于18 mmHg时则不然。表面压力释放后，灌注的反应性充血峰值随加热而增加。在方案III中，在施加3.7和18 mmHg期间测量皮肤变形（蠕变和松弛），加热使组织更硬，变形更小。结果发现，对于表面压力低于18 mmHg，皮肤温度升高会显著增加皮肤灌注和组织硬度。这些发现的临床意义可能与评估温度和压力对皮肤血流和变形的影响以及将温度用作治疗压疮的治疗方式的疗效有关。
