Mechanisms of the cause of pressure sore in skin blood vessels and its prevention

我们之前已经证明，在两种大鼠高血压模型中，动脉中胶原的合成和沉积增加。由于按重量计算，静脉中通常含有与动脉一样多的胶原蛋白，因此确定高血压对静脉胶原蛋白的影响是很有意义的。30周龄SHR和WKY的动脉血压分别为208(SY.+-)。[)3.3毫米汞柱和120(正弦+-)。[)分别为3.4 mm Hg。自发性高血压患者的静脉血压通常很低，并没有明显升高。[)3.0 MMH&lt；@D22@&>D2O)和WKY(-23()sy.+-.[)5.6 MMH&lt；@D22@&gt；D2O)。在自发性高血压大鼠，血压升高的动脉和肠系膜动脉的胶原合成和沉积(总胶原含量)增加。相比之下，血压仅轻微升高的下腔静脉和肠系膜静脉的胶原合成和沉积的任何标志物都没有改变。似乎对血管胶原合成的刺激是由动脉细胞压力增加的直接作用提供的，而不是由释放到全身循环的体液因子提供的。血压升高如何刺激动脉胶原合成和伴随的纤维化仍有待观察。

We have previously shown that, in two models of hypertension in rats, there is increased synthesis and deposition of collagen in the arteries. Since the veins normally contain as much collagen as the arteries on a weight-per-weight basis, it was of interest to determine the effects of hypertension on venous collagen. The arterial blood pressure of 30 weeks old SHR and WKY were 208(]SY.+-。[)3.3 mmHg and 120(]SY.+-。[)3.4 mmHg, respectively. The venous blood pressures were normally very low and were not significantly increased in SHR (-13(]SY.+-。[)3.0 mmH<@D22@>D2O) and WKY (-23(]SY.+-。[)5.6 mmH<@D22@>D2O). In SHR,it was shown that collagen synthesis (Prolyl hydroxylase activites) and deposition (total collagen content) are increased in the aorta and mesenteric arteries where blood pressure is elevated. By contrast, there were no alterations in any of the markers of collagen synthesis and deposition in vena cava and mesenteric veins, where blood pressure was only slightly elevated.It would appear that the stimulus for vascular collagen synthesis is provided by a direct effect of the increased pressure on the arterial cells rather than by a humoral factor released into the general circulation. It remains to be seen as to just how the increased blood pressure stimulates arterial collagen synthesis and the accompanying fibrosis.