Mechanisms of the cause of pressure sore in skin blood vessels and its prevention
Project/Area Number |
08672620
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
応用薬理学・医療系薬学
|
Research Institution | Nagano College of Nursing |
Principal Investigator |
IWATSUKI Kazuhiko Nagano College of Nursing・Nursing, Professor, 看護学部, 教授 (20004666)
|
Co-Investigator(Kenkyū-buntansha) |
CHIBA Shigetoshi Shinshu University・School of Medicine, Professor, 医学部, 教授 (30004659)
|
Project Period (FY) |
1996 – 1997
|
Project Status |
Completed (Fiscal Year 1997)
|
Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1997: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1996: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | blood vessels / pressure sore / blood pressure / prolyl hydroxylase activity / total collagen content / コラーゲン生合成 / コラーゲン代謝 / プロリルハイドロキシラーゼ / 血管壁 |
Research Abstract |
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.
|
Report
(3 results)
Research Products
(6 results)