| Autor: |
Scott, Cynthia K., Persico, Francis J., Carpenter, Karen, Chasin, Mark |
| Předmět: |
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| Zdroj: |
Angiology; May1980, Vol. 31 Issue 5, p320-330, 11p |
| Abstrakt: |
It has been postulated that flunarizine's ability to increase tissue perfusion may be due to either antivasoconstrictor activity, or its effects on red blood cell deformability, or both. In studies reported here, the ability of flunarizine to influence human red blood cell membranes has been demonstrated in a number of systems: (1) Calcium accumulation in the red blood cell is related to a loss of deformability; flunarizine inhibited 45Ca accumulation in red blood cells with an 1C50 of 46 ± 7 μM. (2) Flunarizine caused a significant increase in deformability, as measured by its ability to decrease ischemia-induced hyperviscosity. (3) Flunarizine had the ability to prevent the discoid-echinocyte transformation induced by metabolic depletion in ischemic blood as a result of storage. These alterations in red blood cells can all be explained by the localization of one site of action of flunarizine in the membrane of red blood cells, resulting in an inhibition of calcium accumulation and maintenance of normal red blood cell deformability. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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