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PROSTACYCLIN AND THROMBOXANE A(,2) I...
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SIMON, DAVID M.
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PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS).
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS)./
作者:
SIMON, DAVID M.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 1985,
面頁冊數:
124 p.
附註:
Source: Dissertation Abstracts International, Volume: 46-05, Section: B, page: 1525.
Contained By:
Dissertation Abstracts International46-05B.
標題:
Pharmacology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8514210
PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS).
SIMON, DAVID M.
PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS).
- Ann Arbor : ProQuest Dissertations & Theses, 1985 - 124 p.
Source: Dissertation Abstracts International, Volume: 46-05, Section: B, page: 1525.
Thesis (Ph.D.)--Rush University, College of Health Sciences, 1985.
The high incidence of vascular disease in patients with diabetes mellitus may be accounted for by an imbalance between platelet thromboxane (TX) synthesis and vascular prostacyclin (PGI(,2)) production. The influence of spontaneous diabetes, as seen in the Chinese hamster, on washed platelet TX synthesis, aggregation and vascular PGI(,2) synthesis was investigated using bioassay and radioimmunossay (RIA) techniques.Subjects--Topical Terms:
634543
Pharmacology.
PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS).
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PROSTACYCLIN AND THROMBOXANE A(,2) IN THE DIABETIC CHINESE HAMSTER (BLOOD PLATELETS).
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Source: Dissertation Abstracts International, Volume: 46-05, Section: B, page: 1525.
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Thesis (Ph.D.)--Rush University, College of Health Sciences, 1985.
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The high incidence of vascular disease in patients with diabetes mellitus may be accounted for by an imbalance between platelet thromboxane (TX) synthesis and vascular prostacyclin (PGI(,2)) production. The influence of spontaneous diabetes, as seen in the Chinese hamster, on washed platelet TX synthesis, aggregation and vascular PGI(,2) synthesis was investigated using bioassay and radioimmunossay (RIA) techniques.
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Washed diabetic platelets demonstrated an increased aggregation response to arachidonic acid (AA). The Ed(,50) for AA to induce platelet aggregation was 1.9 x 10('-6) M for diabetic platelets and 8.7 x 10('-6) M for control platelets. At a dose range of 10('-7) to 10('-4) M AA, washed platelets from diabetic hamsters produced from 37% to 124% more TA(,2) than did control platelets. Thrombin (0.05 - 1.00 units/ml) induced platelet TX production was 96% to 177% higher in platelet samples from diabetic hamsters, although no difference in aggregation was observed.
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Using in vitro bioassay techniques, diabetic aortas produced 9.2 (+OR-) 2.1 ng/mg tissue of PGI(,2) activity compared to 3.6 (+OR-) 0.9 ng/mg tissue produced by control aortas (p < 0.02). These data were confirmed using a specific RIA for the stable PGI(,2) metabolite, 6-keto PGF(,1)-alpha. Renal cortex specimens excised from diabetic hamsters produced decreased quantities of 6-keto PGF(,1)-alpha compared to control renal cortex. (Diabetic 0.26 (+OR-) 0.08 ng/mg tissue, control 0.34 (+OR-) 0.09 ng/mg tissue, x (+OR-) SEM, N = 6, p < 0.05.).
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These results indicate that diabetic Chinese hamster AA metabolism is enhanced leading to increases in platelet TX and aortic PGI(,2) production. However, PGI(,2) production in renal cortex is depressed, indicating regional differences in AA metabolism.
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