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Biomedical subjects

E Han

Publications and source records attributed to E Han.

23 records · Page 2Linked to original sources
PubMed1992

[Non-activated platelet cytoplasmic ionized calcium in patients with acute ischemic stroke and healthy controls].

Non-activated platelet cytoplasmic ionized calcium was measured in Aequorin-loaded Gel-filtered platelets in 43 patients with acute ischemic stroke and 32 healthy controls. Platelet cytoplasmic ionized calcium is 2,596 +/- 0,674 mumol/L in controls, 3,370 +/- 1,339 mumol/L in the patients with acute ischemic stroke. Platelet cytoplasmic ionized calcium is increased in the stroke patients as compared to controls (P < 0.01). This indicates that there may be a lower threshold in platelet of stroke patient for activation. Moreover, increased platelet cytoplasmic ionized calcium may be a risk factor for thrombus propagation and aggravation of clinical manifestation.

Adult↗
PubMed1991

Endothelin-1 and human platelet activity.

Endothelin-1, a peptide produced by endothelium, causes vascular smooth muscle contraction possibly by mobilizing intracellular calcium. Shifts in ionized calcium may also play a role in platelet activation. Accordingly, the effects of endothelin on platelet ionized calcium and aggregation were studied. The measurements were made in aequorin-loaded gel-filtered human platelets derived from healthy donors. Endothelin even in a final concentration of 10(-6) M did not cause a measurable change in platelet ionized calcium or aggregation. When tested in combination with collagen, thrombin and platelet activating factor, endothelin showed no synergistic effect. These observations raise the possibility that endothelin may not interact with platelets in a physiologically significant way.

Adult↗
PubMed1991

[Effect of chronic antiplatelet treatment on platelet activating factor-induced platelet activity in stroke].

The effect of chronic antiplatelet treatment on PAF--induced platelet aggregation, ATP--release, and cytoplasmic ionized calcium was studied in 20 acute ischemic stroke patients. Chronic antiplatelet treatment failed to suppress these PAF--induced platelet responses. We speculate that selective PAF antagonists may be useful in suppressing PAF--induced platelet activation, and thereby possibly improve the treatment of stroke.

Adenosine Triphosphate↗