抄録
To clarify the mechanism of increasing platelet aggregation in ischemic diseases, the following experiments were carried out.
1) Maximum platelet aggregability (MPA) before and after O2 inhalation were estimated in 6 patients (2 a victim of strokes, 2 a victim of old myocardial infarctions, and 1 a victim of cor pulmonale, and 1 a victim of hypertensive) who were given O2 of 2 liter/min via nasal canal for dyspnea. After the O2 inhalation of 60 minutes, the ADP and epinephrine induced MPAs were suppressed compared to the MPAs before the inhalation. In the collagen induced MPAs of the same above condition, a decreasing trend was recognized.
2) The ADP induced and the epinephrine induced MPAs in the venous blood showed higher trends compared to the same two kinds of MPAs in the arterial blood, but in the collagen induced MPA, there were no differences found (between the venous and the arterial blood). MPAs were measured in 6 patients; 3 of whom were victims of cerebral thrombosis, 2 of whom were victims of ischemic heart diseases, and 1 who suffered from hypertensive.
3) The MPAs in the ischemic blood (by arm ligation) were defined in 10 healthy persons. After the 5 minute legations, the MPAs were suppressed.
4) After the O2 bubblings, the MPAs in 8 healthy persons increased.
After the N2 bubblings the MPAs did not change significantly, but after the CO bubblings, the MPAs decreased markedly.
