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Mechanisms of platelets-aggregation in the interaction between platelets and vascular walls
72 EFFECT OF PROPRANOLOL ON CYCLIC NUCLEOTIDES OF ISCHEMIC DOG HEART. 2nd Department of Internal Medicine, Nagoya K.Ogawa, T.Nakamura, K.Mori. University School of Medicine, Nagoya, Japan. Effects of ischemia on myocardial adenyl cyclase, phosphodiesterase and cyclic nucleotides (C-AMP & C-GMP) of dogs were studied. Enzymatic activities and concentrations of cyclic nucleotides were determined in the infarcted and non-infarcted area at the early stage following the ligation of coronary artery with or without propranolol administration. Adenyl cyclase activity was measured by the method of Krishna. Phosphdiesterase activity was assayed by the measurement of hydrolysis of C-AMP and cyclic nucleotides were assayed by a radioimmunoassay of Cailla et al. Adenyl cyclase activity in the infarcted area increased significantly compared with the non-infarcted area at 15 min and continued for 60 min. There was no change of phosphodiesterase activity in the infarcted area at the early stage of myocardial ischemia. The concentration of C-AMP in the both infarcted and non-infarcted area at 60 min was significantly higher than the sham operated control. That of C-GMP in the infarcted area also significantly elevated compared with control at 15 min. But, when propranolo1 was given , the concentration of C-AMP of the infarcted area at 6n min and that of non-infarcted area at 15 min and 60 min decreased significantly. While, the concentration of C-GMP of the infarcted area increased significantly compared with control at 15 min and 60 min. These results suggested that the stability of the ischemic cardiac muscle was induced by the administration of propranolol.
MECHANISMS OF PLATELETS-AGGREGATION IN THE INTERACTION BETWEEN PLATELETS AND VASCULAR WALLS. K. Okamoto, Y. Eshita and N. Shibata. Department of Internal Medicine, The Center for Adult Diseases, Osaka, Osaka, Japan. Recently, it has been well known that metabolites of arachidonic acid (A.A.) produced in platelets play an important role in the first step of thrombus formation and another metabolite of A.A. (prostacycline, PG12) in vascular walls inhibits platelets-aggregation. However, it is still unknown how the above mentioned metabolites of-A.A. do involve in platelets-aggregation. In this paper, mechanisms of platelets aggregation in the interaction between platelets and vascular walls were studied. In order to clarify the inhibitory mechanism of platelets-aggregation by vascular walls, bovine carotid arteries and human aorta were used with several agents acting on Ca2+. The results obtained were as follows: 1) Microsomes from arteries were capable of producing anti-aggregating substance (PGI2) even after 2 weeks in keeping at 4°C. 2) Platelets-aggregation was inhibited in the presence of a Ca2+-chelating agent or agents inhibiting Ca2+-influx into the cell and their effects were counteracted by an addition of CaC12. 3) Myosin B prepared by us from platelets lost its Ca2+ -sensitivity after washing with NaHC03 at 25°C which was characteristic of actomyosin from smooth muscle. And, the regulatory protein endowing the washed myosin B with Ca2+-sensitivity was isolated from the myosin B. 4) In electron microscope, it was shown that microfilaments consisting of actin were formed in aggregating platelets, but not formed in non-aggregating platelets. In summary, it was suggested that Ca2+influx into platelets is a key step in the aggregation studied.
MECHANISMS OF PLATELETS-AGGREGATION IN THE INTERACTION BETWEEN PLATELETS AND VASCULAR WALLS. K. Okamoto, Y. Eshita and N. Shibata. Department of Internal Medicine, The Center for Adult Diseases, Osaka, Osaka, Japan. Recently, it has been well known that metabolites of arachidonic acid (A.A.) produced in platelets play an important role in the first step of thrombus formation and another metabolite of A.A. (prostacycline, PG12) in vascular walls inhibits platelets-aggregation. However, it is still unknown how the above mentioned metabolites of-A.A. do involve in platelets-aggregation. In this paper, mechanisms of platelets aggregation in the interaction between platelets and vascular walls were studied. In order to clarify the inhibitory mechanism of platelets-aggregation by vascular walls, bovine carotid arteries and human aorta were used with several agents acting on Ca2+. The results obtained were as follows: 1) Microsomes from arteries were capable of producing anti-aggregating substance (PGI2) even after 2 weeks in keeping at 4°C. 2) Platelets-aggregation was inhibited in the presence of a Ca2+-chelating agent or agents inhibiting Ca2+-influx into the cell and their effects were counteracted by an addition of CaC12. 3) Myosin B prepared by us from platelets lost its Ca2+ -sensitivity after washing with NaHC03 at 25°C which was characteristic of actomyosin from smooth muscle. And, the regulatory protein endowing the washed myosin B with Ca2+-sensitivity was isolated from the myosin B. 4) In electron microscope, it was shown that microfilaments consisting of actin were formed in aggregating platelets, but not formed in non-aggregating platelets. In summary, it was suggested that Ca2+influx into platelets is a key step in the aggregation studied.