The Role of humoral Agents Released by Platelet Aggregation in the Pathogenesis of Transient Ishchemic Attacks
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概要
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For the purpose of investigating the role of the humoral agents released by platelet aggregation in the pathogenesis of transient cerebral ischemic attacks (TIA), the products of platelet suspension which was aggregated by Thrombin was infused as a bolus into the internal carotid artery in rabbits. Before injection, formed elements were filtered off by the use of a milipore filter. The injected material was supposed to contain substances released by platelet aggregation, such as serotonin, histamin, ADP and so on as well as various prostaglandins, among which the existence of thromboxane A2(TXA_2)possessing a potent vasoconstricting effect was known.Before and after the injection, the cortical CBF(coCBF), EEG and systemic arterial pressure (SAP) were continuously monitored under controlled respiration. According to the pattern of response of coCBF following injection of Thrombin-added PRP (T-PRP), a total of 29 rabbits were divided into three groups. In the first group(7/29), the coCBF decreased markedly immediately after the injection, which was accompanied by supression of EEG. Such an ischemic change lasted for 5-10 minutes and then gradually subsided. In two additional rabbits which exhibited the same ischemic pattern, India ink was intravenously administered when the fall of coCBF was at its maximum. This revealed considerable non-filling of the capillary networks of the cerebral cortex in the injected side.The responsible agent for this remarkable cerebral ischemia was considered to be TXA_2.In the second group(9/29), a biphasic pattern (initial brief ischemia followed by more prolonged hyperemia) was observed. In the third group(13/29), transient but prominent hyperemia was observed. In the two latter groups, there were only slight supressions of EEG as compared to the first group. India ink perfusion of the brain, carried out in the two additional rabbits exhibiting this hyperemic pattern, revealed a patent cerebral microcirculation. This transient hyperemia seen in the second and the third groups was considered to be due to the action of some unknown substance which had a potent vasodilating effect. Recently found Prostacyclin (PGI.)was suggested as a possible agent which caused the hyperemic response. The result of the present study is considered to indicate that the dual control system of platelet aggregation and vascular tonus by TXA_2 and Prostacyclin as proposed by Moncada et al.^<14)>is also effective to the cerebral vessels.
- 日本脳神経外科学会の論文
著者
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Mii Koji
Department Of Emergency Medicine Faculty Of Medicine University Of Tokyo
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Asano Takao
Department Of Applied Chemistry Seikei University
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Sano Keiji
Department Of Hepato-biliary-pancreatic Surgery Japanese Red Cross Medical Center
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Tamura Akira
Department Of Biochemistry Kyoto Pharmaceutical University
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Tamura Akira
Department Of Neurosugery University Of Tokyo Hospital Tokyo Japan
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Asano Takao
Department Of Neurosugery University Of Tokyo Hospital Tokyo Japan
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Sano Keiji
Department Neurosurgery University Of Tokyo
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Sano Keiji
Department Of Neurosugery University Of Tokyo Hospital Tokyo Japan
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Sano Keiji
Deparmtent Of Neurosurgery:faculty Of Medicine University Of Tokyo
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