Platelet activation, as measured by the up-regulation of CD62p, is an early process, occurring not only within the dialyser, but across the entire length of the ECC. As CD62p remained unaltered after the administration of LMWH 10 min before the actual start of HD, this kind of activation is independent of LMWH. Considering PF4 however, a sharp increment was observed after the administration of LMWH and before the start of HD. This finding suggests that the PF4 release observed early in clinical HD is largely independent from the ECC, and is probably the result of LMWH-induced detachment from the endothelium. As the platelet serotonin content was relatively reduced and the plasma serotonin levels were elevated, platelets from chronic HD patients might be depleted due to chronic repetitive activation. Based on these data, it appears first, that PF4 is an inferior marker of platelet activation in clinical HD and second, that LMWH is a major contributor to HD-induced bio-incompatibility.
Regular fluctuations in pupil size of the cat were measured and the properties, nervous pathways, and origin of these oscillations were investigated. The rhythm of pupil movements under control conditions appeared to be either locked to the central respiratory cycle or to the artificial ventilatory cycle. These movements were only seen in lightly anesthetized or tranquilized cats, but not in alert or deeply anesthetized cats (ether, halothane or pentobarbital). The fluctuations proved to be independent of sympathetic innervation but related to variations in parasympathetic outflow. At least two sources for pupil oscillations appeared to be involved: central respiratory activity and respiratory blood pressure fluctuations that modulated pupil width via sinoaortic baroreceptors. Lung movements per se, as a third possible factor, did not modulate pupil width, whereas electrical stimulation of the afferent lung vagi did; therefore the role of this mechanical factor is not clear. A review of the pertinent literature shows that in the organism there are many phenomena exhibiting respiratory oscillations. It seems likely that these oscillations have the same origin as the respiratory pupil fluctuations.
Cortical spreading depression (CSD) is a wave of increased electrocortical activity and vasodilation, followed by sustained decreased activity and prolonged vasoconstriction. Although the discovery of CSD has been ascribed to Leão, rather than vasoconstriction, he only observed a depression of neural activity combined with vasodilation, with much weaker stimulation than used by his followers. There is a longstanding belief that CSD underlies migraine aura, with its positive symptoms such as mosaic patterns and its negative symptoms such as scotoma, and a similar propagation speed and vasoreaction pattern. However, there are many arguments against this theory. CSD is difficult to evoke in man, and electroencephalography (EEG) readings are not flattened during migraine (as opposed to EEG during CSD). Moreover, in contrast to CSD, migraine can occur bilaterally, and is not accompanied by a disrupted blood-brain barrier, increased cerebral metabolism, or cerebral cell swelling. Calcitonin gene-related peptide, which is thought to be characteristic of migraine pain, is increased in the blood from the external jugular vein during migraine in humans, but not during CSD in cats or rats. Moreover, CSD does not explain the appearance of premonitory symptoms or allodynia, long before the actual onset of aura. In addition, there is a variation in the pain mechanisms of migraine and CSD, and in their reaction to transcranial magnetic stimulation and several pharmacologic interventions. Finally, the origin of putative CSD in migraine is currently unknown.
In the presence of an arterial stenosis, COX-2 inhibitors enhance shear stress-induced platelet aggregation. This enhancement was prevented by low-dose clopidogrel but not by low-dose aspirin. Clopidogrel might therefore allow COX-2 inhibitors to be used without raising risk of thrombotic occlusion.
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