Citations

The pathogenesis of certain types of focal cerebral ischemia, particularly episodes of focal cerebrovascular insufficiency, is not fully understood. Atherosclerosis, a relatively static process, commonly occurs without producing any neurologic phenomena. However, such episodes rarely occur in cerebral vascular systems unaffected by atherosclerosis. Atherosclerosis plus some transitory pathophysiologic event would explain the clinical events. A list of such events includes vasospasm, transitory systemic hypotension, kinking and external compression of vessels, transitory hypoglycemia, temporary shunts, and thrombosis and multiple emboli. The roles of polycythemia and anemia are mentioned. Evidence is presented that incriminates thrombosis or embolus formation (or both) as the process, secondary to atherosclerosis or associated with atherosclerosis, that produces the focal cerebral ischemia.

This has been a summary of the clinical patterns in certain types of cerebrovascular disease with emphasis on occlusive disease. Knowledge concerning these categories is important in studying the results of various therapeutic technics and in selecting the correct treatment for some subdivisions where effective therapy exists.

Cerebral infarction is attended by extravasation of blood in varying degrees. The present study was undertaken to learn whether anticoagulant therapy increases the extravasation and thereby diminishes or negates possibly favorable therapeutic effects. A series of experiments on dogs is described and the clinical implications are discussed.

Cerebral infaretion currently is the third leading cause of death in the United States. Since atherosclerosis of the cerebral arteries is the basis for the majority of strokes, the authors undertook to define more accurately the distribution of such atherosclerosis, its relation to coronary atherosclerosis, and its relation to such other factors as hypertension, obesity, and cerebral infarction. The results of their study are presented here.

Considerable variation exists in the interplay of the factors influencing the occurrence of strokes and their final outcome. A final statement about the usefulness of anticoagulant drugs in the treatment of cerebrovascular disease must await further study. The current indications for their use include: (1) intermittent insufficiency of the basilar arterial system, (2) intermittent insufficiency of the internal carotid system, (3) thrombosis within the basilar arterial system, (4) recurrent cerebral emboli associated with a likely cardiac source and (5) possibly, recurrent cerebral thromboses.

AbstractVEGF induces vascular permeability (VP) in ischemic diseases and cancer, leading to many pathophysiological consequences. The molecular mechanisms by which VEGF acts to induce hyperpermeability are poorly understood and in vivo models that easily facilitate real-time, genetic studies of VP do not exist. In the present study, we report a heat-inducible VEGF transgenic zebrafish (Danio rerio) model through which VP can be monitored in real time. Using this approach with morpholino-mediated gene knock-down and knockout mice, we describe a novel role of phospholipase Cβ3 as a negative regulator of VEGF-mediated VP by regulating intracellular Ca2+ release. Our results suggest an important effect of PLCβ3 on VP and provide a new model with which to identify genetic regulators of VP crucial to several disease processes.