✓ The authors report and analyze the in vitro contractions of fresh bovine cerebral artery on exposure to blood. The vessel does not contract significantly until blood clots on its surfaces; the contraction begins at the moment of clotting and is maintained as long as extracellular calcium is available. Comparative studies with vasoconstrictor amines suggest that serotonin, liberated from platelets by the clotting process, is responsible for this contraction and that the adherent clot itself concentrates the serotonin on the surface of the vessel. This contraction persists throughout the “viability” of the in vitro preparation, approximately 10 hours. Serotonin is capable of producing this sustained contraction by increasing smooth muscle cell membrane permeability to extracellular calcium, which in turn activates native actinomycin.
Frederick A. Simeone and Philip Vinall
Pablo M. Lawner and Frederick A. Simeone
✓ A patient with a meningioma of the medial sphenoid wing underwent inadvertent intraoperative occlusion of the middle cerebral artery. Neurological deficit and infarction were presumably prevented by immediate administration of pentobarbital followed by extracranial-intracranial bypass.
Colin S. Doyle and Frederick A. Simeone
✓ A young man with a large sphenoid sinus mucocele developed hypopituitarism, headaches, and visual difficulties. Subsequently the lesion caused complete occlusion of both internal carotid arteries in the parasellar region. The headaches and visual difficulty improved after simple transoral drainage of the cyst.
Frederick A. Simeone and Herbert I. Goldberg
Steven J. Barrer, Frederick A. Simeone and Soo S. Han
✓ The case reported is that of an oligodendroglioma presenting only as a lump on the forehead. A thin convex area of bone was found overlying the tumor.
John P. Laurent, Pablo Lawner, Frederick A. Simeone and Eugene Fink
✓ Barbiturates were administered to normal dogs, establishing an isoelectric electrocorticogram. Cortical cerebral blood flows (CBF) and deeper CBF's were respectively measured by krypton-85 (85Kr) and xenon-133 (133Xe). Following barbiturate administration, the two methods of measuring CBF showed a poor coefficient of variation (r = 0.12, p < 0.05). The cortical flows decreased less than the fast compartment flows. A shifting of percentage contribution of flow to the slow compartment (60% increase, p < 0.001) was observed after barbiturate infusion. A selective shunting of blood flow to the slower areas may explain the lowering of intracranial pressure and protection of the deep white matter observed by many authors who use barbiturates in clinical and experimental situations.
James H. Wood, Lauri L. Snyder and Frederick A. Simeone
✓ Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with whole blood, a popular adjunct in the clinical prevention or therapy of the focal ischemic deficits of cerebral vasospasm and acute stroke, were studied in splenectomized dogs. Clipping of the right distal internal carotid and proximal middle cerebral arteries in eight dogs reduced regional cortical blood flow (rCoBF) by 49% to 58% without altering cardiac output (CO), and produced about 10% hemispheric infarction. Eight dogs underwent similar cerebral arterial occlusion and eight dogs underwent arterial manipulation without clipping. Both latter groups received two autologous whole blood infusions within 2 hours, each equal to 20% of the respective dog's total blood volume. Despite significant CO elevations after the infusions, rCoBF in the middle cerebral arterial territory did not rise. These whole-blood infusions did not significantly alter mean arterial blood pressure, hematocrit, intracranial pressure, or, in dogs with clipped cerebral arteries, the relative size of infarction.
These data suggest that nondilutional hypervolemia neither elevates collateral perfusion to ischemic regions of the brain nor reduces infarction. In addition, elevations in CO do not appear to augment blood flow in either ischemic or normal brain.
Frederick A. Simeone, Kevin G. Ryan and John R. Cotter
Elevation of cardiac output, regional cortical blood flow, and ICP after intravascular volume expansion with low molecular weight dextran
James H. Wood, Frederick A. Simeone, Eugene A. Fink and Michael A. Golden
✓ Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with low molecular weight dextran (LMD, molecular weight 40,000), an advocated adjunct in the clinical prevention or therapy of acute stroke and cerebral vasospasm, were studied in splenectomized dogs. Clipping of the right distal internal carotid artery and the proximal middle cerebral artery (MCA) in eight dogs decreased regional cortical blood flow (rCoBF) by 58% without changing cardiac output (CO), and caused 10% ± 5% (SE) hemispheric infarction. Ten other dogs underwent similar cerebral arterial occlusion and were infused twice with LMD within 2 hours; each infusion equaled 20% of the respective dog's total blood volume. Both CO and rCoBF in the territory of the occluded MCA increased significantly by 119% ± 13% and 42% ± 6%, respectively, following the two LMD infusions. Although the mean arterial blood pressure was unaltered, the hematocrit decreased significantly and the intracranial pressure (ICP) increased significantly. The mean hemispheric infarction in these 10 treated dogs was 4% ± 2%. Another nine dogs underwent arterial manipulation without clipping. Two hemodiluting LMD infusions, similar to those in the 10 dogs, significantly elevated CO and ICP but not rCoBF. These data suggest that hypervolemic hemodilution with LMD effectively elevates collateral perfusion to ischemic regions of brain distal to occluded MCA segments and concomitantly raises the CO and ICP.
James E. Lesnick, John J. Michele, Frederick A. Simeone, Steven DeFeo and Frank A. Welsh
✓ The somatosensory evoked potential (SEP) measured in response to median nerve stimulation was correlated with cortical and white matter cerebral blood flow (CBF), adenosine triphosphate (ATP), and lactate levels in 14 cats subjected to graded hemorrhagic hypotension following bilateral carotid artery ligation. Three additional cats served as controls. Regional CBF was determined by the hydrogen clearance method, and the time for conduction of the sensory stimulus from the thalamus to the cortex (the thalamocortical conduction time), was used to assess SEP latency changes. A reproducible sequence of changes occurred in the SEP as ischemia developed. There was an early conduction delay that correlated well with mild white matter ischemia. Amplitude reductions in the SEP began as significant cortical ischemia occurred. The cortical SEP was abolished when white matter CBF and ATP fell to critical levels.