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W A Pulsinelli

Publications and source records attributed to W A Pulsinelli.

67 records · Page 4Linked to original sources
PubMed1982

Moderate hyperglycemia augments ischemic brain damage: a neuropathologic study in the rat.

We compared the effects of glucose injection with those of saline or mannitol on ischemic brain damage and brain water content in a four-vessel occlusion (4-VO) rat model, which simultaneously causes severe forebrain ischemia and moderate hindbrain ischemia. Glucose given before onset of ischemia was followed by severe brain injury, with necrosis of the majority of neocortical neurons and glia, substantial neuronal damage throughout the remainder of forebrain, and severe brain edema. By comparison, saline injection before forebrain ischemia resulted in only scattered ischemic damage confined to neurons and no change in the brain water content. Mannitol injection before 4-VO or D-glucose injection during or after 4-VO produced no greater forebrain damage than did the saline injection. Morphologic damage in the cerebellum, however, was increased by D-glucose injection given either before or during 4-VO. The results demonstrate that hyperglycemia before severe brain ischemia or during moderate ischemia markedly augments morphologic brain damage.

Animals↗
PubMed1980

Regional protein synthesis in rat brain following acute hemispheric ischemia.

Regional protein synthesis was measured in rat brain at intervals up to 48 h following occlusion of the four major arteries to the brain for either 10 or 30 min. Four-vessel occlusions produces ischemia in the cerebral hemispheres and oligemia in the midbrain-diencephalon and brainstem. During the hour following 10 min of ischemia, protein synthesis, measured by incorporation of [14C]valine into protein, was inhibited in the cerebral cortex by 67%. Normal rates of protein synthesis were attained within 4 h of recirculation. In rats subjected to 30 min of ischemia, protein synthesis was inhibited by 83% during the first hour of recirculation in the cortex, caudate-putamen, and hippocampus. Recovery of protein synthesis in these regions was slow (25-48 h). The midbrain-diencephalon showed less inhibition, 67%, and faster recovery (by 12 h). Protein synthesis was unaffected in the brainstem. [14C]Autoradiography revealed that the pyramidal neurons of the hippocampus and areas of the caudate and cortex failed to recover normal rates of protein synthesis even after 48 h. The accumulation of TCA-soluble [14C]valine was enhanced (55-65%) in the cortex, caudate, and hippocampus after 30 min of ischemia; the increase persisted for 12 h. A smaller rise in [14C]valine content (30%) and more rapid normalization of valine accumulation (by 7 h) were observed in the midbrain-diencephalon; no changes were found in the brainstem. In the cortex, recovery was more rapid when the duration of ischemia was reduced. Thus, the degree of inhibition of protein synthesis, the accumulation of valine in the tissue, and the length of time required to reestablish normal values for these processes were dependent on both the severity and the duration of the ischemic insult. Restoration of normal rates of protein synthesis after ischemia was slow compared with the normalization of cerebral energy metabolites.

Animals↗
PubMed1980

Glutathione and ascorbate during ischemia and postischemic reperfusion in rat brain.

Thirty minutes of total cerebral ischemia (decapitation) decreased total glutathione (GSH + GSSG) by 7% but had no detectable effect on the concentration of oxidized glutathione (GSSG), reduced ascorbate, or total ascorbate, In a model of reversible, bilateral hemispheric ischemia (four-vessel occlusion) no changes in glutathione or ascorbate were detected after 30 min of ischemia. During 24 h of reperfusion following such an insult no detectable change in total ascorbate, reduced ascorbate, or oxidized glutathione was noted: however, total brain glutathione declined by 25%. The findings are discussed in relation to the hypothesis that the deleterious effects of ischemia are due to an increase in free radical production which in turn leads to increased lipid peroxidation.

Animals↗
PubMed1979

Local cerebral glucose metabolism during controlled hypoxemia in rats.

2-Deoxy-[14C]glucose metabolism was examined in brains of hypoxic, normotensive rats by autoradiography, which revealed alternating cortical columns of high and low metabolism. Activity in white matter was increased severalfold over that in adjacent gray matter. The columns were anatomically related to penetrating cortical arteries with areas between arteries demonstrating higher rates of metabolism. The results suggest the presence of interarterial tissue oxygen gradients that influence regional glucose metabolism. The relatively greater sensitivity of white matter metabolism to hypoxia may lead to an understanding of white matter damage in postanoxic leukoencephalopathy.

Animals↗
PubMed1977

Painful tic convulsif.

Painful tic convulsif is a syndrome restricted to paroxysmal dysfunction of the fifth and seventh cranial nerves. It occurs primarily in women over the age of 50 years and is usually associated with an ectatic vertebrobasilar artery--less frequently an arteriovenous malformation or cholesteatoma--which compresses the trigeminal and facial nerve roots in the posterior fossa. In rare instances this syndrome may be caused by disseminated sclerosis. Because of the high incidence of posterior fossa lesions in painful tic convulsif, a complete neurological evaluation including computerised transaxial tomography and vertebrobasilar angiography should be performed in every case.

Aged↗
PubMedDate not supplied

Compartmentation of acid-base balance in brain during complete ischemia.

During near complete hyperglycemic brain ischemia, brain lactate levels rise in excess of 16-18 mmol/K and are associated with severe brain infarction. Analyses of pHo, Pt(CO2), and total brain lactate under these circumstances suggest that H+, HCO3, and lactate become unequally distributed between cells and the interstitial space and, perhaps, even between different types of brain cells. In addition, to whatever physiological advantages it may generate, such compartmentalization may be a factor leading to cell death in brain ischemia.

Acid-Base Equilibrium↗
PubMedDate not supplied

A new model of bilateral hemispheric ischemia in the unanesthetized rat.

A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described. During ether anesthesia the rat's vertebral arteries were electrocauterized through the alar foramina of the first cervical vertebra and reversible clasps placed loosely around the common carotid arteries. Twenty-four hr later, the awake rats were restrained and the carotid clasps tightened to produce 4-vessel occlusion. The carotid clasps were removed after 10, 20 or 30 min of 4-vessel occlusion and the animals killed by perfusion fixation 72 hr later. Rats which convulsed during the ischemic or post-ischemic period were excluded from further study. All rats subjected to 20 or 30 min of 4-vessel occlusion demonstrated ischemic neuronal damage. The H1 and paramedian hippocampus, striatum and layers 3, 5 and 6 of the posterior neocortex were the regions most frequently damaged. The advantages of this model are the ease of preparation of large numbers of animals, a high rate of predictable ischemic neuronal damage, a low incidence of seizures and the absence of anesthesia.

Animals↗
PubMedDate not supplied

Behavioral performance of rats following transient forebrain ischemia.

Rats subjected to transient forebrain ischemic injury by the method of four vessel occlusion (4-VO) develop irreversible injury to select populations of vulnerable neurons which include pyramidal cells in the CA-1 region of the hippocampus. This brain area is thought to be crucial for learning and memory. Rats subjected to 30 minutes of 4-VO, and then cerebral reperfusion were tested on a radial 8-arm maze task after they had recovered. The data shows that both 4-VO and control animals improve their performance over trials, but that 4-VO rats are impaired on "working" and "reference" tasks. The data suggest that 4-VO rats' impaired "working" performance is permanent, compared to their transient "reference" impairment. Alterations in sensorimotor activity could not account for these performance deficits since control and 4-VO rats demonstrated equivalent choice time per maze arm. Performance deficits in rats following forebrain ischemic injury may be similar to some of the cognitive deficits found in humans survivors of cerebral hypoxia-ischemia.

Animals↗