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Biomedical subjects

J Choki

Publications and source records attributed to J Choki.

12 recordsLinked to original sources
PubMed1990

Cerebral blood flow, glucose utilization, and electrocorticograms following common carotid artery occlusion in gerbils.

We designed this study to elucidate the relations between cerebral function and glucose metabolism during the early stage of ischemia. We induced focal cerebral ischemia in 28 gerbils by occluding the common carotid artery. We recorded electrocorticograms in 34 gerbils by positioning bipolar electrodes between the anterior and middle cerebral arteries. We related the electrocorticograms to local cerebral glucose utilization measured with [14C]2-deoxyglucose in half the gerbils. A characteristic pattern (a zone of markedly decreased [14C]2-deoxyglucose uptake surrounded by a narrow band of greatly increased uptake) was observed on the autoradiogram in nine of the 14 experimental gerbils (64%). An electrocorticogram recorded from such a band of increased uptake was characterized by transient suppression of electrical activity followed by partial or complete recovery, and local cerebral blood flow in gerbils showing this electrocorticographic type were variable (15.0-43.3 ml/100 g/min). An electrocorticogram recorded from the ischemic core and inner border of this band, even when [14C]2-deoxyglucose uptake was relatively high, was characterized by the complete disappearance of electrical activity just after occlusion; cerebral blood flow in gerbils that showed this electrocorticographic type were consistently less than 15.0 ml/100 g/min. Our investigation suggests that the transient disappearance of electrocorticographic activity in the periphery of ischemia, which has relatively high residual blood flow, may relate to the heterogeneity of glucose consumption during the early stage of ischemia.

Animals↗
PubMed1990

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.

Animals↗
PubMed1984

Clinical and neuroradiological analysis of thrombotic and embolic cerebral infarction.

The clinical and neuroradiological characteristics of cerebral thrombosis and cerebral embolism were established in 109 cases with nonembolic and 120 cases with embolic arterial occlusion of the brain. Cases with cerebral thrombosis due to occlusion of perforating branches were excluded from the study, to equalize the size of the involved arteries in the two groups. More than 60% of patients with cerebral embolism showed a level of consciousness lower than stupor, while less than 15% did so in the thrombotic group. Cortical signs such as aphasia, agnosia, conjugate deviation, etc., were more frequently seen in the embolic group. A mean size of the infarct on CT (Infarct-Index) was significantly larger, and a shift of the midline structure was more frequently noticed in the embolic group than in the thrombotic group. Accordingly, the patients with cerebral embolism showed more unfavorable outcome than those with thrombosis. Hyperdense area developed in 40% of cerebral embolism during the period of observation, while in only 2% of cerebral thrombosis. Recurrence of the attack was very common in cerebral embolism. Forty-four percent experienced more than two episodes of cerebral and/or systemic embolization; of these recurrences 51% (27% of all cases) occurred within 2 weeks before and/or after the present episode that caused the admission. The importance of atrial fibrillation as the source of emboli was reemphasized.

Adolescent↗
PubMed1983

The effect of antidepressant drugs on regional cerebral glucose utilization in the rat.

The 2-deoxyglucose (2-DG) technique is a potentially powerful method for assessing the effect of centrally acting drugs on local neuronal function in the brain. Since little is established on the effect of antidepressant drugs on local functional activity throughout the brain, we have employed this technique to study the effects of desmethylimipramine (DMI), a tricyclic antidepressant, and assessing the effect of centrally acting drugs on local neuronal function in the brain. Since little is established on the effect of antidepressant drugs on local functional activity throughout the brain, we have employed this technique to study the effects of desmethylimipramine (DMI), a tricyclic antidepressant, and assessing the effect of centrally acting drugs on local neuronal function in the brain. Since little is established on the effect of antidepressant drugs on local functional activity throughout the brain, we have employed this technique to study the effects of desmethylimipramine (DMI), a tricyclic antidepressant, and phenelzine, a monoamine oxidase inhibitor used clinically as an antidepressant, on local glucose utilization. The drugs were administered either as an acute dose, or repeatedly for 7 days, or chronically for 28 days. The local metabolic rate of glucose was determined in 30 regions of rat brain. Acute DMI increased glucose utilization in 11 regions whereas, in contrast, chronic DMI decreased glucose utilization in 7 regions of rat brain. Many of the areas affected are those of the telencephalon and diencephalon that receive prominent noradrenergic innervation. This is consistent with the notion that acute DMI treatment leads to enhanced and chronic DMI treatment leads to reduced noradrenergic functioning in the CNS. In contrast to these effects with DMI, phenelzine had little effects on glucose utilization either after acute or chronic dosing.

Animals↗
PubMedDate not supplied

Regional cerebral glucose metabolism during and after bilateral cerebral ischemia in the gerbil.

Cerebral metabolic rate for glucose (CMRG) was measured using the 14C-deoxyglucose technique in a stroke model of the gerbil produced by bilateral common carotid artery occlusion. During 30 minutes of ischemia, 14C-deoxyglucose uptake in the brain was increased along the border zone between the ischemic and nonischemic area and decreased in the ischemic areas. During the early stage of reperfusion (2 or 3 to 30 minutes), CMRG increased 50 to 150% in the cerebral cortex, caudoputamen and thalamus and 270 to 320% in the hippocampus, globus pallidus and amygdala. During the late stage of reperfusion (15 to 45 minutes), heterogeneity of CMRG appeared in the cerebral cortex, caudoputamen and thalamus. CMRG decreased to less than 50% of the control value in the cerebral cortex but remained at 200 to 300% of control in the hippocampus, globus pallidus and amygdala. The latter structures exhibited a larger and more protracted increase in glucose metabolism than the other structures most probably due to the histological vulnerability to ischemia of these structures. The relationship between the transient increase of the glucose metabolism and cell function is discussed.

Animals↗
PubMedDate not supplied

Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil.

The correlation between cerebral glucose utilization and brain surface potassium concentration (BS-K+) was studied during reperfusion following bilateral cerebral ischemia in the gerbil. Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monitored by a potassium sensitive membrane electrode. BS-K+ increased from 3.0 +/- 0.6 mM (mean +/- S.D.) before ischemia to 58.7 +/- 17.3 mM 30 minutes after the occlusion of both common carotid arteries. The rate of decline of BS-K+ after release of occlusion differed between animals. Glucose utilization rate in the cerebral cortex immediately under the potassium electrode was low but homogeneous in 7 animals while in 5 animals the metabolic pattern was heterogeneous with areas of both low and high glucose metabolism. The former animals exhibited a fast recovery of potassium flux while the latter animals showed a slow recovery. Glucose utilization rate and potassium half recovery time were linearly correlated. These studies suggest that the reason that potassium flux may not recover rapidly in postischemic brain tissue is due to the lack of sufficient energy for a rapid re-establishment of the ion gradient across the cell due to the inefficient energy production of anaerobic glycolysis.

Animals↗
PubMedDate not supplied

Cerebrospinal fluid and arterial lactate, pyruvate and acid-base balance in patients with intracranial hemorrhages.

Lactate and pyruvate concentrations and acid-base balance in cerebrospinal fluid (CSF) and arterial blood were determined in patients with intracranial hemorrhages (28 subarachnoid hemorrhages and 15 intracerebral hemorrhages). A greater increase in CSF lactate and lactate-pyruvate ratio (L/P ratio) was observed in patients with impairment of consciousness, focal neurological deficits, poor prognosis, or CSF pressures higher than 300 mm H2O. A combination of CSF lactate greater than 2.5 mM per liter, L/P ration above 20, bicarbonate less than 20.4 mEq per liter, pH below 7.276, or arterial PCO2 below 31.5 mm Hg seems to indicate poor prognosis from intracranial hemorrhage. The mechanism of hyperventilation in acute cerebrovascular diseases and of CSF pH regulation in acid-base disturbances was also discussed.

Acid-Base Imbalance↗