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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory evoked response. This study tests the hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis. By microelectrode techniques, measurements of blood flow, extracellular activity of K+ and H+ as well as evoked potential were made in the baboon neocortex. Reductions in blood flow were obtained by occlusion of the middle cerebral artery and depression beyond the ischemic threshold of electrical function achieved by a reduction of systemic blood pressure which, in the ischemic zones, changed local cerebral blood flow proportionally. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 greater than 6 greater than 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal function is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH.
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PMID:Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. 1 21

Blood flow in the vertebral artery and the upper extremity was studied in five cases of Takayasu's arteritis with subclavian steal by use of ultrasonic Doppler flowmetry and finger plethysmography. The diagnosis of subclavian steal was made by observation of flow reversal in the vertebral artery on the subclavian steal side during grip exercise and, in addition, the vertebral flow change with brachial artery occlusion. The blood flow increase of both internal cartotid and non-affected (non-subclavian steal side) vertebral arteries during a common carotid compression was almost normal in patients with Takayasu's arteritis in this study. During carotid compression on the side of the subclavian steal, ipsilateral vertebral blood flow greatly decreased, and the amplitude the ipsilateral finger plethysmogram decreased slightly or moderately. It is suggested that there are significantly important factors in suppressing sumptoms of vertebrobasilar ischemia in these patients with Takayasu's arteritis with subclavian steal. These factors are believed to be (1) good function of the circle of Willis, (2) good blood supply to the brain stem, and (3) collateral circulation to the distal subclavian artery not via the vertebral artery.
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PMID:Subclavian steal in Takayasu's arteritis. A hemodynamic study by means of ultrasonic Doppler flowmetry. 1 35

Regional cerebral blood flow (rCBF) was measured in normotensive rate (NTR) and spontaneously hypertensive rats (SHR), in a lightly anesthetized state and with control of PaCO2 by artificial ventilation. Without carotid artery ligation, NTR and SHR showed almost identical rCBF values and distribution, despite significantly elevated levels of blood pressure in SHR. Bilateral carotid artery ligation, however, caused much more pronounced decreases of rCBF (ischemia) in SHR than NTR, in regions supplied by the carotid artery. The reduction of rCBF in SHR was rather homogenous and symmetrical. Mechanisms causing the differences between NTR and SHR are discussed.
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PMID:Effect of carotid artery ligation on regional cerebral blood flow in normotensive and spontaneously hypertensive rats. 1 64

Changes in cerebral cortex concentrations of high-energy phosphates, glycolytic metabolites, citric acid cycle intermediates, associated amino acids, and ammonia, were studied after 5, 15 and 30 min of incomplete ischemia in rats anesthetized with 70% N2O or 150 mg.kg-1 of phenobartibal. Previous results have shown that with this type of ischemia (bilateral carotid artery occlusion combined with reduction in blood pressure to 50 mm Hg) cortical blood flow is reduced to below 10% of nitrous oxide values, whether animals are anesthetized with 70% N2O or 150 mg.kg-1 of phenobarbital. In animals under 70% N2O, changes in tissue concentrations of phosphocreatine, ATP, ADP and AMP were similar to those previously obtained in complete ischemia. However, some glucose remained in the tissue, and the lactate concentrations gradually rose to reach excessive values. Changes occuring in glycolytic and citric acid cycle intermediates were similar to those seen in complete ischemia but, after 30 min, there was some reduction in the pool size of amino acids. In those animals given phenobarbital and which lost all EEG activity during ischemia, changes in cerebral metabolites were virtually identical to those observed in nitrous oxide-anesthetized animals. However, some animals exposed to 5 or 15 min of ischemia had some remaining EEG activity. In these, cerebral energy state was significantly less deranged, and levels of glycogen, glucose and pyruvate were higher.
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PMID:Effects of phenobarbital in cerebral ischemia. Part I: cerebral energy metabolism during pronounced incomplete ischemia. 2 84

In twenty dogs, anticoagulated with heparin 300 units/kg, the right cortical sensory evoked response (CSER) to contralateral median nerve stimulation was suppressed during 60 min ischemia induced by periodic infusion of 50 to 100 microliter increments of air via the right internal carotid artery. The post-ischemic recovery of the CSER was followed an additional 60 min in 19 of these animals divided into 2 groups. Ten dogs were subjected to glass-wool filtration of their blood by extracorporeal shunting from femoral artery to femoral vein for one hr prior to infusing air. Nine dogs did not receive glass-wool filtration. Post-ischemic recovery of CSER amplitude, a quantifiable electrophysiologic index of neuronal function, was significantly greater in the filtered group than in the non-filtered group. 14C-antipyrine autoradiographic blood flow studies were performed in 3 dogs. One was studied at the end of a 60 min ischemic CSER suppression period and showed severe flow disruption by air embolism. Two dogs, one from each group, were studied at the conclusion of the 60 min recovery period. In the filtered animal, cortical blood flow exceeded the threshold for CSER maintenance while cortical flow rates in the unfiltered animal fell below this threshold. The enhanced postischemic neuronal recovery in the filtered group as indicated by the CSER in attributed to the preservation of injury zone nutrient blood flow that is supported by collateral circulation.
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PMID:Extracorporeal glass-wool filtration of whole blood enhances post-ischemic recovery of the cortical sensory evoked response. 3 63

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.
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PMID:A new model of bilateral hemispheric ischemia in the unanesthetized rat. 3 14

Cerebral ischemia was produced by a combination of vascular occlusion and mild systemic hypotension in 2 groups of rabbits. Arterial blood pressure, arterial pH, arterial blood gases, blood glucose and PCV were monitored and recorded before, during and for 3 hours after reperfusion. Return of EEG activity, vasomotor control, spontaneous ventilation and corneal reflex were also recorded. At 4, 8, 12, 24 and 48 hours after reperfusion, the rabbits' neurologic status was assessed according to an arbitrary scale based on motor function. The 2 groups differed in return of reflexes and motor function. Eighty percent of the rabbits ischemic for 20 minutes and 75% of the rabbits ischemic for 30 minutes survived. The graduated response of motor function to cerebral ischemia is attributed to the ventilatory and circulatory support given the rabbits for the first 3 hours after reperfusion. The graduate response of motor function to ischemia supports the suggestion that motor function can be used as an index of neurologic damage.
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PMID:Survival of rabbits after prolonged cerebral ischemia. 3 15

Dopamine (DA), serotonin (5-HT), tryptophan (TRP), 5-hydroxyindole acetic acid (5-HIAA), and GABA were assayed spectrofluorometrically in various regions of 16 human post-mortem brains with acute and old cerebral infarction. In both recent and older strokes a total depletion of DA and 5-HT in the necrotic tissue was associated with mild reduction of these compounds in remote non-ischemic areas of the injured, and less of the contralateral cerebral hemispheres. 5-HIAA was significantly reduced in acute ischemic necrosis, while the perifocal edema zone showed considerable accumulation of both 5-HT and 5-HIAA. Marked elevation of the 5-HT precursor TRP and of GABA was present in both the necrotic center and perifocal edema of acute infarcts, which also showed a mild reduction of total proteins. The degradation zone surrounding old infarcts showed a mild decrease of both 5-HT and 5-HIAA with normal TRP levels, indicating normalization of the previously increased 5-HT metabolism and turnover after decrease of acute cerebral edema. These data which confirm previous studies in experimental cerebral ischemia and stroke indicate that disorders in the metabolism of brain monoamines and other putative neurotransmitters contribute to the development of postischemic brain damage and the complicating cerebral edema. They are also in keeping with the concept that unilateral focal ischemia produces bilateral effects on brain monoamines.
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PMID:Changes of some putative neurotransmitters in human cerebral infarction. 3 76

In cats air embolism of the brain was produced by injecting 0.6 ml blood foam into the innominate artery proximal to the origin of both common carotid arteries. Air embolism caused transient ischemia of the brain, reaching a maximum within 1 min after injection. Resolution of the air embolism began a few minutes later and was completed within 15 min in the center and within 30 min in the border zone of the main supplying arteries. During this phase tissue perfusion was inhomogenous with reduced flow rates in some areas and reactive hyperemia up to 300% in others. This resulted in venous hyperoxia and a decrease of arteriovenous oxygen difference to as low as 2 ml/100 ml blood. Reactive hyperemia was accompanied by brain swelling and an increase in intracranial pressure from 3.6 +/- 1.2 to 12.3 +/- 2.0 mm Hg. The reason for hyperemia was a decrease of cortical pH which fell from 7.33 +/- 0.03 to 7.03 +/- 0.05, and which caused a dilation of pial arteries up to 260%. Immediately after embolism, the EEG flattened and oxygen consumption decreased. After normalization of flow, oxygen consumption returned to normal, but EEG only partially recovered. Air embolism had little effect on the water and electrolyte content of the brain, and produced very little damage to the blood-brain barrier.
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PMID:Arterial air embolism in the cat brain. 4 47


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