Treatment of intraoperative middle cerebral artery occlusion with pentobarbital and extracranial-intracranial bypass

1979 ◽  
Vol 51 (5) ◽  
pp. 710-712 ◽  
Author(s):  
Pablo M. Lawner ◽  
Frederick A. Simeone
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Artery Occlusion ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ 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.

Posttraumatic bilateral middle cerebral artery occlusion

1975 ◽  
Vol 42 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Skip Jacques ◽  
C. Hunter Shelden ◽  
D. Thomas Rogers ◽  
Anthony C. Trippi
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Content Type ◽  
Pathophysiological Mechanisms ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The authors report a case of bilateral posttraumatic middle cerebral artery occlusion. Previously reported unilateral cases are reviewed and possible pathophysiological mechanisms disscussed.

Indomethacin-mediated improvement following middle cerebral artery occlusion in cats

1985 ◽  
Vol 62 (6) ◽  
pp. 874-881 ◽  
Author(s):  
Robert J. Dempsey ◽  
Mark W. Roy ◽  
Kathleen L. Meyer ◽  
David L. Donaldson
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Opposite Hemisphere ◽  
Content Type ◽  
Beneficial Effects ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ Focal cerebral ischemia initiates multiple detrimental effects in the brain. Chief among these are the regional development of ischemic edema, decreased local perfusion, altered neuronal function, and eventual infarction. To determine if pretreatment with the cyclo-oxygenase inhibitor, indomethacin, would result in improvement in these parameters, adult cats were given indomethacin or control solvent (4 mg/kg intraperitoneally twice daily) and were studied for periods up to 24 hours after right middle cerebral artery occlusion. The interaction of anesthetic agents with indomethacin was also examined in separate groups of experimental animals using pentobarbital and ketamine. In cats allowed to recover from pentobarbital anesthesia, indomethacin reduced gray and white matter edema at 6 and 24 hours after occlusion (p < 0.05). This was noted in densely ischemic areas (indomethacin = 84.3%, control = 87.5%), in “penumbra” regions (indomethacin = 82.5%, control = 85.3%), and in nonischemic zones (indomethacin = 81.5%, control = 82.3%) at 24 hours. Somatosensory evoked potential amplitude and central latency were also improved in the indomethacin group (p < 0.05), as was cerebral perfusion (p < 0.05). In animals anesthetized with continuous ketamine administration, cerebral edema and perfusion as well as evoked potentials were not significantly improved in any region by indomethacin. Regional cerebral blood flow in the group was increased by indomethacin in the nonischemic opposite hemisphere (indomethacin = 64.7 cc/100 gm/min, control = 48.5 cc/100 gm/min, p < 0.05), but not in the penumbra region of the ischemic hemisphere (indomethacin = 15.0 cc/100 gm/min, control = 18.6 cc/100 gm/min, p < 0.05), when measured 4 hours after occlusion. This suggested a steal phenomenon. Beneficial effects of indomethacin were evident in the presence of pentobarbital, but not after ketamine anesthesia. This suggests a synergism dependent on decreased arachidonic acid production from pentobarbitalstabilized membranes coupled with diminished production of cyclic endoperoxides from available arachidonate due to inhibition of cyclo-oxygenase with indomethacin.

Pathophysiology and treatment of focal cerebral ischemia

1992 ◽  
Vol 77 (3) ◽  
pp. 337-354 ◽  
Author(s):  
Bo K. Siesjö
Keyword(s):  
Free Radicals ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Lesion ◽  
Glutamate Antagonists ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.

Melatonin and calpeptin synergistically protect against post-reperfusion injury in a rat middle cerebral artery occlusion stroke model

2021 ◽  
Vol 4 (4) ◽  
pp. 592-612
Author(s):  
Ye Feng ◽  
Qian Xu ◽  
Raymond Tak Fai Cheung
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Reperfusion Injury ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Stroke Model ◽  
Cerebral Artery Occlusion

Cerebral ischemia induces oxidative injury and increases the intracellular calcium ion concentration to activate several calcium-dependent proteases such as calpains. Calpain activation leads to various necrotic and apoptotic processes. Calpeptin is a potent, cell-permeable calpain inhibitor. As a strong antioxidant and free radical scavenger, melatonin shows beneficial effect in rodent models of focal cerebral ischemia when given prior to ischemia or reperfusion. This study was focused on the neuroprotective effects of melatonin and/or calpeptin given after onset of reperfusion. For this purpose, right-sided middle cerebral artery occlusion (MCAO) for 90 minutes followed by 24 or 72 hours of reperfusion was performed in male Sprague Dawley rats, then, melatonin 50 or 150 µg/kg, calpeptin 10, 15 or 50 µg/kg or a combination of melatonin 50 µg/kg plus calpeptin 15 or 50 µg/kg were injected via an intracerebroventricular route at 15 minutes after onset of reperfusion. Melatonin or calpeptin tended to reduce the relative infarct volume and significantly decreased the neurological deficit at 24 hours. The combination achieved a greater protection than each of them alone. Melatonin, calpeptin or the combination all decreased Fluoro-Jade B (FJB)+ degenerative neurons and cleaved/total caspase-3 ratio at 24 hours. These treatments did not significantly impact the density of surviving neurons and ED-1+ macrophage/activated microglia. At the 72-hour-reperfusion, melatonin or the combination decreased the relative infarct volume and neurological deficit. Nevertheless, only the combination reduced FJB+ degenerating neurons at 72 hours. In conclusion, a combination of melatonin and calpeptin exerted synergistic protection against post-reperfusion injury in a rat MCAO stroke model.

Histochemical studies in the zone of ischemia following middle cerebral artery occlusion in cats

1972 ◽  
Vol 37 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Vance D. MacDonald ◽  
Thoralf M. Sundt ◽  
R. K. Winkelmann
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Enzyme System ◽  
Artery Occlusion ◽  
Tissue Reaction ◽  
Specific Enzyme ◽  
Content Type ◽  
Cerebral Artery Occlusion ◽  
Enzyme Changes

✓ Representative enzymes in brain were studied by histochemical techniques at intervals varying between 6 hours and 8 weeks after permanent middle cerebral artery occlusion in 18 cats. Unequivocal enzyme changes did not develop until 12 hours after occlusion, and no specific enzyme system was demonstrated to fail prior to others. That the ischemia of the first 6 hours is reversible in the cat was further substantiated by histological studies in a separate group of animals subjected to temporary middle cerebral artery occlusion for 6 hours. This study demonstrated progressive axonal changes, after the period of reversibility, bordering the core area of ischemia and resembling neural tissue reaction to injury in the spinal cord. Correlation of this study with previous biochemical determinations suggests that a self-induced and self-perpetuated toxicity might explain, in part, progressive changes in ischemic areas.

scholarly journals A Promising Approach to Integrally Evaluate the Disease Outcome of Cerebral Ischemic Rats Based on Multiple-Biomarker Crosstalk

2017 ◽  
Vol 2017 ◽  
pp. 1-10
Author(s):  
Guimei Ran ◽  
Yixuan Wang ◽  
Haochen Liu ◽  
Chunxiang Wei ◽  
Tao Zhu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Mathematic Model ◽  
Artery Occlusion ◽  
Disease Outcome ◽  
Multiple Biomarkers ◽  
Cerebral Artery Occlusion

Purpose. The study was designed to evaluate the disease outcome based on multiple biomarkers related to cerebral ischemia.Methods. Rats were randomly divided into sham, permanent middle cerebral artery occlusion, and edaravone-treated groups. Cerebral ischemia was induced by permanent middle cerebral artery occlusion surgery in rats. To form a simplified crosstalk network, the related multiple biomarkers were chosen as S100β, HIF-1α, IL-1β, PGI2, TXA2, and GSH-Px. The levels or activities of these biomarkers in plasma were detected before and after ischemia. Concurrently, neurological deficit scores and cerebral infarct volumes were assessed. Based on a mathematic model, network balance maps and three integral disruption parameters (k,φ, andu) of the simplified crosstalk network were achieved.Results. The levels or activities of the related biomarkers and neurological deficit scores were significantly impacted by cerebral ischemia. The balance maps intuitively displayed the network disruption, and the integral disruption parameters quantitatively depicted the disruption state of the simplified network after cerebral ischemia. The integral disruption parameteruvalues correlated significantly with neurological deficit scores and infarct volumes.Conclusion. Our results indicate that the approach based on crosstalk network may provide a new promising way to integrally evaluate the outcome of cerebral ischemia.

Induced seizures as therapy of experimental strokes in dogs

1971 ◽  
Vol 34 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Ronald R. Reed ◽  
Conrad Ciesel ◽  
Guy Owens
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Oxidative Metabolism ◽  
Collateral Circulation ◽  
Seizure Activity ◽  
Artery Occlusion ◽  
Content Type ◽  
Elevated Rate ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ Intracerebral pO2, as measured in normal dog brains by a modified mass spectrometer, was found to increase following seizure activity and remain elevated at least 2 hours. These results were found with both drug- and electrically-induced seizures. The pO2 increased to a greater degree in brain tissue rendered ischemic by middle cerebral artery occlusion. A transient reflex hypertension was observed with seizure activity, but hypertension alone failed to produce significant pO2 changes. Since oxidative metabolism has been shown by other investigators to proceed at an elevated rate during seizure activity, the increased pO2 must reflect improved collateral circulation following seizure activity.

High-soy diet decreases infarct size after permanent middle cerebral artery occlusion in female rats

2005 ◽  
Vol 289 (1) ◽  
pp. R103-R108 ◽  
Author(s):  
Derek A. Schreihofer ◽  
Khoi D. Do ◽  
Ann M. Schreihofer
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Estrogen Treatment ◽  
Cerebral Artery Occlusion

Estrogen is a powerful neuroprotective agent in rodent models of ischemic stroke. However, in humans, estrogen treatment can increase risk of stroke. Health risks associated with hormone replacement have led many women to consider alternative therapies including high-soy diets or supplements containing soy isoflavones, which act as estrogen receptor ligands to selectively mimic some of estrogen's actions. We hypothesized that a high-soy diet would share the neuroprotective actions of estrogen in focal cerebral ischemia. Female Sprague-Dawley rats were ovariectomized and divided into three groups: isoflavone-free diet + placebo (IF-P), isoflavone-free diet + estradiol (IF-E), or high-soy diet + placebo (S-P). Two weeks after being placed on diets, rats underwent left permanent middle cerebral artery occlusion (MCAO). Reductions in ipsilateral cerebral blood flow were equivalent across groups (∼50%). Twenty-four hours later neurological deficit was determined, and brains were collected for assay of cerebral infarct by TTC staining. In the IF-P rats MCAO produced a 50 ± 4% cerebral infarct. Estrogen and high-soy diet both significantly reduced the size of the infarcts to 26 ± 5% in IF-E rats and to 37 ± 5% in S-P rats. Analysis at five rostro-caudal levels revealed that estrogen treatment was slightly more effective at reducing infarct size than high soy diet. Overall neurological deficit scores at 24 h correlated with infarct size; however, there were no statistically significant differences among the treatment groups. These data show that 2 wk of a high-soy diet is an effective prophylactic strategy for reducing stroke size in a rat model of focal cerebral ischemia.

Quantitative measurement of neurological deficit after mild (30 min) transient middle cerebral artery occlusion in rats

2007 ◽  
Vol 1130 ◽  
pp. 181-187 ◽  
Author(s):  
Kouji Wakayama ◽  
Munehisa Shimamura ◽  
Masataka Sata ◽  
Naoyuki Sato ◽  
Koji Kawakami ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurological Deficit ◽  
Quantitative Measurement ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion
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