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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using electron microscopy, we investigated the small arteries and veins in ischemic lesions induced by occlusion of the ostium of the middle cerebral artery in 42 rats. We observed endothelial denudation in the small arteries of rats receiving occlusion for greater than 6 hours. When the occluding cylinder was removed to allow for reperfusion, however, 2 hours of occlusion was sufficient for endothelial denudation to occur. Medial smooth muscle cells seemed to be more vulnerable to ischemia than endothelial cells because ultrastructural changes in the former cells preceded endothelial denudation. Moreover, endothelial denudation definitely exacerbated vascular changes so that medial necrosis appeared to be complete beneath the denuded areas, allowing erythrocytes, platelets, and exogenous tracers to penetrate into the cytoplasm of smooth muscle cells. These arterial lesions seemed to be repaired 10 days after removal of the occluding cylinder following 2 hours of occlusion. On the other hand, small veins in the ischemic lesion did not show endothelial denudation or medial necrosis. Our study suggests that arterial changes in ischemic lesions play a role in exacerbating the brain edema caused by recirculation after ischemia.
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PMID:Effect of recirculation on exacerbation of ischemic vascular lesions in rat brain. 202 94

The cerebral protective effect of eptazocine, an opioid mu-antagonist-kappa-agonist, was investigated using mice and rats subjected to ischemia. 1) Decapitation or concussive head injury (20 g, 30 cm)-induced ischemia in mice: Eptazocine (3,10 mg/kg) prolonged the gasping duration or the survival time in a dose-dependent manner. 2) Ischemic brain edema induced by bilateral carotid arterial occlusion (BLCO) in rats: Administration of eptazocine just after BLCO treatment significantly prevented the incidence of ischemic seizures, lethality and an increase in cerebral water content. 3) Acute ischemic changes in cerebral energy metabolism in mice: 2-min BLCO treatment decreased the cerebral contents of phosphocreatine and ATP, and it increased the contents of AMP and lactate, resulting in a 34% decrease in energy charge potential and an increase in lactate/pyruvate ratio. Such changes were improved by eptazocine (3, 10 mg/kg) and ethylketocyclazocine (3 mg/kg), a kappa-agonist. 4) Respiratory function in mouse brain mitochondria preparations: Eptazocine increased the State 3 respiration and respiratory control index (RCI:State 3/State 4), and it prevented a decrease in RCI induced by 3-min ischemia. These results suggest that eptazocine may improve cerebral ischemic disorders through an activation and/or protection of mitochondrial energy-producing systems.
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PMID:[Protective effect of eptazocine, a novel analgesic, against cerebral ischemia in mice and rats]. 205 80

The cerebral protective actions of a new thyrotropin releasing hormone (TRH) analogue, YM-14673, [Na-[[(S)-4-oxo-2-azetidinyl-carbonyl]-L-histidyl-L-prolinamide] dihydrate), were compared with those of CDP-choline (cerebral metabolic enhancer) and naloxone in rats rats subjected to unilateral carotid artery ligation and anoxic exposure (Levine rats). Drugs were administered intraperitoneally or orally 20, 80, and 140 min after anoxia. YM-14673 (0.03 to 1 mg/kg i.p. and 0.3 to 10 mg/kg p.o.) decreased the incidence of neurological deficits, such as hemiplegia and convulsion followed by coma and death, for 48 h after ischemia and anoxia. Both the increase in the brain water content and the degeneration of neurons in the cerebral cortex and thalamus were prevented by YM-14673 at a dose of 0.1 mg/kg (i.p.). CDP-choline (400 mg/kg i.p.), which is currently used in the therapy of cerebral vascular diseases, and naloxone (3 mg/kg i.p.) also decreased the incidence of the neurological deficits. These results suggest that YM-14673 protects Levine rats against neurological deficits, presumably by attenuating the development of brain edema and preventing neuronal damage. This compound may be useful in the therapeutic treatment of cerebral vascular diseases.
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PMID:Pharmacological actions of a new TRH analogue, YM-14673, in rats subjected to cerebral ischemia and anoxia. 211 71

Arachidonic acid is liberated from damaged cell membranes during ischemia and is the source of vasoactive prostanoids. In this study, specific drugs that influence AA metabolism were investigated for their effects on brain edema and energy metabolites during ischemia. The agents tested were: methylprednisolone (phospholipase A2 inhibition), indomethacin (cyclooxygenase inhibitor), trapidil (TXA2 synthetase inhibitor), and OP-41483 (prostacyclin derivative). Cerebral ischemia was produced using bilateral common carotid artery occlusion in spontaneously hypertensive rats. Brain water content and concentrations of ATP, pyruvate, and lactate were determined 3 hr after occlusion. Compared with its vehicle, methylprednisolone significantly reduced water content and lactate concentration and maintained high levels of ATP. Indomethacin had no effect on brain water content nor metabolite levels. Trapidil decreased water content and lactate levels and increased levels of ATP and pyruvate. OP-41483 had no effect on water content and lactate, but maintained ATP and pyruvate at high levels. These results indicate that some of the AA metabolites may play an important role in the development of brain edema and in the impairment of energy metabolism.
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PMID:Role of arachidonic acid metabolism on ischemic brain edema and metabolism. 211 11

Perfluorochemicals were developed as a blood substitute and were reported to have an advantage in oxygen transport compared with blood. The present study was undertaken to investigate the therapeutic effects of a perfluorochemical, FDA, on brain edema and metabolites in acute cerebral ischemia. Cerebral ischemia was induced in SHR by BLCO followed by recirculation. The FDA administration resulted in (a) the significant inhibition of brain edema as shown by brain water content in the treated group, and (b) significant amelioration of metabolic impairments as shown by lesser degree of ATP and pyruvate decrease and lactate accumulation. The TpO2 was compared between FDA-infused and nontreated group during ischemia. The FDA-infused group had significantly higher TpO2 than nontreated group. These results indicate that the improvement of brain edema and metabolite levels were due to alleviation of ischemic hypoxia by FDA under the same ischemic insult.
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PMID:Effects of fluosol-DA on brain edema, energy metabolites, and tissue oxygen content in acute cerebral ischemia. 211 12

Kainic acid (KA) is a potent neuroexcitatory drug widely used in the experimental study of seizure activity. Subcutaneous injection of KA into rats (10 mg/kg in saline 10 mg/ml; pH 7.0) induced longlasting status epilepticus followed by damage of CNS tissue in the entorhinal/pyriform cortex and in the hippocampus. The studies covered by this report demonstrated the formation of cytotoxic brain edema characterized by massive swelling of perineuronal and perivascular astroglia with microcirculation disturbance after KA injection, resulting in parenchymal necrosis of the affected region; furthermore perivenous hemorrhages and necroses corresponding to herniation lesions of the brain appear. Tracer studies with Na-fluorescein, Evans blue, albumin, and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. Treatment of brain edema with dexamethasone did not influence the incidence and severity of edematous brain damage. Treatment with mannitol, however, completely prevented the lesion in 54% of animals injected with KA. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic KA intoxication. It is suggested that in this model brain edema develops due to massive ionic imbalance caused by KA induced persistent neuronal excitation. In addition the model demonstrates the possible pathogenetic role of selective astrocytic swelling in the production of local hippocampal ischemia followed by herniation and its sequels. Such pathology originating from astrocytes probably may occur also in closed brain injury.
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PMID:Some mechanisms of brain edema studied in a kainic acid model. 213 Jun 48

The effects of intraventricularly administered atrial natriuretic peptide (ANP) on the brain water, sodium, and potassium contents in ischemic brain edema were investigated. By use of a three-vessel occlusion model, ischemic brain edema was produced in the rat brain by 15 minutes of global ischemia followed by recirculation. Water content was measured by means of a drying/weighing method; sodium and potassium contents were measured by means of flame photometry. The effects of intraventricular administration of ANP were evaluated by a comparison between the groups given 2 and 5 micrograms of atriopeptin II (treated) and those given 0.9% NaCl (sham-treated). The treated groups showed significant decreases in brain water (P less than 0.02) and sodium (P less than 0.01) contents at 15 and 30 minutes after recirculation, whereas the brain potassium contents remained unaltered. Before ischemia and immediately after 15 minutes of ischemia, intraventricularly administered ANP did not significantly change the brain water, sodium, or potassium contents. There was no significant difference in the effect on the amount of brain water and sodium between the two doses (2 and 5 micrograms). These effects of ANP were thought not to be mediated by primary changes in serum osmolality and sodium and potassium concentrations, because intraventricular administration of ANP did not change them significantly. The present results reveal that, in ischemic brain edema, ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation.
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PMID:Effect of atrial natriuretic peptide on ischemic brain edema: changes in brain water and electrolytes. 214 1

Postischemic events cause exacerbation of brain injury, not only in the postischemic area but also in the area originally free from the ischemic insult. The present study was performed in rats. After the animals were anesthetized with a mixture of 70% N2O, 0.5% halothane, a focal ischemia was induced by occlusion of the right MCA by means of a silicone rubber cylinder introduced from the internal carotid artery. Three hours after the MCA occlusion, the embolus was pulling out from the artery by an attached nylon surgical thread. Three hours after the recanalization, animals were decapitated to acquire water content of the brain, local CBF, or local CMRgl. After recirculation, water content markedly increased in the MCA area whereas the CBF returned near normal. However, the CMRgl decreased below half of the normal value. In the neighboring, originally nonischemic area, water content remained within the normal limit although the CBF markedly decreased and the CMRgl increased. Deductions from these data were as follows: (a) If the brain tissue cannot recover from the ischemic-induced injury, restored blood flow may exacerbate the brain edema; and (b) the edematous brain tissue affects the neighboring area with lowering blood flow and rising glucose consumption.
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PMID:Uncoupling of blood flow and glucose metabolism in the neighboring postischemic edematous brain area. 214 97

Oxygen-derived free radicals have been postulated to be involved in brain edema and cell death secondary to ischemia and traumatic injury. Using a model of vasogenic brain edema produced by a permanent occlusion of the left MCA in rats, we have studied the role of superoxide radicals in pathogenesis of ischemic edema. The levels of NBF in ischemic brain were increased by 222%, 420%, and 614%, respectively, at 1, 4, and 24 hr after the MCAO. Topical application of superoxide dismutase to the injured cortex through a modified cranial window significantly reduced the NBF levels, indicating the involvement of superoxide radicals in ischemic brain. Liposome-entrapped SOD, when IV injected 5 min after the MCAO, significantly reduced the degree of edema at 24 hr. Our data indicate that superoxide radicals play an important role in the pathogenesis of vasogenic edema in cerebral ischemia.
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PMID:Pathogenesis of vasogenic edema in focal cerebral ischemia. Role of superoxide radicals. 216 62

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-to-brain sodium transport in ischemic brain edema. 216 71


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