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

Acutely increased intraabdominal pressure can lead to multisystem organ dysfunction. Organ dysfunction consists of acute pulmonary failure secondary to compressive atelectasis and associated with high peak inspiratory pressures and impaired gas exchange, acute renal failure with marked oliguria without hypernaturia, intestinal and hepatic ischemia possibly leading to bacterial translocation or necrosis with peritonitis, increased intracranial pressures which may cause brain dysfunction or aggravate head injury edema, venous thrombosis and thromboembolism, and abdominal wall ischemia or necrosis. The diagnosis is made clinically in a patient with high peak inspiratory pressures, oliguria and an apparently tight abdomen, although urinary bladder pressure > or = 20 cm H2O pressure is suggestive. However, chronically increased intraabdominal pressure as is seen in the morbidly obese, pregnancy and cirrhosis may be misleading. As to treatment, once the diagnosis is made, the patient's abdomen should be opened and the tension relieved. The intestinal contents need to be protected and evaporative water loss minimized by either closing the skin and not the fascia or, if this is not possible, using an impermeable protective dressing. If the abdomen is difficult to close at the primary operation, it is best to prevent the development of an acute abdominal compartment syndrome by closing only the skin or leaving it open and using an impermeable dressing. In conclusion, the acute abdominal compartment syndrome has become increasingly recognized as a cause for multisystem organ failure. Recognition of the problem or prevention is mandatory for optimal patient survival.
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PMID:Multisystem organ failure secondary to increased intraabdominal pressure. 1144 Mar 93

The significance of mild-hypothermia as a treatment of brain ischemia-induced neuronal cell death was investigated by measurement of hippocampul excitatory amino acids, brain lactate and energy-charge just after 10 min of transient forebrain ischemia in a rat model with four vessels occluded. After 10 min of ischemia, cerebral circulation was restored. At that time, in the control group transient increases of hippocampul aspartate and glutamic acid levels were observed. Furthermore, brain lactate levels were also elevated but the energy-charge was reduced. These significant changes were observed in the non-isoflurane anesthesia and mild-hypothermia rats (control group). However, in rats with treatment of either isoflurane or mild-hypothermia, the excessive amount of amino acids and the significant fluctuation of brain metabolic/energy pathway seen in the control group were suppressed. Particularly, in the combined treatment group, these increased and decreased phenomena induced by brain ischemia were significantly inhibited. In a group of pre- and post-treatment of mild-hypothermia, the maximum peak of lactate was significantly less than that seen in the control group, although the sustained increased level of lactate was detected. These results indicate that the combined treatment with isoflurane anesthesia and mild-hypothermia is a suitable treatment for the brain dysfunction induced by ischemia and that the sustained hypothermia may help restore brain lactate levels after brain ischemia because of the lasting anaerobic metabolism.
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PMID:[Changes in brain metabolites under combined mild-hypothermia and isoflurane anesthesia in rat with temporal brain ischemia]. 1079 19

Stroke is the major cause of adult brain dysfunction. In an experimental approach to evaluate the possible beneficial effects of administration of neurotrophic factors in stroke, we have used a model of distal middle cerebral artery (MCA) occlusion in adult rats. In this model, we found: (1) a permanent reduction of brain-derived neurotrophic factor (BDNF) and its full-length receptor, TrkB, in the infarcted core; (2) a transient increase in BDNF immunoreactivity in the internal region of the border of the infarct (penumbra area) at 12 h after MCA occlusion; (3) increased truncated TrkB immunoreactivity in astrocytes surrounding the area of the infarction; and (4) increased full-length TrkB immunoreactivity in scattered neurons, distant from the infarct, in ipsilateral and contralateral cortices at 24 and 48 h after MCA occlusion. We next studied the regulation of TrkB expression by BDNF, after ischemia, and its neuroprotective effects in vivo. In control non-ischemic rats, grafting of mock- or BDNF-transfected fibroblasts (F3A-MT or F3N-BDNF cell lines, respectively) in the medial part of the somatosensory cortex increased truncated TrkB immunoreactivity in neighboring astrocytes. Grafting alone also increased full-length TrkB in the vicinity of the mock graft (at 24 and 48 h) and the BDNF-grafted graft (at 4 days). Interestingly, ischemic animals grafted with the mock-transfected cell line did not show any further regulation of TrkB receptors. However, ischemic animals grafted with the BDNF cell line showed an up-regulation of full-length TrkB expression in neurons located in the internal border of the infarct. Analysis of nuclear DNA fragmentation in situ, combined with microtubule-associated protein 2 immunohistochemistry, revealed that most cells dying in the borders of the infarct (penumbra area) at 48 h following MCA occlusion were neurons. No differences in the infarct size were found between MCA occluded, mock-transfected MCA-occluded, and BDNF-transfected MCA-occluded rats. Moreover, cell death was similar in nongrafted and mock-grafted rats subjected to MCA occlusion. However, the number of cells with nuclear DNA breaks was significantly reduced in the penumbra area close to the BDNF graft in ischemic rats. Thus, our results show that BDNF specifically up-regulates its full-length TrkB receptor in cortical neurons of the penumbra area and prevents their death in an in vivo model of focal ischemia.
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PMID:Brain-derived neurotrophic factor reduces cortical cell death by ischemia after middle cerebral artery occlusion in the rat. 1130 22

To investigate whether postischemic cerebral dysfunction occurs via the interleukin-1 beta/nitric oxide (IL-1beta/NO) pathway, we examined the effects of an IL-1beta antagonist on long-term potentiation (LTP) impairment and excessive NO production in the rat hippocampus after 10-min global ischemia. Intracerebroventricilar administration of the IL-1beta antagonist attenuated NO production and rescued LTP impairment in the perforant path-dentate gyrus synapses, observed 1 day and 4 days after ischemic insult, respectively. There was an inverse relationship between LTP in the dentate gyrus synapses and hippocampal NO production. Centrally applied IL-1beta mimicked the consequences of transient ischemia in LTP formation and hippocampal NO production in non-ischemic rats. These findings indicate that the IL-1beta/NO pathway is involved in the hippocampal LTP impairment observed in the postischemic brain.
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PMID:Involvement of interleukin-1beta/nitric oxide pathway in the postischemic impairment of long-term potentiation of the rat hippocampus. 1168 45

A 70-year-old motorist driving on the wrong side of the road caused a car-to-car head-on collision and died some minutes later. The autopsy revealed a lethal rupture of the right heart ventricle. The insurance company argued that driving on the wrong side was an act of gross negligence so that the damage was not covered by the full comprehensive insurance. Surprisingly, the microscopic examination of the myocardium performed by a clinical pathologist brought to light a severe myofibrillar degeneration (MFD) which was interpreted as diagnostic of acute myocardial infarction. It was supposed that this could have caused an incapacity of the driver to control his car, which in turn would commit the insurance to payment. A critical re-evaluation of the heart tissue material, however, revealed the pattern of trauma-induced hypercontraction banding of the myocardium along the cleft edges but no findings suggestive of myocardial infarction. Thus, the accident was not the result of a cardiac attack. But there was a severe preexisting pathology including cardiac hypertrophy, scarring of the myocardium, siderophages of the lungs, and an infarction of the pons, so that a cerebral dysfunction was the most plausible explanation for the accident. Thus, gross negligence had to be denied, and the insurance company was obliged to pay. This observation points to the existence of two different variants of MFD: Clinical pathologists are familiar with "tyical" MFD occurring in reperfusion after ischemia, in catecholamine toxicity, and around infarct necroses. But hypercontraction banding, regularly found along penetrating heart lesions and well known to forensic pathologists, is uncommon in clinical pathology.
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PMID:[Traumatic heart rupture or infarct?]. 1236 34

Neonatal seizures are the most common manifestation of underlying cerebral dysfunction. Hypoxic-ischemic encephalopathy is the cause of seizures in 40-60% of newborns. Previous work from our laboratory demonstrates that seizures associated with a hypoxic-ischemic insult results in aggravation of neuronal cell death, specifically within the hippocampus. The latter occurs in the setting of spontaneously occurring hyperthermia of 1.5 degrees C. The purpose of this study was to determine whether preventing the onset of seizure induced hyperthermia would be neuroprotective. Three groups of 10-day old rat pups received unilateral hypoxic-ischemic insults for 30 min followed by KA-induced seizures. Hyperthermia was prevented by lowering the environmental temperature ("relative hypothermia") to 29 degrees C such that the seizuring rat pups were normothermic. In one group, the prevention of hyperthermia occurred immediately following hypoxia-ischemia, whereas in the other group it occurred at the onset of seizures. The third group of rat pups (controls) remained at their nesting temperature and therefore became hyperthermic during seizures. Early (3 days) and late (20 days) neuropathology was assessed. Rat pups in whom hyperthermia was prevented during seizures displayed a significant reduction in brain damage compared to controls (p<0.05). Assessment of hippocampal brain damage also showed a significant improvement in neuronal necrosis at 20 days of recovery compared to 3 days of recovery (p<0.05). The results indicate that preventing spontaneous hyperthermia in this model of hypoxic-ischemic seizures in the newborn is neuroprotective.
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PMID:Preventing hyperthermia decreases brain damage following neonatal hypoxic-ischemic seizures. 1514 Jun 43

Evidence suggests that S-nitrosylation is a biological process involved in cerebral ischemia. The aim of the present study was to elucidate the effects of S-nitrosylated (SNO) polyethylene glycol-conjugated (PEG) hemoglobin (Hb) developed as an artificial oxygen carrier, which can absorb free NO and translocate NO to a sulfhydryl (SH) moiety, on ischemic cerebral dysfunction. Long-term potentiation (LTP) in the perforant path-dentate gyrus synapses of the rat hippocampus was evaluated as functional outcome 4 days after transient incomplete cerebral ischemia (2-vessel occlusion: 2VO, 10 min). SNO-PEG-Hb (250 mg/kg, i.v.) administered on Day 0, 1, 2, or 4 (immediately, 24 h, 48 h, or 96 h after reperfusion, respectively) alleviated 2VO-induced LTP impairment with a therapeutic time window. The effect was significant when SNO-PEG-Hb was administered on Day 1 or 2. SNO-PEG-Hb altered NOS features observed in the vehicle-treated 2VO rat, upregulation of eNOS, nNOS, and iNOS expressions at mRNA and protein levels; SNO-PEG-Hb further upregulated eNOS and nNOS and downregulated iNOS expressions. These findings suggest that SNO-PEG-Hb might have protective effects on the rat hippocampus from ischemia/reperfusion-induced functional damages, thereby increasing the therapeutic potential as an artificial oxygen carrier for use in the area of oxygen therapy.
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PMID:An S-nitrosylated hemoglobin derivative protects the rat hippocampus from ischemia-induced long-term potentiation impairment with a time window. 1549 65

Astrocytes play many roles essential for normal brain activity. The ability of these cells to recover after temporary focal cerebral ischemia is likely to be one important determinant of the extent of brain dysfunction and tissue damage. We have assessed astrocytic function based on the incorporation of radiolabel from 1-14C-acetate into glutamine at 1 hour of recirculation after middle cerebral artery occlusion for 2 or 3 hours in rats. There were marked differences in the response between subregions within the tissue subjected to ischemia, but the overall pattern of changes was similar after each ischemic period. The striatum, which forms part of the severely ischemic focal tissue during arterial occlusion, showed a large (44% to 68%) decrease in glutamine labeling compared with equivalent tissue from the contralateral hemisphere. In contrast, 14C-glutamine content was not significantly altered in perifocal tissue in the cerebral cortex, which was subjected to more moderate ischemia. Cortical focal tissue also was not significantly affected, but the response was much more variable between rats. In these brain subregions, the extent of recovery of the 14C-acetate metabolism after ischemia was not a good predictor of the likelihood of subsequent infarct development. Interestingly, a similar pattern of responses persisted when recirculation was extended to 4 hours. These results indicate that many astrocytes, particularly in the cortex, remain viable and capable of at least some complex oxidative metabolism during the first few hours of recirculation.
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PMID:Astrocytic function assessed from 1-14C-acetate metabolism after temporary focal cerebral ischemia in rats. 1567 39

Hypoxia-ischemia is a leading cause of morbidity and mortality in the perinatal period with an incidence of 1/4000 live births. Biochemical events such as energy failure, membrane depolarization, brain edema, an increase of neurotransmitter release and inhibition of uptake, an increase of intracellular Ca(2+), production of oxygen-free radicals, lipid peroxidation, and a decrease of blood flow are triggered by hypoxia-ischemia and may lead to brain dysfunction and neuronal death. These abnormalities can result in mental impairments, seizures, and permanent motor deficits, such as cerebral palsy. The physical and emotional strain that is placed on the children affected and their families is enormous. The care that these individuals need is not only confined to childhood, but rather extends throughout their entire life span, so it is very important to understand the pathophysiology that follows a hypoxic-ischemic insult. This review will highlight many of the mechanisms that lead to neuronal death and include the emerging area of white matter injury as well as the role of inflammation and will provide a summary of therapeutic strategies. Hypothermia and oxygen will also be discussed as treatments that currently lack a specific target in the hypoxic/ischemic cascade.
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PMID:Pathophysiology of an hypoxic-ischemic insult during the perinatal period. 1584 8

Neurodevelopmental changes may underlie the brain dysfunction seen in schizophrenia. While advances have been made in our understanding of the genetics of schizophrenia, little is known about how non-genetic factors interact with genes for schizophrenia. The present analysis of genes potentially associated with schizophrenia is based on the observation that hypoxia prevails in the embryonic and fetal brain, and that interactions between neuronal genes, molecular regulators of hypoxia, such as hypoxia-inducible factor 1 (HIF-1), and intrinsic hypoxia occur in the developing brain and may create the conditions for complex changes in neurodevelopment. Consequently, we searched the literature for currently hypothesized candidate genes for susceptibility to schizophrenia that may be subject to ischemia-hypoxia regulation and/or associated with vascular expression. Genes were considered when at least two independent reports of a significant association with schizophrenia had appeared in the literature. The analysis showed that more than 50% of these genes, particularly AKT1, BDNF, CAPON, CCKAR, CHRNA7, CNR1, COMT, DNTBP1, GAD1, GRM3, IL10, MLC1, NOTCH4, NRG1, NR4A2/NURR1, PRODH, RELN, RGS4, RTN4/NOGO and TNF, are subject to regulation by hypoxia and/or are expressed in the vasculature. Future studies of genes proposed as candidates for susceptibility to schizophrenia should include their possible regulation by physiological or pathological hypoxia during development as well as their potential role in cerebral vascular function.
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PMID:Gene regulation by hypoxia and the neurodevelopmental origin of schizophrenia. 1663 32


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