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

During ECC, dogs ventilate spontaneously according to classical physiology. Further, given the CO2 clearance insured by the ECC oxygenator, many hours of reversible apnea are tolerated without sequellae. Surgical removal of the lungs shows that an emptied chest still responds to chemical drives, but the absent lung-recoil causes hyperinflation with lethal failure. Finally, liquid ventilation induces metabolic acidemia through phasic gut ischemia and respiratory muscle strain that destroys the delicate lung structure.
Bull Mem Acad R Med Belg 1994
PMID:[Aspects of pathological physiology of the dog in extracorporeal circulation]. 755 34

Na/Ca exchange is an important regulatory mechanism of the cytosolic free Ca2+ concentration in most cells. This transporter, localized at the level of the plasma membrane, represents with the plasma membrane Ca2+ ATPase, one of the two systems allowing active Ca2+ extrusion from the cells. Renewed interest for this system comes from recent advances in the molecular biology of the exchanger and the identification of the major role played by the exchanger in Ca2+ extrusion from cardiac cells. These recent progresses may allow a better understanding of the role played by Na/Ca in Physiology and in Physiopathology, e.g. in cardiac ischemia.
Bull Mem Acad R Med Belg 1996
PMID:[Na/Ca exchange]. 896 56

In order to assess effects of global ischemia in tasks of spatial learning and working memory, male Wistar rats were subjected to four vessel occlusion (4 VO) for periods of 5, 10, and 20 min and compared with sham-operated controls over four test phases, from 6 to 54 weeks after surgery. Rats were assessed on acquisition in the water maze, a task that is sensitive to ischemic impairments, before testing in Skinner box and water maze working memory tasks, which both require the short-term storage of information, but make different demands on spatial information processing. Phases 1 and 3 assessed spatial learning in a standard water maze procedure (12 and 10 training days, 2 trials/day with a 10-min intertrial interval: ITI). Phase 2 involved training and testing in delayed non-matching-to-position task in the Skinner box, with delays of 2-10 s between the information and choice stages. Phase 4 examined working memory in a water maze delayed matching-to-position task with 4 trials/day, an ITI of 30 s, and a novel platform position on each day. Ischemic rats showed duration-related impairments in water maze acquisition and working memory, but not in the less spatially demanding Skinner box task. Since water maze acquisition deficits were seen both before and after testing in the Skinner box the lack of effect cannot be attributed to time or to prior training. Ischemic deficits were more marked in Phase 3 than in Phase 1 of acquisition, suggesting that impairment may be progressive. Histological assessment showed that cell loss was largely confined to the hippocampal CA1 field and was linearly related to duration of occlusion. At the maximal level of loss (5.7 mm before the interaural line) the 20-min group showed 90% loss, the 10-min group 60% loss, and the 5-min group, which did not differ from controls, less than 10% loss. Only the 20-min group showed significant damage beyond the CA1 field, ranging from 30-40% loss in the CA3 field to 5% loss in one striatal area. No cortical damage was seen. The extent of CA1 cell loss correlated modestly with water maze acquisition (Phase 3) and working memory scores, but not with trials to criterion in the Skinner box task. There were significant correlations between different measures both within and between water maze tasks, but not Skinner box tasks, suggesting that the two types of procedure engaged different cognitive processes. The results indicate that the intrahippocampal damage induced by 4 VO impaired tasks which required processing of allocentric spatial information, but did not impair the storage of limited spatial information in working memory.
Neurobiol Learn Mem 1997 May
PMID:Differential effects of global ischemia on delayed matching- and non-matching-to-position tasks in the water maze and Skinner box. 915 61

Each year, thousands of peoples die, suffering from an anatomical or functional loss of their intestine; these patients would benefit from bowel transplantation; the difficulties of bowel transplantation are as follows: 1. the physiological characteristics of the small bowel, and the fact that denervation, lymphatics interruption and ischemia, independently from rejection, may disturb its function; 2. secondly, the organ is septic; thus, its transplantation causes major infectious problems; 3. at last, the immunological characteristics of the intestinal allograft. Bowel transplantation causes a two-way immunological conflict, not only a standard rejection response, but also a graft-versus-host disease, similar to that observed after bone marrow transplantation; this reaction is caused by the lymphoid tissue conveyed within the bowel graft. The introduction of a new immunosuppressive molecule, FK 506, in combination with profound antibiotic prophylactic regimens, decontamination protocols and vigorous anti-viral protection (against cytomegalovirus and Epstein-Barr), have significantly improved the results. Bowel transplantation has recently reached clinical application. The one-year survival rate of intestinal grafts reaches now 70%. Still, there is no doubt that, due to its microbiological and immunological characteristics, the small bowel will remain the most challenging abdominal organ to transplant.
Bull Mem Acad R Med Belg 1998
PMID:[Intestinal transplantation: a clinical reality in 1998]. 976 Jul 59

The mechanisms of cellular lesions induced by lung ischemia and reperfusion are not fully understood and, in particular, the consequences of pulmonary ischemia and reperfusion injury on mitochondrial function have not been previously investigated. Therefore, we studied the respiratory function of isolated pulmonary mitochondria in a swine model of lung ischemia and reperfusion. We demonstrated that prolonged hypothermic (4 degrees C) ischemia induces significant lesions of the mitochondrial respiratory chain, particularly if ischemia is followed by normothermic reperfusion. These results should be integrated in the cellular alterations induced by the ischemia-reperfusion injury. In another swine model mimicking controlled non-heart beating donors, we demonstrated that thirty minutes of cardiac arrest do not promote significant alteration of the mitochondrial respiratory function. In contrast, forty-five minutes of cardiac arrest, induced significant mitochondrial lesions. This pulmonary tolerance to normothermic cardiac arrest might be explained by the presence of air in the lung airways, allowing some aerobic metabolism after circulatory arrest. These results suggested that lung grafts might be harvested from non-heart beating donors after thirty minutes of cardiac arrest, significantly increasing the pulmonary graft pool.
Bull Mem Acad R Med Belg 2001
PMID:[Lung transplantation and mitochondrial function]. 1192 26

A major goal in the treatment of acute ischemia of a vascular territory is to restore blood flow to normal values, i.e. to "reperfuse" the ischemic vascular bed. However, reperfusion of ischemic tissues is associated with local and systemic leukocyte activation and trafficking, endothelial barrier dysfunction in postcapillary venules, enhanced production of inflammatory mediators and great lethality. This phenomenon has been referred to as "reperfusion injury" and several studies demonstrated that injury is dependent on neutrophil recruitment. Furthermore, ischemia and reperfusion injury is associated with the coordinated activation of a series of cytokines and adhesion molecules. Among the mediators of the inflammatory cascade released, TNF-alpha appears to play an essential role for the reperfusion-associated injury. On the other hand, the release of IL-10 modulates pro-inflammatory cytokine production and reperfusion-associated tissue injury. IL-1beta, PAF and bradykinin are mediators involved in ischemia and reperfusion injury by regulating the balance between TNF-alpha and IL-10 production. Strategies that enhance IL-10 and/or prevent TNF-alpha concentration may be useful as therapeutic adjuvants in the treatment of the tissue injury that follows ischemia and reperfusion.
Mem Inst Oswaldo Cruz 2005 Mar
PMID:The balance between the production of tumor necrosis factor-alpha and interleukin-10 determines tissue injury and lethality during intestinal ischemia and reperfusion. 1596

Oxidative stress underlies many forms of vascular disease as well as tissue injury following ischemia and reperfusion. The major source of oxidative stress in the artery wall is an NADPH oxidase. This enzyme complex as expressed in vascular cells differs from that in phagocytic leucocytes both in biochemical structure and functions. The crucial flavin-containing catalytic subunits, Nox1 and Nox4, are not found in leucocytes, but are highly expressed in vascular cells and upregulated with vascular remodeling, such as that found in hypertension and atherosclerosis. The difference in catalytic subunits offers the opportunity to develop "vascular specific" NADPH oxidase inhibitors that do not compromise the essential physiological signaling and phagocytic functions carried out by reactive oxygen and nitrogen species. Nitric oxide and targeted inhibitors of NADPH oxidase that block the source of oxidative stress in the vasculature are more likely to prevent the deterioration of vascular function that leads to stroke and heart attack, than are conventional antioxidants. The roles of Nox isoforms in other inflammatory conditions are yet to be explored.
Mem Inst Oswaldo Cruz 2005 Mar
PMID:Mechanisms for suppressing NADPH oxidase in the vascular wall. 1596 5

Hemolytic episodes such as sickle cell disease, malaria and ischemia-reperfusion occurrence are often associated to the statement of an inflammatory response which may develop or not to a chronic inflammatory status. Although these pathological states are triggered by distinct etiological agents, all of them are associated to high levels of free heme in circulation. In this review, we aim to focus the very recent achievements that have led to the statement of free heme as a proinflammatory molecule, which may play a central role during the onset and/or persistence of inflammation during these pathologies.
Mem Inst Oswaldo Cruz 2005 Nov
PMID:Heme and innate immunity: new insights for an old molecule. 1641 Sep 72

Environmental enrichment (EE) results in improved learning and spatial memory, as well as attenuates morphological changes resulting from cerebral ischemia in adult animals. This study examined the effects of daily EE on memory deficits in the water maze and cerebral damage, assessed in the hippocampus and cerebral cortex, caused by neonatal hypoxia-ischemia. Male Wistar rats in the 7th postnatal day were submitted to the Levine-Rice model of neonatal hypoxia-ischemia (HI), comprising permanent occlusion of the right common carotid artery and a period of hypoxia (90 min, 8%O(2)-92%N(2)). Starting two weeks after the HI event, animals were stimulated by the enriched environment (1h/day for 9 weeks); subsequent to the stimulation, performance of animals in the water maze was assessed. HI resulted in spatial reference and working memory impairments that were completely reversed by EE. Following the behavioral study, animals were killed and the hippocampal volume and cortical area were estimated. There was a significant reduction of both hippocampal volume and cortical area, ipsilateral to arterial occlusion, in HI animals; environmental stimulation had no effect on these morphological measurements. Presented data indicate that stimulation by the daily environmental enrichment recovers spatial memory deficits caused by neonatal hypoxia-ischemia without affecting tissue atrophy in either hippocampus or cortex.
Neurobiol Learn Mem 2007 Jan
PMID:Effects of daily environmental enrichment on memory deficits and brain injury following neonatal hypoxia-ischemia in the rat. 1693 Oct 63

Among the astonishing Einstein's papers from 1905, there is one which unexpectedly gave birth to a powerful method to explore the brain. Molecular diffusion was explained by Einstein on the basis of the random translational motion of molecules which results from their thermal energy. In the mid 1980s it was shown that water diffusion in the brain could be imaged using MRI. During their random displacements water molecules probe tissue structure at a microscopic scale, interacting with cell membranes and, thus, providing unique information on the functional architecture of tissues. A dramatic application of diffusion MRI has been brain ischemia, following the discovery that water diffusion drops immediately after the onset of an ischemic event, when brain cells undergo swelling through cytotoxic edema. On the other hand, water diffusion is anisotropic in white matter, because axon membranes limit molecular movement perpendicularly to the fibers. This feature can be exploited to map out the orientation in space of the white matter tracks and image brain connections. More recently, it has been shown that diffusion MRI could accurately detect cortical activation. As the diffusion response precedes by several seconds the hemodynamic response captured by BOLD fMRI, it has been suggested that water diffusion could reflect early neuronal events, such as the transient swelling of activated cortical cells. If confirmed, this discovery will represent a significant breakthrough, allowing non invasive access to a direct physiological marker of brain activation. This approach will bridge the gap between invasive optical imaging techniques in neuronal cell cultures, and current functional neuroimaging approaches in humans, which are based on indirect and remote blood flow changes.
Bull Mem Acad R Med Belg 2008
PMID:[See the thinking brain: a story about water]. 1881 31


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