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

The presence of a lupus anticoagulant (LA) is paradoxically associated with a high incidence of arterial and venous thrombosis. In a patient with a lupus-like systemic disease, having received phenindione for 11 years, LA was discovered in association with recurrent deep venous thrombosis, a right atrial thrombus, coronary occlusion, arterial hypertension, thrombopenia, and anticardiolipin antibodies without anti-DNA antibodies. Renal cortical ischemia was detected by a tomographic scan. Renal biopsy showed glomerular ischemia and diffuse interstitial fibrosis. After a one-year anticoagulant and steroid therapy, LA has disappeared despite a high level of anticardiolipin antibodies, and renal function remains normal.
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PMID:[Renal cortex ischemia, right atrial thrombosis and coronary occlusion in anti-phospholipid antibody syndrome]. 251 17

The influence of partial hepatic ischemia (32%) prior to partial hepatectomy (68%) has been studied in the rat. 3H-thymidine incorporation into the hepatic DNA was significantly suppressed in both 20 min and 30 min ischemia depressed the survival following partial hepatectomy (p less than 0.001). Three cases of ruptured hepatocellular carcinomas were treated: one case by emergency hepatectomy, and two cases by hepatectomy following TAE. Hepatic insufficiency and post-operative death occurred to only the case given an emergency hepatectomy. Thus, it is felt that a ruptured hepatoma should first be treated by TAE and then surgically resected.
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PMID:[Influence of hepatic ischemia on liver regeneration following hepatectomy, with special reference to the therapeutic choice for ruptured hepatoma]. 254 49

The area of cerebral resuscitation has become an exciting area of research in critical care medicine. It is a complicated field, however, which has seen attempts to protect the brain using a single therapy such as barbiturates ultimately disappoint investigators in the field. It is likely that much more work needs to be done in understanding the intracellular metabolic and biochemical effects of ischemia before therapies can be designed that are likely to be effective. This work might ultimately require knowledge of how ischemia or hypoxia interrupt cellular RNA and DNA machinery before these effective therapies can be developed. Before we are discouraged by the difficulty of the task, however, it is useful to review how much progress has been made in understanding the pathophysiology of ischemic brain injury in the past decade, so that we may be challenged to continue our efforts in this exciting area of critical care medicine.
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PMID:Current concepts in brain resuscitation. 256 85

To determine the timing and location of renal cell regeneration after ischemic injury to the kidney and to assess whether exogenous epidermal growth factor (EGF) enhances this regenerative repair process to accelerate recovery of renal function, experiments were undertaken in rats undergoing 30 min of bilateral renal artery clamp ischemia followed by reperfusion for varying time intervals. Renal cell regeneration, as reflected by incorporation of radiolabeled thymidine within the kidney, began between 24 to 48 h and reached a peak at 72 h after renal ischemia. As demonstrated by histoautoradiography, renal thymidine incorporation was essentially confined to tubule cells. Morphometric analysis of histoautoradiograph sections of renal tissue demonstrated that the majority of labeled cells were found in renal cortex, but some labeled cells were also located in the inner stripe of the outer medulla, suggesting that injury to medullary thick ascending limbs also occurs in this ischemic model. Exogenous EGF administration produced increases in renal thymidine incorporation compared with non-treated animals at 24, 48, and 72 h after ischemic injury. This accelerated DNA replicative process was associated with significantly lower peak blood urea nitrogen (BUN) and serum creatinine levels, averaging 63 +/- 20 and 3.1 +/- 0.4 mg/dl in EGF-treated ischemic rats compared with 149 +/- 20 and 5.1 +/- 0.1 mg/dl, respectively, in nontreated ischemic rats, and was also associated with a return to near normal BUN and serum creatinine levels in EGF-treated animals approximately 4 d earlier than that observed in nontreated animals. This report is the first demonstration that EGF accelerates the repair process of a visceral organ after an injurious insult.
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PMID:Epidermal growth factor enhances renal tubule cell regeneration and repair and accelerates the recovery of renal function in postischemic acute renal failure. 259 59

To study the effects of glucagon-insulin (G-I) infusion on protein synthesis and DNA synthesis in a condition with partial hepatic ischemia, G-I or saline was infused via portal vein for 40 minutes before and after a period of partial hepatic ischemia or following a period of partial hepatic ischemia. Protein synthesis was measured by 14C-leucine incorporation into proteins in incubated liver slices and DNA synthesis by 3H-thymidine incorporation into DNA. Protein synthesis in the postischemic liver was significantly recovered faster and more completely in G-I treated rats. G-I infusion enhanced the DNA synthesis of postischemic liver significantly, peaking 48 hours after the period of partial hepatic ischemia. However, the dosage of G-I infused in this investigation couldn't increase the hepatic tissue blood flow measured by hydrogen gas clearance method. On the histological examination, mitotic index was significantly higher in G-I treated group than in control. These results suggest that G-I infusion could be beneficial effects on the liver in situation with partial ischemic injury and that G-I infusion could remarkably augment hepatic tissue repair following ischemic damage.
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PMID:[Beneficial effects of glucagon-insulin infusion on hepatic protein synthesis and DNA synthesis in partial hepatic ischemia]. 267 61

Although free radicals have been suggested to contribute to ischemic brain damage for more than 10 years, it is not until quite recently that convincing evidence has been presented for their involvement in both sustained and transient ischemia. The hypothesis is examined against current knowledge of free radical chemistry, as it applies to biological systems, and of cellular iron metabolism. It is emphasized that those advents have changed our outlook on free radical-induced tissue damage. First, it has been realized that damage to DNA and proteins may be an earlier event than lipid peroxidation, perhaps also a more important one. Second, evidence now exists that the triggering event in free radical-induced damage is a disturbance of cellular iron metabolism, notably delocalization of protein-bound iron, and its chelation by compounds that trigger site-specific free radical damage. Third, methods have been developed that allow the demonstration of partially induced oxygen species in tissues, and scavengers have become available that can curb free radical reactions. As a result of these events, it has been possible to demonstrate formation of free radicals in oxygen toxicity, trauma, and ischemia, and their participation in the cell damage that is incurred in these conditions, particularly in causing vascular pathology and edema. It is suggested that in ischemia, free radical damage becomes pathogenetically important when the ischemia is of long duration, when conditions favor continued delivery of some oxygen to the ischemic tissue, and particularly when such partially oxygen-deprived tissue is reoxygenated.
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PMID:Free radicals and brain damage. 270 75

Glucocorticoids (GCs) are highly pathogenic if secreted in excess. Recent work shows that such deleterious consequences include damage to the hippocampus, a principal neural target site for GCs. Excessive chronic exposure to GCs accelerates senescent hippocampal neuron loss, while the presence of GCs at the time of neurological insults, such as seizure or hypoxia-ischemia, exacerbates hippocampal damage. The present study determines whether GCs endanger hippocampal neurons through the same mechanism by which they damage lymphocytes. GC-induced lymphocytolysis involves cleavage of chromosomal DNA, most likely through steroid induction of a nuclease that produces a characteristic ladder of fragmented DNA. Moreover, inhibition of DNA repair using the poly(ADP-ribose) synthetase inhibitor benzamide exacerbates GC-induced lymphocytolysis. We replicated this GC-induced fragmentation of DNA in thymocytes, but observed the absence of a similar fragmentation in DNA from primary hippocampal cultures under conditions in which GCs exacerbate the toxic effects of the excitotoxin kainic acid. Furthermore, under such conditions benzamide did not worsen the GC/kainic acid toxicity. These observations suggest that GCs endanger hippocampal neurons through a different mechanism, one that seems likely to be less sterotyped and simple than this cascade of apoptosis in lymphocytes.
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PMID:Glucocorticoid endangerment of hippocampal neurons does not involve deoxyribonucleic acid cleavage. 272 59

DNA synthesis was studied in liver nuclei of Wistar rats after 30% liver tissue resection, 2 hr ischemia of 70% liver tissue or 2 hr ischemia of 70% liver tissue with resection of intact lobes. DNA synthesis was markedly increased in ischemic lobes and was especially high in ischemic lobes if simultaneous resection of intact lobes occurred; maximum of the synthesis was observed within 32 hrs after the operation. Proliferation stimulating extracts, isolated from liver tissue within 48 hrs after the resection or after ischemia, intensified the regenerating processes in the resected liver tissue; the first preparation (from resected liver tissue) exhibited the most distinct effect as compared with the second extract (from ischemic liver tissue). Proliferation stimulating extracts did not affect the cytochrome P-450, content of which was decreased after resection and ischemia. The data obtained suggest the important role of proliferation stimulating factors in regeneration of liver tissue after ischemia or resection; these factors proved to be possible to isolate from ischemized and reperfused liver tissue; the medicinal effect of resection was shown.
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PMID:[Regeneration ability of ischemic liver and the effect of liver resection and extracts stimulating proliferation]. 274 22

The use of various types of cultured mammalian renal tubular epithelial cells in the study of cell injury has been reviewed. Permanent cell lines, primary explant cultures, monolayers from individually microdissected tubules, isolated cells and organ cultures have been used. In the majority of studies, cultured cells of normal tissue origin have been treated with a noxious agent and alterations in growth, morphology, biochemical and immunological properties studied. Earliest studies examined infection by parasites and bacteria and the effects of plant and bacterial toxins, carcinogens, metabolic and transport inhibitors, cytoskeletal perturbants, general inhibitors of protein, glycoprotein, DNA and RNA synthesis. More recent studies have concentrated on the effects of specific nephrotoxins, such as heavy metals and aminoglycoside antibiotics and of ischemia which have bearing on the pathogenesis of acute renal failure. An additional approach has been to culture diseased renal epithelia of cystic, diabetic or tumor origin and compare their properties with those of normal cultured tubular epithelia. Future studies using cultured renal tubular cells will be valuable in elucidating the cellular and subcellular mechanisms of renal epithelial cell injury in disease.
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PMID:Use of cultured renal tubular cells in the study of cell injury. 300 63

The objective of this study was to determine if DNA damage caused by ischemic insult (blood depletion) causes an alteration in the activity of endogenous mouse kidney poly(ADP-ribose) synthetase. The results show that kidneys made nonviable by warm (37 degrees C) in vitro ischemia (organ storage to study the effects of blood loss at normal body temperature) and in vivo ischemia (surgical depletion of the blood supply by arterial clamping) exhibit decreased levels of enzyme activity. Kidneys made nonviable by cold (0 degrees C) storage injury (organ storage as utilized for transplantation), however, possess elevated levels of enzyme activity. The DNA isolated from ischemic kidneys was shown to have a stimulatory effect upon exogenous calf thymus poly(ADP-ribose) synthetase. Also, electron microscopy analysis of DNA from ischemic kidneys showed that cold storage injury leads to the formation of large (average size = 500 bases) single-stranded regions. The results suggest that the activities of both endogenous and exogenous poly(ADP-ribose) synthetase are related to the nature of DNA damage resulting from ischemic insult.
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PMID:In vivo ischemia and storage injury cause alterations in the activity of poly(adenosine diphosphate ribose) synthetase. 311 78


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