Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five of 80 (6.2%) nulliparous women sustained uterine trauma in association with midtrimester abortion induced by intra-amniotic prostaglandin F2alpha and intravenous oxytocin. All five women suffered cervical lacerations, one extending to the lower uterine segment of the corpus and another associated with myometrial necrosis caused by cornual sacculation and ischemia. No uterine trauma was observed among 95 parous women aborted in the same fashion during this study. The different mechanisms of cervical dilation in the parous woman and the nullipara are offered as an explanation for this difference. Thirty-nine other cases of uterine injury associated with the use of intraamniotic prostaglandin F2alpha from the literature were reviewed, and found to indicate that midtrimester abortion induced by intra-amniotic prostaglandin F2alpha is associated with a significant risk of uterine trauma in the nullipara. The risk seems to increase with the use of oxytocin and with increasing gestational age.
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PMID:Uterine trauma associated with midtrimester abortion induced by intra-amniotic prostaglandin F2alpha with and without concomitant use of oxytocin. 88 3

Much of the morbidity and mortality in sickle cell disease (SCD) is caused by tissue ischemia and infarction resulting from vascular occlusion. Research in this area has been dominated by the hypothesis that vascular occlusion in SCD is due primarily to microvascular obstruction by sickle erythrocytes (SS RBC), yet there is no direct evidence that microvascular occlusion is responsible for any of the vasocclusive complications of SCD. In this paper an alternate hypothesis is proposed: that thrombotic occlusion of larger arteries and veins is an important factor in many of the vasocclusive complications of SCD. Large-vessel cerebral arterial disease (intimal hyperplasia with superimposed thrombosis) has clearly been established as the most important cause of stroke in SCD, and considerable evidence suggests that pulmonary arterial thrombosis/embolism is a major cause of pulmonary infarction and hypertension. The involvement of large-vessel thrombosis in painful crisis, aseptic necrosis of bone, priapism, leg ulcers, retinopathy, and miscarriage has not been adequately investigated. Large-vessel occlusion in SCD is probably a consequence of the abnormal adhesive and procoagulant properties of SS RBC, which produce endothelial damage, secondary intimal proliferation, and thrombosis. Techniques currently used to treat large-vessel occlusion in other disorders (antiplatelet and anticoagulant agents, thrombolytic therapy, angioplasty, endarterectomy, and vascular bypass surgery) should be considered in sickle cell subjects with large-vessel occlusion, especially in the cerebral vasculature.
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PMID:Large-vessel occlusion in sickle cell disease: pathogenesis, clinical consequences, and therapeutic implications. 189 Sep 82

An acute ischemia has almost its origin in a mechanical obstruction of the vessel caused by embolus, thrombose or dissection. An ischemia caused by medicament, excepted the erronated intraarterial injection of vasoconstrictive medicament, is very seldom encountered in the clinic. We describe the case of a young woman who was referred to our clinic for investigation and treatment of an acute ischemia of both limbs. In her past medical history she was treated because of a liver insufficiency occurring after a spontaneous abortion and received methylergometrine (Methergin) for uterine stimulation. Because of this unusual manifestation in a young patient with a complicated past medical history we considered the possibility of a drug induced ischemia caused by ergotamine-derivate. The rapid recovering after treatment with chlorpromazine and nifedipine confirmed the suspected diagnosis. A well defined therapy of this rare complication has not been described; vasodilatators, nitroglycerin, calcium-antagonists and even streptokinase and balloon dilatation are proposed.
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PMID:[Drug-induced acute arterial occlusion]. 222 77

Apoptotic cells were histochemically demonstrated by the TdT-mediated biotinylated dUTP nick end-labeling (TUNEL) method in formalin-fixed and paraffin-embedded sections of the human endometrium and placental villi. In 53 endometrial biopsy specimens, labeled nuclei were identified in 16 samples showing a desquamating change, associated with menstruation, functional bleeding or adenocarcinoma. Cells in the normal proliferative and secretory phases were unlabeled. The labeled nuclei in the gland and stroma corresponded well to the so-called apoptotic bodies. Placental tissues at various stages of gestation were obtained by spontaneous abortion, intrauterine fetal death or normal delivery. Syncytiotrophoblastic cells in an early gestational stage (7-12 weeks) and in the term placenta were focally labeled, and the labeled cells possessed pyknotic nuclei and densely eosinophilic cytoplasm. In the early gestational chorionic villi with marked hydropic degeneration or in hydatidiform mole, the stromal cells were frequently labeled. Villous cells in coagulation necrosis (infarction) also revealed strong signals. The apoptotic bodies were not recognizable histologically in these labeled villi. The placenta at the 20th to 33rd week of gestation lacked labeling. From a technical point of view, it should be noted that cells in the foci showing ischemia or coagulation necrosis were labeled positively.
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PMID:Apoptotic cells in the human endometrium and placental villi: pitfalls in applying the TUNEL method. 757 70

Plasma levels of triglycerides, cholesterol, cholesterol esters, phospholipids, lipoperoxides, vitamin E and erythrocyte glutathione peroxidase activity showed no significant differences between 40 women with habitual abortion and controls. However, the levels of free fatty acids (FFA), which are extremely cytotoxic compounds, were significantly higher in women with habitual abortion (HA) than in controls (16.8 +/- 6.7 vs. 8.6 +/- 3.7 mg/100 ml, p < 0.01, respectively). The high amounts of FFA in HA women during pregnancy were probably due to a continuous and/or excessive stress-dependent discharge into the blood of catecholamines from autonomic nerve endings. These catecholamines can induce a strong uterine vasoconstriction and placental ischemia-hypoxia which, in association with additional insults caused by reoxygenation, might lead to eventual miscarriage.
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PMID:Blood levels of lipids, lipoperoxides, vitamin E and glutathione peroxidase in women with habitual abortion. 785 5

The authors report the case of a 30-year-old woman with Takayasu's disease revealed by acute leg ischemia and complicated by abortion during the fourth month of pregnancy. Clinically suspect lesions were confirmed by angiography showing a severe stenosis at the aorto-iliac bifurcation complicated by overlying mild ectasic lesions and a large thrombus. A total occlusion of embolic origin was noted in the right popliteal artery. An attempt to open up the thrombosis at the bifurcation led unfortunately to massive rethrombosis requiring implantation of an aorto-iliac prosthesis. Histopathological examination of the aortic surgical specimen indicated Takayasu's disease; the placenta showed multiple infarcts. The complete angiographic study revealed no arterial involvement in any other region. Five months after the initial operation, rapid development of claudication in both lower limbs suggested stenosis at the prosthesis implantation sites which was confirmed by angiography. Initiation of general corticosteroid therapy led to partial remission in less than two weeks. The unusual feature in this case was the revelation of the affection by distal arterial embolic manifestations, which have been reported only exceptionally in the literature. Moreover, isolated involvement of the aorto-iliac bifurcation constitutes a rare form of Takayasu's disease. With respect to therapy, the implantation of a prosthesis was complicated by severe stenoses of the junction zones, which is unfortunately an event in the course of this affection. The normality of biologic inflammation studies did not suggest an initial need for corticosteroid therapy, especially in the case of an isolated arterial manifestation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterial embolic manifestations in the legs revealing isolated aorto-iliac Takayasu's disease]. 790 28

Apoptosis is an organized, energy dependent process, which leads to cell death. Its definition is based on distinct morphological features [10] and demonstration of internucleosomal DNA degradation [27], executed by selectively activated DNAses [4, 22]. The morphologic hallmarks of apoptosis include chromatic margination, nuclear condensation and fragmentation, and condensation of the cell with preservation of organelles. The process is followed by fragmentation of the cell into membrane-bound apoptotic bodies, which undergo phagocytosis by nearby cells without associated inflammation [10, 11]. Apoptosis characteristically occurs in insolated single cells. The duration of apoptosis is estimated to be from 12 to 24 hours, but in cell culture visible morphologic changes are accomplished in less than two hours [10, 16]. Non-apoptotic cell death, a prototype of which is cell death due to ischemia (oncosis), is characterized by depletion of intracellular ATP stores, swelling of the cell with disruption of organelles and rupture of the plasma membrane [15]. Groups of necrotic cells and inflammation are found in tissues [10, 15]. The significance of apoptosis has mostly been studied using the TUNEL assay that detects DNA strand breaks in tissue sections and allows quantification of apoptotic cells by light microscopy [6]. Common experience seems to be that the TUNEL assay is prone to false positive or negative findings. This has been explained by the dependence of the staining kinetics on the reagent concentration [17], fixation of the tissue [2] and the extent of proteolysis [17]. Active RNA synthesis [12] and DNA damage in necrotic cells [17, 19] may cause non-specific staining. To obtain reliable and reproducible results, TUNEL assay should be carefully standardized by using tissue sections treated with DNAse (positive control of apoptosis). Quantification of apoptosis should include enough microscopic fields and identification of the cell type undergoing apoptosis. The specificity of the results can be substantiated by combining other methods with TUNEL, such as assessment of the pattern of DNA fragmentation or evaluation of the morphological features. Even though there is high variation in the results obtained in consecutive studies under the same circumstances, increasing evidence shows that TUNEL-positive cardiomyocytes and internucleosomal DNA fragmentation are associated with various cardiac diseases, including acute myocardial infarction and heart failure [reviewed in 5, 9]. Some morphological features of apoptosis have been observed in TUNEL-positive cardiomyocytes using light microscopy (Figure 1) or confocal microscopy [20]. Electron microscopic evidence of apoptosis has been found in the degenerating conduction system [7], in experimental heart failure [23], and in human hibernating myocardium [3]. In acutely ischemic myocardium the interpretation of the findings remains controversial, since only non-apoptotic cell morphology has been found in electron microscopy [8, 19]. One explanation might be abortion of the apoptotic program due to the lack of ATP before the morphologic features are fully evident [14]. Another explanation is the possibility that non-apoptotic cell death and apoptosis share common mechanisms in the early phases of the processes [14, 19]. The exact mechanisms of ischemic cell death remain to be clarified and the classification between apoptosis and non-apoptosis cell death to be specified. Recently, caspase activation has emerged as the central molecular event leading to apoptosis, preceding DNA degradation and the development of apoptotic morphology [22, 25]. New methods have been developed to demonstrate caspase activation [1, 13]. Inhibition of caspase may be an efficient way to prevent apoptotic cardiomyocyte death as well as to define and specifically probe the significance of apoptotic cell death in cardiac diseases.
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PMID:Morphologic criteria and detection of apoptosis. 1041 42

A 16-year-old girl developed acute left choreic movements during her fourth week of pregnancy. She had sometimes had transient ischemic attacks since she was 10 years old. During the eighth week of pregnancy, a brain MRI showed old ischemic lesions deep in the right frontal white matter. Her angiograph revealed a complete obstruction of the terminal portion of the right internal carotid artery with a developed moyamoya net work. After her abortion, all involuntary movements completely subsided. The choreic movements might have been caused not only by ischemia, but also by enhanced dopaminergic sensitivity mediated by elevations in female sex hormones due to pregnancy.
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PMID:[A case of chorea gravidarum with moyamoya disease]. 1096 57

Necrosis and apoptosis have been initially identified as two exclusive pathways for cell death. In acute brain lesions, such as focal ischemia, this binary scheme is challenged by demonstrations of mixed morphological and biochemical characteristics of both apoptosis and necrosis in single cells. The resulting difficulty in defining the nature of cell death that is triggered by severe insults has dramatically impeded the development of therapeutic strategies. We show that in the early stages of cerebral infarction, neurons of the so-called "necrotic" core display a number of morphological, physiological, and biochemical features of early apoptosis, which include cytoplasmic and nuclear condensations and specific caspase activation cascades. Early activation cascades involve the death receptor pathway linked to caspase-8 and the caspase-1 pathway. They are not associated with alterations of mitochondrial respiration or activation of caspase-9. In contrast, pathways that are activated during the secondary expansion of the lesion in the penumbral area include caspase-9. In agreement with its downstream position in both mitochondria-dependent and -independent pathways, activation of caspase-3 displays a biphasic time course. We suggest that apoptosis is the first commitment to death after acute cerebral ischemia and that the final morphological features observed results from abortion of the process because of severe energy depletion in the core. In contrast, energy-dependent caspase activation cascades are observed in the penumbra in which apoptosis can fully develop because of residual blood supply.
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PMID:Specific caspase pathways are activated in the two stages of cerebral infarction. 1154 23

Mycophenolate mofetil (MMF) is a new immunosuppressive drug used to reduce acute rejection after heart transplantation. As with other immunosuppressive drugs, MMF therapy is associated with several adverse effects. However, the direct effects of MMF on myocardial tissue has not been yet evaluated. The aim of the work was thus to evaluate the effects of MMF on isolated cardiomyocytes (CM) in normal conditions and in an in vitro model of simulated ischemia (SI; substrate-free hypoxia) and reperfusion (R; reoxygenation). Myocyte-enriched cultures were prepared from newborn rat heart ventricles. The transmembrane potentials were recorded using conventional microelectrodes and the cell contractions were monitored with a photoelectric device. In basal conditions, MMF (10(-6) and 10(-5) M) exerted no significant effects on the survival and on the electrical and contractile activities of CM in culture, even during long-term exposure (up to 48 h). SI per se led to a gradual decrease and then an abortion of the spontaneous automaticity and electromechanical activity of CM. Pretreating CM with either 10(-6) or 10(-5) M MMF was able to reduce the SI-induced cell dysfunctions. The presence of MMF at these concentrations did not hamper the post-SI functional recovery of CM during reoxygenation. At 10(-5) M, MMF applied during reoxygenation only permitted a better recovery of CM. However, the mitochondrial function after reoxygenation, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl-tetrazolium bromide (MTT) test, was not significantly influenced by the addition of MMF before as well as after ischemia. Conversely, MMF was able to reduce in this model the postischemic rise in xanthine and hypoxanthine. These data from CM-enriched model show that MMF: (i) had no cytotoxic effect, (ii) displayed a cytoprotective effect during SI, and (iii) exerted its beneficial effect at least partly through the decrease in the xanthine oxidase-dependent free radical production.
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PMID:Physiological and metabolic actions of mycophenolate mofetil on cultured newborn rat cardiomyocytes in normoxia and in simulated ischemia. 1514 80


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