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)

Fourteen patients with diffuse tumors of the liver were treated with temporary occlusion of the hepatic artery (HA) by an external tourniquet followed by infusion and systemic chemotherapy. Three patients had primary neoplasms (one hepatocarcinoma and two cholangiocarcinomas) and eleven had metastatic disease (nine from carcinoma of the colon and rectum, one from retroperitoneal liposarcoma, and one from pulmonary small cell cancer). Infusion chemotherapy in all patients was based on 5-FU, Mitomycin and Vincristine. Systemic chemotherapy was FIVB in metastatic carcinoma and Adriamycin in primary liver tumors. All patients showed improvement of the performance status according to the Karnofsky Index. Objective response (OR) was present in 54% of cases. At present, median survival time in 12.5 months. Aggressive treatment combining hepatic ischemia with infusion and systemic polychemotherapy seems to provide an effective method of palliation in diffuse tumors of the liver. Delayed occlusion by an external tourniquet appears safer than intraoperative ligation of the HA.
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PMID:Temporary occlusion of the hepatic artery plus infusion and systemic chemotherapy for inoperable cancer of the liver. 616 63

Chronic thrombotic mesenteric ischemia is a well-described but infrequently encountered disease in the practice of clinical vascular surgery. Viewing it as a three-stage process and tailoring the management to this concept will help to achieve maximal success in prompt diagnosis, appropriate revascularization, and resection when needed. Aggressive intravenous nutritional support will help bolster these patients against the complications and mortality associated with management for each stage, while helping to restore the deficits engendered preoperatively by the disease itself.
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PMID:Mesenteric ischemia: nutritional impact and capturing the golden operative moment. 681 Jul 35

The literature on the treatment of pediatric vascular injuries was reviewed. Aggressive treatment of arterial ischemia is clearly indicated, since children with uncorrelated arterial thrombosis are almost certain to develop a growth abnormality in the affected extremity. Alternatives to operative treatment have not been well described. Operative treatment is technically difficult and results are strongly influenced by age. To emphasize this relationship, we combined 10 cases of arterial thrombosis treated operatively in children under age 2 years complied form the literature with five similar cases reviewed retrospectively in our hospital. In these 15 patients the etiology was iatrogenic in 100%. Sixty-seven percent (10 of 15) were treated with simple thrombectomy, and only one patient (7%) received a graft. At up to 8 years of follow-up, only 26% (3 of 15) were normal, 47% (7 of 15) had thrombosis, 20% (3 of 15) had suffered tissue loss, and there had been one perioperative death. We conclude that operative treatment of an ischemic although viable limb in a small child might best be deferred if simple thrombectomy has failed or if a more complex procedure would be required at the outset, with the hope that any growth abnormality that developed could be reversed by definitive reconstruction when the child is larger.
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PMID:Pediatric vascular injuries. 724 48

Overall surgical experience in dealing with extracranial angiopathology on the basis of 300 cases submitted to surgical reconstitution is hereby presented, together with long term observations covering a period of 1-10 years. Particular emphasis is given to the concept of prophylaxis which has to be considered as the major goal of contemporary operative approach, by means of "preventing" ischemic episode rather than "reducing" an already established infarct. Spectrum of surgical indications covers mainly transient attacks of brain ischemia with attention focused upon the selective group of patients with "impending stroke" semiology, who although considered asymptomatic, are by no means as such if carefully investigated. "Avant garde" philosophy of operative approach as instituted is fully outlined, with all merits of a fully justified surgical aggression, accordingly discussed.
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PMID:Extracranial angiopathology, within the scope of justified surgical aggression and particular emphasis upon "impending stroke". Surgical considerations with 1-10 years follow-up report of 300 operated cases. 741 59

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overloaded right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of "hemodynamic instability" after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.
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PMID:Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. 748 82

Pre-eclampsia is a frequent, unpredictable syndrome which is dangerous for both mother and foetus. The concept of placental ischemia has gained wide acceptance among the numerous theories put forward to explain the illness. The setting up of preeclampsia seems to be scheduled in two steps: (1) an absolute or relative placental ischemia due to vascular diseases or hypertrophic placenta, or most often secondary to implantation defect, particularly anomaly with the invasive trophoblast; (2) a diffuse endothelial disease. The connection between these two steps is incompletely disclosed. The authors demonstrate that the maternal immune system which is strongly stressed during all the stages of normal gestation is implicated in pre-eclampsia. Its role is probably not univocal. Foeto-trophoblastic antigens could be poorly recognised. This defect of recognition could lead to the abnormalities of trophoblastic invasion observed in pre-eclampsia. Pre-eclampsia does not seem to be accompanied by an immunological rejection of the foetus. Some genetically predisposed patients do not have a sufficiently competent immune system to neutralise one or more of the toxic products released by the ischemic placenta. Certain types of pre-eclampsia could be auto-immune, with the auto-antibodies directed against certain types of phospholipids or trophoblastic constituents. A disequilibrium between oxidation and anti-oxidation mechanisms involving neutrophils could lead to aggression of the endothelium which is observed in pre-eclampsia. Pre-eclampsia could represent a form of immuno-dystrophy, with the excessive production of adverse cytokines locally, directed against the trophoblast. Without directly implicating the immune system as the trigger of pre-eclampsia, it seems that its role is unclear. In some cases it develops protective mechanisms which, when overwhelmed or inadequate, allows pre-eclampsia to occur. In other cases it can form part of the cascade of aggressions leading to the abnormalities encountered. The integration of these abnormalities in the pathophysiological models, could help improve the classification of pre-eclampsia. This attempt will lead to a more adapted preventive and therapeutic management of pre-eclampsia.
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PMID:Pre-eclampsia: physiology and immunological aspects. 890 80

Lower-extremity ischemia can lead to impaired healing of saphenous vein excision sites in patients with significant peripheral vascular disease (PVD). Five patients who required infrainguinal revascularization for wound necrosis of the harvest site after coronary artery bypass grafting are described. The male/female ratio was 2:3 with a mean age of 67 (range 45-87) years. The most commonly associated problems were insulin-dependent diabetes mellitus (80%) and congestive heart failure (60%). The saphenous vein was harvested from the thigh and leg in three patients and exclusively from the leg in the others. Manifestations of ischemia ranged from persistent ulceration to complete wound disruption threatening limb loss. Impaired healing was isolated to infragenicular wounds in all patients. Pedal pulses were not detected in any of the affected extremities. Determination of the ankle/brachial pressure indices (ABI) revealed values of < 0.5 in three affected limbs. Non-compressible vessels resulted in falsely raised ABI of > 1.0 in the remaining two limbs; however, Doppler waveform analysis in these patients demonstrated significant PVD. Aggressive wound care and antibiotic therapy were continued for mean of 9 weeks before operative intervention. Infrainguinal reconstruction included femoropopliteal (two), femorotibial (two) and popliteal-tibial bypass (one). Autologous arm and saphenous veins in addition to expanded polytetrafluoroethylene grafts were used effectively. Limb salvage and wound healing were achieved in 100% of the patients without untoward sequelae. It is concluded that unrecognized PVD in patients undergoing coronary artery bypass grafting can lead to significant morbidity. Patients at risk may be identified with a combination of history, physical examination and non-invasive testing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vein harvest ischemia: a peripheral vascular complication of coronary artery bypass grafting. 795 53

It is well known that reperfusion damage of ischemic myocardium may be attributed to alterations in the antioxidant defense system against free radical aggression. In addition, the degree of myocardial damage may depend on the duration and severity of ischemia that precedes reperfusion. We carried out serial ischemic experiments (10, 30, 60 and 120 min) in ex-vivo rat hearts followed by 30 min reperfusion and we assayed the glutathione-dependent enzymatic activities (selenium-dependent glutathione-peroxidase: GSH-Px; selenium-independent glutathione peroxidase: GST-Px; glutathione-transferase: GST and glutathione-reductase: GS-SG-Red), Catalase activity (CAT) and non-proteic thiol compounds (NP-SH) at the end of reperfusion. We found a significant reduction of NP-SH, GSH-Px and CAT in ischemic/reperfused hearts from 30 min on, while GST activity was increased. In addition, we observed the appearance of a selenium-independent glutathione peroxidase activity (GST-Px) belonging to the GST system. In conclusion, we found the longer the duration of ischemia the greater the inbalance between the myocardial antioxidant system especially the GST activation, suggesting in particular for GST-Px, a role in the control of the damage against oxygen toxicity during ischemia/reperfusion.
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PMID:Myocardial antioxidant defense mechanisms: time related changes after reperfusion of the ischemic rat heart. 801 40

Inflammatory reactions induce the production of reactive oxygen species (ROS): the reverse sequence of these events is also true. Moreover, many components of these reactions interact with a synergistic effect. In this short comprehensive review we analyze some of these interactions which may have pathological effects. Inflammatory reactions are triggered off by exogenous or endogenous aggressions and are characterized by cellular and vascular events. The activated leucocytes leave the circulating blood and reach the site of the aggression where they release a large amount of ROS as well as the content of their granules. The granular content is made in a large part by molecules with killing and degradative activities such as myeloperoxidase, defensins, elastase, collagenase, cathepsins and lysozyme. The inflammatory reaction is beneficial for humans when its effects are limited to the pathogens. The insufficiency of a component of the inflammatory reaction such as the production of ROS which is seen, for example in chronic granulomatous disease, leads to severe and recurrent bacterial infections. In other situations inflammatory reactions are deleterious because they are directed against normal tissues instead or in addition to pathogens. In some cases the behaviour of the phagocytes is modified because they have been primed by inflammatory molecules such tumor necrosis factor, LPS, interleukins or interferons. Priming often leads to a decreased speed of locomotion of the leucocytes with an increased susceptibility to their stimuli. The combination of these effects leads to a premature release by the phagocytes of their killing and degradative factors. Production of ROS such as that seen during irradiation, drug metabolism, or ischemia followed by reperfusion for example, induces inflammatory reactions with a secondary amplification of ROS production. Acute ROS production can also lead to thrombosis, whereas chronic ROS production can induce a chronic inflammatory reaction of the endothelium with atherosclerosis as a possible consequence. Some examples are also given to show that ROS might control positively or negatively the activity of inflammatory molecules. The multiplicity of the cross reactions between ROS and inflammation allows to suggest that drugs that disconnect these two events might be therapeutically used.
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PMID:[Reactive oxygen species and inflammation]. 801 8

Colon ischemia is a well-recognized clinical entity that often occurs spontaneously in patients over the age of 50 years. Many previous cases of nonspecific colitis are now felt to have been secondary to an ischemic event. In contrast to patients with acute mesenteric ischemia and extensive necrosis of the small bowel, the majority of patients with isolated colon ischemia follow a benign clinical course. Most patients present days, weeks, or months after the initial ischemic insult, and many may not have any recognizable antecedent episode of colon ischemia. However, some patients develop a fulminant form of the disease that causes colon infarction and death if not treated early. A high index of suspicion is necessary to make the diagnosis in the hospitalized patient. Endoscopy is recommended to confirm the diagnosis and the extent of injury and to monitor progression or resolution of disease. Aggressive management is of paramount importance to minimize the damage to the ischemic colon and reduce the otherwise high in-hospital mortality rate. Surgical intervention is indicated for patients with evidence of peritonitis or transmural infarction or perforation of the colon and for patients with chronic symptomatic colitis or stricture.
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PMID:Ischemic colitis. 837 27


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