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)

Four hundred eighty-eight consecutive carotid endarterectomies were performed on 417 patients. Stroke, as a procedure-related complication, occurred in 12 patients, or 2.4 per cent of cases. Five causes of operative or postoperative stroke were identified: 1) operative embolization, 2) postoperative hypertensive episodes with cerebral hemorrhage, 3) technical error, 4) conversion of ischemic infarct to hemorrhagic infarct, and 5) clamp-time ischemia. The use of several modalities evolved as routine in an effort to reduce mortality and morbidity: 1) minimal manipulation of the artery until after cross clamping to prevent microembolization; 2) routine direct arterial blood pressure monitoring and control during and after surgery; 3) routine operative arteriography to detect and correct technical errors at the time of surgery; 4) liberal use of CAT scans preoperatively to avoid surgery on patients with small, unrecognized infarcts; and 5) stump pressure measurement and selective shunting to prevent ischemia during the endarterectomy. The anatomical-pathological combination of a high bifurcation and high plaque is identified as a high-risk situation.
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PMID:The causes and prevention of stroke associated with carotid artery surgery. 707 27

The adjunctive use of ACE-inhibitors with thrombolytic therapy early during acute myocardial infarction offers theoretic advantages. In the acute phase, captopril may scavenge free radicals, blunt the catecholamine response, elicit coronary vasodilation and increase prostacyclin and bradykinin levels. In the chronic phase remodelling may be attenuated. At present, a large number of controlled clinical trials mainly focussing on the effects of ACE-inhibition in the chronic phase is under way. Only few studies concentrate on the effect of acute intervention with ACE-inhibitors in ischemia-reperfusion i.e. thrombolysis in myocardial infarction. In the Captopril And Thrombolysis pilot study (CAT pilot-study) 3 mg and 6.25 mg captopril was tolerated well as adjunctive therapy to intravenous streptokinase. Decrease in mean arterial blood pressure (36 +/- 11%) after 6.25 mg was comparable to the control group (30 +/- 7%). Furthermore noradrenaline levels decreased dose dependently to 47 +/- 6 and 38 +/- 7% from baseline respectively. These results prompted a large nationwide acute intervention trial with captopril in 300 patients receiving thrombolytic therapy: the Captopril And Thrombolysis Study (CATS). The primary hypothesis of CATS supposes a very early effect of converting enzyme inhibition on evolving myocardial damage due to ischemia and the consequences of early reperfusion. This will be evaluated by serial echocardiography, Holter monitoring and neurohumoral measurements immediately upon thrombolysis and during the first year after myocardial infarction. Blinded data show a favourable blood pressure response, with systolic hypotension below 100 mm Hg occurring only in 0.2% of patients.
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PMID:Angiotensin-converting enzyme inhibition during thrombolytic therapy in acute myocardial infarction: the Captopril and Thrombolysis Study (CATS). 812 21

Myocardial ischemia in vivo is associated with dramatic electrophysiologic alterations that occur within minutes of cessation of coronary flow and are rapidly reversible with reperfusion. This suggests that subtle and reversible biochemical alterations within or near the sarcolemma may contribute to the electrophysiologic derangements. Our studies have concentrated on two amphipathic metabolites, long-chain acylcarnitines and lysophosphatidylcholine (LPC), which have been shown to increase rapidly in ischemic tissue in vivo and to elicit electrophysiologic derangements in normoxic tissue in vitro. Incorporation of these amphiphiles into the sarcolemma at concentrations of 1 to 2 mole%, elicits profound electrophysiologic derangements analogous to those observed in ischemic myocardium in vivo. The pathophysiological effects of the accumulation of these amphiphiles are thought to be mediated by alterations in the biophysical properties of the sarcolemmal membrane, although there is a possibility of a direct effect upon ion channels. Inhibition of carnitine acyltransferase I (CAT-I) in the ischemic cat heart was found to prevent the increase in long-chain acylcarnitines and LPC and to significantly reduce the incidence of malignant arrhythmias including ventricular tachycardia and fibrillation. This review focuses on the electrophysiologic derangements that are observed during early ischemia and presents data supporting the concept that accumulation of these amphiphiles within the sarcolemma contributes to these changes. The potential contribution of these amphiphiles to the increases in extracellular potassium and intracellular calcium are examined. Finally, recent data pertaining to the accumulation of long-chain acylcarnitines on cell-to-cell uncoupling are presented. In addition to the events reviewed here, there are many other alterations that occur during early myocardial ischemia, but the results from multiple studies over the past two decades indicate that the accumulation of these amphiphiles contributes importantly to arrhythmogenesis and that development of specific inhibitors of CAT-I or phospholipase A2 may be a promising therapeutic strategy to attenuate the incidence of lethal arrhythmias associated with ischemic heart disease in man.
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PMID:Recent insights pertaining to sarcolemmal phospholipid alterations underlying arrhythmogenesis in the ischemic heart. 826 1

Generation of free radicals during reperfusion after organ ischemia has been implicated in the pathogenesis of ischemic injury. We have previously shown that a combination of intravenous polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) and catalase (PEG-CAT), at a dose of 10,000 U/kg each, is effective in reducing infarct size in a focal cerebral ischemia model in the rat. It is not clear whether PEG-SOD alone is sufficient to reduce ischemic brain injury. In this study we determined the therapeutic efficacy of PEG-SOD and its dose-response curve. In a range of 1,000-30,000 U/kg, PEG-SOD exhibited a U-shaped dose-response curve. Only 10,000 U/kg significantly reduced infarct size [control 121 +/- 12 mm3 (mean +/- SE), n = 35; PEG-SOD 95 +/- 10 mm3, n = 36, P < 0.05]. PEG-SOD at the doses tested did not have significant acute hemodynamic effects but had a tendency to improve postischemic hypotension. This beneficial effect of PEG-SOD on blood pressure did not appear to fully account for the treatment effect of PEG-SOD on infarct size. The narrow therapeutic dose range of PEG-SOD in this study and similar findings of SOD in other investigations may contribute to the inconsistent protective effects of SOD preparations in ischemia-reperfusion injury in the literature.
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PMID:Polyethylene glycol-conjugated superoxide dismutase in focal cerebral ischemia-reperfusion. 834 41

An experiment was conducted to determine whether the oxygen and carbon dioxide gas tensions in liver tissue (PtO2 and PtCO2, respectively) reflect the state of microcirculation and/or metabolism in the ischemic liver. Subjects were divided into three groups: group 1, 30 min ischemia; group 2, 60 min ischemia; group 3, four times of intermittent 15 min ischemia after every 10 min of reperfusion. PtO2, PtCO2 and tissue blood flow (TBF) were measured by mass spectrometry, comparatively studied with the serum GOT level as an indicator of liver tissue damage. Furthermore, the time point at which the PtCO2 increase for 1 min initially became less than 1/2 of the maximum value was located on the transit curve of PtCO2, referred to as the critically anaerobic (CA) point, with which new indices of critically anaerobic score (CAS) and time (CAT) (see details in text) were developed. The profiles of PtO2 and PtCO2 during ischemia and reperfusion were clearly demonstrated, and the CA point was observed 12.7 +/- 2.9 min after induction of ischemia. PtO2 was positively correlated with TBF and negatively with the serum GOT level. Furthermore, not only CAS but also CAT were significantly correlated with PtO2, TBF, and the serum GOT level. It was concluded that PtCO2 reflects the state of anaerobic tissue metabolism during ischemia and PtO2 reflects the magnitude of microcirculatory disturbance and tissue injury caused by ischemia/reperfusion. Therefore, continuous monitoring of not only PtO2 but also PtCO2 is beneficial for patients undergoing hepatic surgery with ischemia.
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PMID:Continuous measurement of tissue oxygen and carbon dioxide gas tensions in dog liver in ischemia/reperfusion. 898 64

An in vivo rat model of isolated intestinal ischemia-perfusion was developed. This is used to compare the effects of crosslinked hemoglobin (PolyHb) versus crosslinked hemolobin-superoxide dismutase-catalase (PolyHb-SOD-CAT) on free radical generation in ischemia-reperfusion. Fasted, anesthetized male Sprague Dawley rats underwent midline laparotomy with cannulation of the abdominal aorta and inferior vena cava. Ligation was carried out at the renal pedicles bilaterally and the aorta and vena cava proximally at the diaphragm and distally above the femoral bifurcation. The system was flushed of blood with 20 ml of lactated Ringer's solution. The portal vein was then cannulated with distal clamping at the porta hepatis so that isolated intestinal perfusion could be achieved with the aorta as the inlet and the portal vein as the outlet. Following a 90 minute ischemic time, perfusates containing modified hemoglobin (5 g/dl) and 4-hydroxybenzoate (5 mM) were infused at 0.8 ml/min for 10 min. Portal vein effluent samples were collected at 2.5 minute intervals. Hydroxyl radical generation was assessed by an aromatic hydroxylation technique with 4-hydroxybenzoate (4HB). Reaction of hydroxyl radical with 4HB produces 3,4 dihydroxybenzoate (3,4 DHBA). In the PolyHb group, the levels of 3,4-DHBA increased 10.75-13.58 x-fold above pre-perfusion values compared to 2.25-3.75 x-fold in PolyHb-SOD-CAT group. This indicates that PolyHb-SOD-CAT is effective in reducing in vivo hydroxyl radical generation following reperfusion. Since free radicals may play a major role in the pathogenesis of ischemia-reperfusion injury, this suggests a role for PolyHb-SOD-CAT as a possible protective perfusate in intestinal reperfusion injury.
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PMID:Crosslinked hemoglobin-superoxide dismutase-catalase scavenges free radicals in a rat model of intestinal ischemia-reperfusion injury. 908 38

The effects of PolyHb (intermolecularly crosslinked hemoglobin) and PolyHb-SOD-CAT (intermolecularly crosslinked hemoglobin, superoxide dismutase and catalase) on the production of hydroxyl radical was studied using a rat hindlimb model of ischemia-reperfusion. Hydroxyl radical generation was assessed by an indirect assay based on the hydroxylation of 4-hydroxybenzoate. The hydroxylation product, 3,4 dihydroxybenzoate (3,4 DHBA), was analyzed by high performance liquid chromatography and electrochemical detection. The identification of 3,4 DHBA was confirmed by analysis of authentic standard and an in vitro hydroxyl radical generation system. Ischemia was induced in both hindlimbs by ligation of the infrarenal aorta. After a 4hr ischemic period, hindlimbs were simultaneously perfused with PolyHb-SOD-CAT (5 g/dl) into one limb and PolyHb (5 g/dl) into the other limb via femoral arterial catheters. Each perfusate also contained the hydroxyl radical trap, 4-hydroxbenzoate (5 mM). Femoral venous effluents were analyzed for the presence of the 3,4 DHBA. Data indicates that greater 3,4 DHBA production occurs during PolyHb perfusion as compared to PolyHb-SOD-CAT. These preliminary results show that perfusion with PolyHb-SOD-CAT may alleviate oxidative stress in a model of ischemia-reperfusion.
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PMID:Reduction of hydroxyl radical generation in a rat hindlimb model of ischemia-reperfusion injury using crosslinked hemoglobin-superoxide dismutase-catalase. 908 37

We investigated the involvement of oxygen-derived free radicals in the pathogenesis of the intrauterine growth retardation (IUGR) induced in Sprague-Dawley rats by ischemia-reperfusion. On day 17 of gestation, rats received saline, superoxide dismutase (SOD, 50,000 U/kg), catalase (CAT, 50,000 U/kg), or SOD + CAT subcutaneously 1 h before induction of 30 min of ischemia of the right uterine horn. On day 21 the placental level of lipid peroxides was significantly increased (P < 0.001 vs. sham-operated group) and IUGR was induced (P < 0.001 vs. left horn) in the saline-treated group n = 6). Pretreatment with SOD + CAT (n = 6) significantly inhibited the increase in placental lipid peroxides and prevented IUGR. The effect of ischemia-reperfusion on uterine blood flow, with or without pretreatment with radical scavengers, was investigated in separate experiments by laser-Doppler flowmetry. The induction of hypoperfusion 3 h after ischemia (blood flow -40 +/- 5%, n = 6, P < 0.05) was blocked by pretreatment with SOD + CAT (n = 6). Results indicate that oxygen-derived free radicals may be important in the development of postischemic uteroplacental hypoperfusion and of ischemia-reperfusion-induced IUGR in the rat.
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PMID:Role of oxygen-derived free radicals in free growth retardation induced by ischemia-reperfusion in rats. 912 27

The aim of this study was to determine whether the administration of free radical antagonists, immediately before and during the early minutes of reperfusion, improves muscle survival 24 hr after a period of ischemia. Rabbit rectus femoris muscles were isolated, made ischemic for 3 1/2 hr and treated with either desferrioxamine (DFX), an Fe3+ chelator, superoxide dismutase and catalase (SOD & CAT), which quench superoxide and hydrogen peroxide, or allopurinol, an inhibitor of xanthine oxidase (XO). After 24 hr reperfusion, muscle viability (+/-s.e.m.), measured by the nitro blue tetrazolium (NBT) vital staining technique, was 41.6 +/- 11.3% for saline-treated ischemic controls, 30.6 +/- 7.6% for DFX-treated, 46.7 +/- 10.3% for SOD & CAT-treated, and 43.3 +/- 9.5% for allopurinol-treated muscles. None of the treated groups differed significantly from the ischemic control group. Tissue myeloperoxidase, ATP and reduced glutathione levels, and plasma lactate dehydrogenase (LDH) and aspartate transaminase (AST) levels were increased by ischemia and reperfusion in all groups, but the changes did not differ between the treatment groups. Levels of XO in the rabbit muscle were determined and found to be very low in both normal and postischemic muscle. As XO is the target enzyme of allopurinol, its absence provides a basis for the lack of effect of this agent. However, it is not clear why DFX and SOD & CAT had no protective effect.
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PMID:Influence of postischemic administration of oxyradical antagonists on ischemic injury to rabbit skeletal muscle. 939 70

The term "spontaneous", when attributed to a stenotic or obliterative arterial lesion, could seem ambiguous and doesn't completely explain the anatomical substrate that is the basis of this morbid condition. However, it is true that injuries can occur without the patient being aware of any traumatic event, and can cause a symptomatology arising suddenly and, apparently, "spontaneously". In this study, three cases of patients observed for acute or chronic lower limb ischemia are presented. All patients were male, young and underwent an angiographic examination that demonstrated, in an otherwise normal arterial tree, filling defects or obstruction involving the popliteal artery. Two patients underwent a reconstructive surgical procedure. The third was medically treated. CAT or MNR examinations were performed in order to exclude developmental defect such as an anomalous course of popliteal artery determined by a displacement due to medial head of the gastrocnemius muscle. Actually in these three cases, a definite etiology of the arterial damage was not demonstrated and therefore it is suggested that a physical effort could have injured an already weakened arterial structure.
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PMID:[So-called "spontaneous" lesions of the popliteal artery]. 954 84


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