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

This study was done to evaluate the response of myopathic hearts from dystrophic hamsters to 30 minutes of ischemia followed by 30 minutes of reperfusion. Hearts from male and female normal animals recovered 77 +/- 6% and 64 +/- 5% of their contractile force respectively following reperfusion whereas only 34 +/- 8% (male) and 34 +/- 7% (female) recovery was seen in myopathic hearts (P less than 0.01). Substantial sustained contractures were observed during reperfusion in hearts from dystrophic animals irrespective of gender whereas none were seen with control hearts. Reperfusion produced a rapid release of CPK that peaked at 5 minutes (approximate coronary effluent concentration of 40 mU/ml) and remained elevated for the reperfusion duration. Peak CPK values for normal hearts were reached at 10 minutes following reperfusion, were significantly lower from the myopathic hearts and returned to near control levels at the end of the 30 minute reperfusion period. Reducing Ca2+ in the perfusion medium by up to 80% or perfusing the hearts with the Ca2+-channel blocker verapamil produced no beneficial effects. Changes in the above parameters produced by ischemia or heart rate alterations throughout the perfusion sequence were not different between normal and myopathic hearts. This study shows a sensitivity of myopathic hearts that is manifested during reperfusion. Possible mechanisms for this reduced tolerance are discussed.
 ...
PMID:Reduced tolerance to reperfusion-associated injury in hearts from myopathic hamsters. 405 41

The possibility that myocardial ischaemia alters the defence mechanisms against oxygen toxicity has been investigated. Ischaemia was induced in isolated, perfused rabbit hearts by reducing coronary flow from 25 ml/min to 1 ml/min for 90 min. Two different degrees of ischaemic damage have been achieved using either spontaneously beating or electrically stimulated hearts. The effects of post-ischaemic reperfusion were also followed for 30 min. Tissue activity of superoxide dismutase (SOD), glutathione peroxidase and reductase (GPD and GRD) have been determined together with tissue content of reduced and oxidized glutathione (GSH and GSSG) and of protein SH groups. The changes in myocardial ATP and CP content and release of CPK and of GSH and GSSG were also determined. Systolic and diastolic pressures were continuously monitored. In the spontaneously beating hearts ischaemia induced a reduction of tissue GSH and protein SH groups. On reperfusion there was a recovery of mechanical function, a transient release of GSH into the coronary effluent and an increase of tissue GSH. In the paced hearts, ischaemia resulted in 50% reduction of mitochondrial SOD activity together with a reduction of tissue GSH and protein SH groups. Reperfusion induced a massive release of CPK and of GSH and GSSG, a further reduction of tissue GSH concomitant with an increase of GSSG and no recovery of mechanical function. GPD and GRD activity were not affected by ischaemia and reperfusion. These data indicate that severe ischaemia induces a reduction of the protective mechanisms against oxygen toxicity.
 ...
PMID:Oxygen-mediated myocardial damage during ischaemia and reperfusion: role of the cellular defences against oxygen toxicity. 406 39

Three cases (one, newborn infant and two infants--one of them recently published--) who present electrocardiographic and enzymatic alterations comparative with diagnosis of ischemia and myocardial infarction are reported. Rarity of this entity in infants is stressed as most of published cases are secondary to ananomolous coronary artery. Etiology of the cases presented shows a myocardiac fibrosis with Schwachman's syndrome in one case, a coronary thrombosis secondary to a disseminated intravascular coagulation in a second case, and finally a generalized hypoplasia of coronary arteries. Hypoxia appears in these cases a factor acting in favour of myocardial ischemia. Diagnostic criteria of acute myocardial infarction are based on typical electrocardiogram and rise of isoenzymes of LDH and CPK-MB. Although rare, it is a diagnosis to be considered in cases of unknow cardiac insufficiency in newborns and infants.
 ...
PMID:[Myocardial infarction and myocardial ischemia in newborn children and infants, not secondary to an abnormal coronary]. 666 Jun 44

This study was aimed to evaluate the effect of catecholamine on the myocardium reperfused after hypothermic global ischemia, by changes of hemodynamics, biochemistry and ultrastructure. Under cardiopulmonary bypass (CPB) at flow rate 80 ml/kg/min., the aorta was clamped for 60 min. at 28 degrees C of myocardial temperature and reperfused for 60 min. in 26 mongrel dogs. They were divided into 4 groups by infusion of physical saline solution (control), epinephrine 1 microgram/kg/min. (group 1), epinephrine 0.1 microgram/kg/min. (group 2) and dobutamine 5 micrograms/kg/min. (group 3) during reperfusion. The hemodynamic parameters and myocardial isoenzyme (m-AST, MB-CPK) of coronary sinus venous blood were measured before CPB, 30 and 60 min. after declamp. The myocardial adenosine triphosphate (ATP), creatine phosphate (CP), water content, tissue Ca content and fine structure with score of mitochondrial membrane and cristae were examined in epicardium and endocardium at the end of experiment. Hemodynamic parameters after declamp were higher in group 1, 2 and 3 than control (p less than 0.05). The water content and tissue Ca content in group 1 were higher than control. The ATP of endocardium was lowest but CP was no significant difference among four groups. The mitochondrial score in group 1 was lower than control. These data suggest that epinephrine and dobutamine increase hemodynamics and tissue Ca content on the reperfused myocardium following 60 min. of hypothermic global ischemia, but they do not improve depletion of ATP and disruption of myocardial ultrastructure. High dose of epinephrine accentuates ischemic damage of reperfused myocardium after hypothermic global ischemia.
 ...
PMID:[Effect of catecholamine on reperfused myocardium following hypothermic global ischemia]. 674 11

Five hundred fifty-nine patients undergoing aortocoronary operation were analyzed retrospectively according to the type of myocardial protection implemented during the period of ischemia. In Group 1 (253 patients), a rapid method of hypothermic cardioplegia alone was utilized. In Group 2 (306 patients), slower infusion of the same solution with topical hypothermia was implemented. Cardiac isoenzymes (CPK-MB, LDH1, LDH2, serum glutamic oxaloacetic transaminase [SGOT]) and myocardial infarct index (MII) were measured postoperatively for 48 hours. Immediately after operation, a significant difference was found between Groups 1 and 2 in the CPK-MB isoenzyme mean value levels--12.1 versus 18.6 IU, p less than 0.01--and MII mean values--5.2 versus 8.1, p less than 0.01. CPK-MB variances between subgroups receiving two, three, and four grafts were significantly different in favor of Group 1. Differences were also found in LDH1, LDH2, total lactic dehydrogenase (LDH), and SGOT: Group 2 levels were significantly higher than in Group 1. There were ten intraoperative infarctions in Group 2 and none in Group 1. In 45% of the patients in Group 2, inotropic agents were necessary in the postoperative period versus none in Group 1. Spontaneous cardiac rhythm following ischemia occurred in 89.7% of the patients in group 1 versus 29% in Group 2. A method of pressurized high-flow rapid cardioplegia with intermittent reperfusions alone, seems to provide adequate protection of the myocardium during ischemia over a slower low-flow method of infusion combined with topical hypothermia.
 ...
PMID:Pressurized rapid cardioplegia versus administration of exogenous substrate and topical hypothermia. 704 26

The sensitivity of cardiac enzymes (GOT, a-HBDH, LDH, LDH-1, CPK and CPK-MB) was studied in the isolated rat heart subjected to 0 (non-ischemic), 20, 30 and 40 min of total global ischemia (0 ml/min) followed by reperfusion in which three consecutive perfusate samples were collected for enzymatic measurements. Cardiac function, estimated by peak tension (Tp), maximal rate of tension development (Tc) and relaxation (Tr) decreased to 0 with ischemia and recovered with reperfusion to 100% in the 20 min, 50% in the 30 min and 10% in the 40 min ischemic groups. In these three groups, enzymatic release, measured as the relative increment (RI) with respect to the control samples, gave significantly higher values than those of non-ischemic hearts (P less than 0.001). LDH-1 was the most sensitive enzyme (P less than 0.0005) for the detection of ischemia in these experimental conditions.
 ...
PMID:Sensitivity of enzymatic release due to ischemia in the isolated rat heart. 718 46

The present study was undertaken to investigate the sequential metabolic and histological changes occurring in dog leg muscles as a consequence of ischemia. The left hind limbs of 45 dogs were amputated at the middle of their thighs and after preserving them in ice water and room temperature for 6 and 12 hours, re-circulation was established. Observation was undertaken on 1) activity of muscle enzymes-CPK, GOT-m, and LDH in the venous blood from the re-circulated limbs, and 2) histological changes of muscles through light microscopy and electron microscopy. Leakage of muscle enzymes into the serum was little in the group preserved in ice water for 6 hours, but resulted in a marked increase in the group preserved in room temperature for 6 hours and 12 hours ischemic groups. This remarkable leakage of muscle enzymes seems to reflect the amount of muscle degeneration. Histologically prominent changes of muscles were characterized by cell swelling and separation of sarcoplasma from endomysium through light microscopic study, and by widening of myofibril space, virtual absence of glycogen granules in sarcoplasma, swelling of mitochondria and appearance of intramitochondrial dense body through electron microscopic study. These histological changes of muscles are well correlated with the leakage of muscle enzymes and demonstrated some extent of irreversible changes had developed already, even in the group preserved in ice water for 6 hours.
 ...
PMID:[The sequential metabolic and histological changes occurring in dog leg muscles as a consequence of ischemia (author's transl)]. 732 Jun 1

Dexamethasone (6 mg/kg) given intravenously to anesthetized cats exerted no significant hemodynamic effect on control open-chest cats or in cats subjected to acute myocardial ischemia by coronary artery ligature. However, dexamethasone normalized elevated S-T segments toward preischemic values, and prevented much of the increase in plasma CPK activity following coronary artery ligation. Moreover, dexamethasone prevented loss of CK activity within ischemic myocardial tissue five hours after the onset of ischemia. Dexamethasone also reduced the extent of ischemic damage as assessed by a nitro-blue tetrazolium staining technique, providing anatomic verification of the reduced ischemic damage. Moreover, dexamethasone prvented the swelling and vacuolization of myocardial lysosomes in the ischemic region, indicating a stabilization of lysosomal membranes within the heart. These data indicate that lysosomal disruption is an important consequence of myocardial ischemia and that early treatment with dexamethasone prevents the loss of myocardial lysosomal and cellular enzymes as reflected in normalization of the ECG and plasma CK activity of ischemic cats. In this way, dexamethasone may act to retard the spread of the developing infarct within the ischemic myocardium.
 ...
PMID:Mechanism of the beneficial effect of dexamethasone on myocardial cell integrity in acure myocardial ischemia. 739 11

Aprotinin, a naturally occurring protease inhibitor, in concentrations of 10(6) KIU/L was found to have no effect on myocardial performance in normally perfused isolated rat hearts, before ischemia. Given during the preischemic period, the drug had a significant protective effect on the reperfused hearts, following cardioplegic ischemia: better contractility upon reperfusion (p < 0.011), faster decline of the ischemic contracture, higher coronary flow (p < 0.025), lower AV-difference (p < 0.05), and lower CPK levels (p < 0.01).
 ...
PMID:Role of protease inhibition in myocardial preservation following ischemia and reperfusion. 753 8

Prolonged global ischemia followed by reperfusion during coronary artery bypass graft (CABG) surgery leads to a burst of oxygen free-radical generation and subsequent myocardial impairment. Blood samples were collected at different time periods from the right atrium of patients (n = 55) who underwent CABG surgery. Free-radical activity was measured by assays for thiobarbituric acid reactive species (TBARS), mainly malondialdehyde (MDA), at zero minute (before aortic cross-clamp), one minute and 10 minutes after declamping i.e. reperfusion. There was a significant increase (p < 0.001) in the level of MDA at one minute of reperfusion which continued to be elevated up to 10 minutes. This increase was significantly correlated with aortic cross-clamp time (r = 0.525, p < 0.05). The activity of CPK and CPK-MB was raised by two fold (p < 0.001) after release of the clamp. Plasma Troponin-T level was estimated in 10 patients during CABG surgery and a significant increase (p < 0.01) was observed at one minute as well as 10 minutes of reperfusion which correlated well (r = 0.81, p < 0.01) with the severity of ischemia. The concomitant rise in TBARS (marker of free-radical activity), CPK, CPK-MB and Troponin-T (indicators of myocardial damage) on reperfusion implies that there is free-radical mediated damage to the cardiac membrane during CABG surgery.
 ...
PMID:Evidence for free-radical mediated injury during coronary artery bypass surgery. 759 Aug 34


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>