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)

The aim of this prospective study was to document postoperative myocardial infarction (PMI) by technetium pyrophosphate scan using single-photon emission computed tomography (TcPPi-SPECT) in 28 patients undergoing elective coronary bypass grafting (CABG). The relationships of intraoperative electrocardiographic myocardial ischemia, hemodynamic responses, and pharmacological requirements to this incidence of PMI were correlated. Radionuclide cardioangiography and TcPPi-SPECT were performed 24 h preoperatively and 48 h postoperatively. A standard high-dose fentanyl anesthetic protocol was used. Twenty-five percent of elective CABG patients were complicated with PMI, as documented by TcPPi-SPECT with an infarcted mass of 38.0 +/- 5.5 g. No significant difference in demographic, preoperative right and left ventricular function, number of coronary vessels grafted, or aortic cross-clamp time was observed between the PMI and non-PMI groups. The distribution of patients using preoperative beta-adrenergic blocking drugs or calcium channel blocking drugs was found to have no correlation with the outcome of PMI. As well, no significant differences in hemodynamic changes or pharmacological requirements were observed in the PMI and non-PMI groups during prebypass or postbypass periods, indicating careful intraoperative control of hemodynamic indices did not prevent the outcome of PMI in these patients. However, the incidence of prebypass ischemia was 39.3% and significantly correlated with the outcome of positive TcPPi-SPECT, denoting a 3.9-fold increased risk of developing PMI. Prebypass ischemic changes in leads II and V5 were shown to correlate with increased CPK-MB release (P less than 0.05) and tends to occur more frequently with lateral myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postoperative myocardial infarction documented by technetium pyrophosphate scan using single-photon emission computed tomography: significance of intraoperative myocardial ischemia and hemodynamic control. 255 62

This study was performed to compare the incidence of prebypass myocardial ischemia in patients receiving fentanyl and enflurane for anesthesia along with either pancuronium or vecuronium. Ninety-eight patients with normal left ventricular function were randomly allocated to receive either pancuronium 0.15 mg.kg-1 or vecuronium 0.15 mg.kg-1 in a double-blind manner after fentanyl 40 micrograms.kg-1 for induction of anesthesia for elective coronary artery bypass grafting (CABG). Premedication included diazepam 0.15 mg.kg-1 po, morphine 0.10 mg.kg-1, and scopolamine 0.005 mg.kg-1 im. Two lead Holter monitor recordings (leads V6 and V9) from the time of arrival in the operating suite to institution of cardiopulmonary bypass were analyzed for ischemia by a cardiologist blinded to the choice of muscle relaxant. Intraoperatively, heart rates greater than 90 beats.min-1 and systolic blood pressure +/- 20% of ward values were treated with propranolol, enflurane, or phenylephrine. Nitroglycerin was infused for ECG signs of ischemia or pulmonary hypertension. After induction of anesthesia the heart rate and cardiac index were consistently decreased in patients receiving vecuronium and also lower in these patients compared with those receiving pancuronium. Thirty-two per cent of patients receiving pancuronium received propranolol for heart rates greater than 90 beats.min-1 versus 7% of those who received vecuronium (P approximately 0.01). Eight patients developed 13 episodes of ischemia after administration of the muscle relaxant: four who received pancuronium (n = 44; 9%) and four receiving vecuronium (n = 54; 7%). Four episodes occurred at induction or tracheal intubation, two in each group. There were four perioperative myocardial infarctions as determined by ECG and CPK-MB levels, two in each group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The incidence of myocardial ischemia during anesthesia for coronary artery bypass surgery in patients receiving pancuronium or vecuronium. 256 17

Twenty adult mongrel dogs were divided into three groups. Group I: control (n = 7), group II: limb ischemia for 6 hours followed by reperfusion (n = 6), and group III: administration of alpha-tocopherol after 6 hours of ischemia, and reperfusion (n = 7). In group II, serum CPK and LPO increased after reperfusion with peak levels of 38,000 +/- 9,800 mU/ml and 20.4 +/- 3.7 nmol/ml respectively, which were significantly higher than those in group I. (CPK: p less than 0.02, LPO less than 0.03). In group III, the peak levels of serum CPK and LPO were regulated to the low level of 1,060 +/- 290 mU/ml and 9.2 +/- 4.5nmol/ml, respectively, which were significantly lower than those in group II. (CPK: p less than 0.02, LPO less than 0.04). Additional 13 dogs were divided into two groups in order to assess tissue LPO in the limb, liver, and kidney. Group A: control (n = 5), group B: reperfusion after 6 hours of ischemia (n = 8). Tissue LPO level of 1.89 +/- 0.74nmol/mg-protein in the gastrocnemius muscle in group B was significantly higher than that in group A (p less than 0.02), although there was no significant difference in the gracilis muscle, liver, and kidney. These results prove indirectly the participation of lipid peroxidative reaction by active oxygen in the mechanism of development of reperfusion injury, and suggest the preventive effect of alpha-tocopherol to reperfusion injury.
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PMID:[An experimental study of tissue injury associated with reperfusion in ischemic limbs]. 259 7

Pneumatic cuff with manometer has become a routine apparatus being applied in surgery of the hand. Ischaemia of the upper extremity procured by means of pneumatic cuff with controlled pressure maintained for 30 minutes to 2 hours and 20 minutes appeared to be safe. The following enzymes were studied: lactic dehydrogenase (LDH) creatine kinase (CPK), aldolase and total protein as well as its electrophoretic decomposition, moreover seromucoid and also 9 selected glycoproteins. There were changes indicating metabolic disturbances during the time from the 3 rd h. upon the removal of the cuff to as late as the third 24-hours inclusive. Significant deviations were disclosed with regard to the rise in levels of: creatine kinase, alpha 1 and alpha 2 globulins, protein of acute phase (inflammatory)--seromucoid and 5 glycoproteins as well as a drop in albumins level. The rise in the value of metabolic enzymes was more significant when the application of the cuff was longer than 1 hour. A similar behaviour was observed in some of the selected glycoproteins qualified to the acute phase proteins. In patients, in whom the cuff was applied for 2 hours or longer, there were transient side effects of ischaemia, which under proper management terminated without traces. In own material neither local nor general permanent changes were noted after imposed ischaemia, which is ample evidence that the technique of ischaemia used in the cited time compartments is safe and useful in surgical procedure involving the extremities particularly the upper ones. Nevertheless, disclosed deviations in a number of metabolic parameters show that some injury to ischaemic tissues is found to take place.
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PMID:[Effect of tourniquet ischemia of the arm on changes in selected parameters of muscle metabolism]. 263 95

The purpose of this study is to evaluate the myocardial protective effects of two types of solution during heart transplantation procedure following cold storage in Collins' solution. Based on the concept whether the ischemic time during the procedure is an extension of heart storage or is an usual aortic cross-clamped ischemic time, we compared the effects of our cardioplegic solution (Group I) and Collins' solution (Group II) using isolated working rat heart model. After 30 minutes of global ischemia at 25 degrees C following 2 hours of cold storage, the hearts in Group I exhibited better functional recovery than those in Group II (% recovery of cardiac output was 61.1 +/- 5.4% in Group I and 42.4 +/- 7.4% in Group II, p less than 0.01). In Group II, marked elevation of coronary vascular resistance occurred on reperfusion. CPK release during reperfusion period was greater in Group II (0.41 +/- 0.24 IU/15 min/heart in Group I, 1.92 +/- 1.25 IU/15 min/heart in Group II, p less than 0.01). Myocardial metabolites contents (ATP, TAN, creatine phosphate and lactate) and energy charge were not significantly different between two groups. We conclude that it is harmful to ischemic myocardium to use Collins' solution as myocardial protection during transplantation procedure even if following cold storage in Collins' solution.
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PMID:[Myocardial protection during transplantation procedure following cold storage in Collins' solution]. 267 Nov 86

There is evidence that oxygen free radicals play a role in myocardial ischemic and reperfusion injury. We investigated the effect of ischemia and reperfusion on glutathione status. Reperfusion after prolonged ischemia (60 min) induced an important release of reduced (GSH) and oxidized (GSSG) glutathione, concomitant with an increase of tissue GSSG and no recovery of mechanical function, indicating that reperfusion results in oxidative stress. These alterations are associated with tissue and mitochondrial calcium accumulation, loss of mitochondrial function, and membrane damage. We also determined the arteriocoronary sinus difference for GSH and GSSG of 16 CAD patients undergoing coronary artery bypass. Patients were divided in two groups according to the length of clamping period: 25 +/- 2 min (group 1), and 55 +/- 6 min (group 2). In group 1, reperfusion resulted in a transient release of GSH, GSSG, CPK, and lactate, with return to preclamping values in 10 minutes. In group 2, reperfusion determined a sustained and pronounced release of GSH, GSSG, CPK, and lactate during declamping, suggesting the occurrence of an oxidative stress. Using an in vitro model, administration of alpha-tocopherol bound with albumin showed protection of mitochondrial function, improved recovery of contraction, and reduced oxidative stress during reperfusion.
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PMID:Oxygen free radical-mediated heart injury in animal models and during bypass surgery in humans. Effects of alpha-tocopherol. 269 6

Changes in the serum of CPK-BB isoenzyme were investigated in dogs with intestinal ischemia in order to determine their use as an enzymatic diagnostic test for bowel infarction. The study consisted of 12 mongrel dogs. Group I (n = 6) was assigned as a control and was subjected to lumen obstruction of a jejunal segment 50-60 cm in length. Group II (n = 6) had an intestinal infarction created by ligation of the arteries of a jejunal segment 50-60 cm in length. A catheter was placed into the right atrium through the left jugular vein for blood sampling and monitoring. Blood samples were withdrawn every three hours for biochemical assays. CPK-BB measurements were performed by electrophoresis in agarose gel. CPK-BB remained unchanged in Group I during the course of the study (median range 17 to 20 IU) showing no significant difference from normal levels. Significant elevation of CPK-BB occurred three hours after establishing the ischemia in Group II (median 50 IU) as compared to Group I (p less than 0.05). The highest levels were determined to be 96 and 80 IU at the sixth and ninth hour, respectively. From hour 15 until completion of the experiment, no significant difference was detected between Groups I and II. We conclude that CPK-BB elevation in serum signifies its release from the smooth muscles of the bowel due to ischemic cellular damage.
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PMID:Plasma level of the creatine phosphokinase BB isoenzyme during experimental intestinal ischemia. 271 37

To investigate the potential myocardial ischemic effects of ritodrine, we studied 36 singleton and four twin preterm pregnancies during ritodrine therapy. We serially determined serum creatinine phosphokinase (CPK-MB fraction) and lactic dehydrogenase isoenzymes and performed electrocardiography before and during ritodrine infusion and again within the first 24 hours of oral drug therapy. We observed that serum CPK-MB and lactic dehydrogenase isoenzymes remained within the normal range during therapy periods. The incidence of sinus tachycardia and non-specific T wave changes were 100% and 25%, respectively. In three of four twin pregnancies, ST-T segment depression in leads I, V4, V5, and V6 of the electrocardiogram was noted. Our study suggests that (1) the recommended ritodrine regimen does not produce direct myocardial damage, and (2) ritodrine may cause cardiac ischemia as determined by electrocardiography, which theoretically would progress to myocardial damage if not treated properly.
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PMID:Cardiac isoenzymes and electrocardiographic changes during ritodrine tocolysis. 224 70

Rat left atria or Langendorff hearts were kept at 37 degrees C and stimulated at a rate of 3.33 Hz. They were subjected to hypoxia (deprivation of oxygen) or ischemia (deprivation of oxygen and glucose + acidosis + increased extracellular potassium concentration) for 15 min or 1 h and subsequent reoxygenation for 5 or 15 min. Tissue concentrations of proteins, reduced and oxidized glutathione and conjugated dienes were measured at the end of the experiment. Hypoxia and ischemia decreased the excitability and contractility of the preparations and caused contracture. These effects were partly reversible during reoxygenation. However, in Langendorff hearts reoxygenation caused an increased release of CPK, LDH and glutathione into the perfusion fluid. Ischemia and reoxygenation in atria lowered the tissue concentration of reduced glutathione and increased its oxidized form. Similar changes were seen in atria and Langendorff hearts when oxygen radical production was accelerated by hypoxanthine and xanthine oxidase. No treatment raised significantly the concentration of conjugated dienes. These results seem to exclude an important role of an increased lipid peroxidation for reperfusion injury of isolated heart preparations.
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PMID:No evidence for an increased lipid peroxidation during reoxygenation in Langendorff hearts and isolated atria of rats. 279 63

The protective effect of angiotensin-converting enzyme inhibitors (ACEI) on myocardial ischemia and reperfusion damage was estimated in rat hearts, both in vivo and in vitro. Enalapril 2.5 mg/kg ip pretreatment at 24 and 5 h before coronary occlusion, significantly blunted the rise of CPK (445 +/- 151 vs 649 +/- 244 mu/ml, P less than 0.05) and improved electrocardiogram (ECG) 8 h after coronary occlusion. In global ischemia and reperfusion ex vivo, enalapril improved contractility (0.9 +/- 0.2 vs 0.3 +/- 0.3 g, P less than 0.05) and coronary flow (15.6 +/- 3.3 vs 11.9 +/- 3.1 ml/min/g, P less than 0.05), shortened significantly the duration of reperfusion arrhythmia (3.1 +/- 2.7 vs 9.7 +/- 8.1 min, P less than 0.05). In Langendorffs heart, captopril remarkably preserved force of contraction (2.1 +/- 0.4 vs 1.4 +/- 0.4 g, P less than 0.01) and coronary flow (2.7 +/- 0.5 vs 3.6 +/- 0.9 ml/min/g, P less than 0.05) in segmental infarction deteriorated by angiotensin I. Captopril 10(-5) M infusion reduced the release of CPK (435 +/- 112 vs 640 +/- 123 mu/min coronary flow, P less than 0.05). This action was almost completely abolished by pretreating and infusing with indomethacin. As a positive control, prostacyclin 5 X 10(-7) M infusion further reduced the release of CPK to 330 +/- 77 mu/min. It is concluded that angiotensin-converting enzyme inhibitor can protect both myocardial ischemia and reperfusion damage in rat hearts. The mechanism of protection was ascribed to reduced production of angiotensin II by ACE inhibition and increased prostacyclin release in the myocardium.
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PMID:Protective effects of captopril and enalapril on myocardial ischemia and reperfusion damage of rat. 282 45


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