Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

25 anesthetized mongrel dogs underwent a left thoracotomy. Creatine kinase (CK) activity was measured in serial blood samples drawn simultaneously from the aorta and a coronary vein. The distribution of myocardial perfusion was determined by a continuous infusion of krypton-81m (half-life 13 sec) into the aortic sinuses. Heart rate and arterial blood pressure were also measured throughout the procedure. In 20 dogs regional myocardial ischemia was produced by ligation of a major branch of the left anterior descending coronary artery. Five of these dogs received 1 microgram.kg-1 nifedipine i.v. and a further 5 received 13 microgram.kg-1. Thoracotomy alone produced a slight rise in plasma CK activity but the arteriovenous difference (AV) across the segment of the heart remained positive over 5 h. Myocardial ischemia in the untreated dogs caused a considerable increase in CK activity and the AV difference became negative at 90 min. Treatment with the lower dose of nifedipine considerably reduced the plasma CK activity and the AV difference did not become negative until 3 h. Regional myocardial perfusion showed a significant improvement. Conversely, the higher dose of nifedipine produced a marked increase in the area of ischemia and an acceleration of CK release from the heart. This was associated with a decrease in arterial pressure and an increase in heart rate. These results show that nifedipine can be beneficial in experimental myocardial infarction but care must be taken to avoid hypotension and increases in heart rate.
 ...
PMID:Effects of nifedipine on creatine kinase release during myocardial ischemia in dogs. 69 37

The efficacy of human extracellular-superoxide dismutase type C (EC-SOD C) to limit infarct size after ischemia and reperfusion was explored and compared to that of EC-SOD C combined with catalase (CAT) and to that of CAT alone. EC-SOD C binds to heparan sulphate proteoglycan on the cell surfaces. Thirty-two pigs were subjected to 45 min of myocardial ischemia followed by 4 h of reperfusion. Control pigs (group A; n = 8) received 300 mL of saline into the great cardiac vein during a 30-min period started 5 min prior to reperfusion; pigs in group B (EC-SOD C; n = 8) got 16.6 mg of EC-SOD C; pigs in group C (EC-SOD C + CAT; n = 8) got 16.6 mg of EC-SOD C together with 150 mg of CAT. Pigs in group D (CAT; n = 8) received 150 mg of CAT. In groups B, C, and D, the drug was dissolved in saline and infused into the great cardiac. Infarct size expressed as percent of area at risk was smaller in groups B (14.5 +/- 16.7%) and C (40.8 +/- 13.3%) than in groups A (78.8 +/- 8.6%) and D (67.2 +/- 18.6%; p less than .05). Creatine kinase (CK) activity in ischemic myocardium was higher in groups B (1740 +/- 548 U/g) and C (1729 +/- 358 U/g) than in groups A (1184 +/- 237 U/g) and D (1251 +/- 434 U/g; p less than .05). There was an inverse relation (r = -.83) between infarct size and CK content. The EC-SOD C infusions resulted in only minimal increases in plasma SOD activities. In conclusion, the presence of SOD on the cell surfaces is of importance in the prevention of reperfusion injury rather than circulating SOD.
 ...
PMID:Effects of recombinant human extracellular-superoxide dismutase type C on myocardial infarct size in pigs. 150 79

A prospective study in 76 newborn with perinatal asphyxia searching for myocardial ischemia was carried out. The disease was found in 51% of the patients. With electrocardiogram, myocardial enzymes, X ray and clinical manifestations the diagnosis was elaborated. No difference in the sex was present, the mean of gestational age was 35 weeks, and with mean birth weight 2,216 g, respiratory distress was present in all the people; only 20.5% developed heart failure and two had heart murmurs; 61.5% showed cardiomegaly. The creatine kinase MB isoenzyme at twelve hours after birth was raised in most of the patients. Respiratory distress syndrome was the principal diagnosis in 38%; hypoxic ischemic encephalopathy and peri-intraventricular hemorrhage was present in 50 and 33% of the patients, respectively. Mortality rate was 33%. Also a comparative study in the infants with and without myocardial ischemia was carried out appearing significative difference in: 1. Cardiomegaly, 2. Hypoxic-ischemic encephalopathy and 3. Creatine kinase MB isoenzyme.
 ...
PMID:[Transient myocardial ischemia in newborn babies with perinatal asphyxia (hypoxic cardiomyopathy)]. 209 33

Seventy patients hospitalized with chest pain after cocaine use were retrospectively evaluated to define the risk and clinical course of acute myocardial infarction (AMI). AMI developed in 22 patients (31%) and transient myocardial ischemia was seen in an additional 9 patients (13%). Coronary risk factors did not distinguish those who developed AMI from those who did not. The presenting electrocardiogram was abnormal in 20 of 22 patients who evolved AMI and in 19 of 48 of those who did not. Creatine kinase levels were elevated in 75% of the patients, including 65% of those who did not develop AMI, but creatine kinase-MB elevations were only observed in the AMI group. The route of cocaine administration did not predict AMI and there was no predilection for a particular coronary vascular bed. The length of time between drug use and onset of AMI pain was often quite prolonged (median interval, 18 vs 1 hour in the non-AMI group). Eight of the patients with AMI underwent cardiac catheterization and 4 had significant coronary narrowing.
 ...
PMID:Acute myocardial infarction and chest pain syndromes after cocaine use. 189 9

The effects of the converting enzyme inhibitor captopril on the susceptibility of the heart to ventricular arrhythmias following ischemia, both in vitro and in vivo, were studied. In isolated rat hearts, captopril, administered either before or at the end of ischemia, reduced ventricular fibrillation upon reperfusion after 15 minutes of local ischemia. Reduction of purine overflow, improvement in contractility, and increase in coronary blood flow occurred concomitantly. In vivo, a closed-chest pig model was used to determine the effects of captopril, administered at the end of ischemia and continued orally, on the susceptibility to ventricular arrhythmias during the chronic phase of myocardial infarction. Myocardial ischemia was induced by 60-minute inflation of a balloon catheter in the left anterior descending coronary artery. Upon reperfusion, an accelerated idioventricular rhythm occurred, both in 10 untreated and in 10 captopril-treated animals. Creatine kinase levels during the reperfusion period were significantly lower after captopril treatment. Two weeks after the short-term experiments, monomorphic ventricular tachycardia could be induced with programmed electrical stimulation in six of eight surviving untreated pigs. In contrast, in none of the six surviving captopril-treated animals was ventricular tachycardia inducible. Thus, early intervention with captopril during the development phase of myocardial infarction may have beneficial effects on the subsequent development of ventricular arrhythmias. Salvage of ischemic myocardium, improvement in ventricular function, beneficial effects on coronary flow, and decreased activity of the sympathetic nervous system may all contribute.
 ...
PMID:Protective effects of captopril against ischemia/reperfusion-induced ventricular arrhythmias in vitro and in vivo. 306 1

Oxygen-derived free radicals and intracellular calcium overload have been implicated as mediators of myocardial ischemia/reperfusion injury. We hypothesized that free radical scavengers or calcium channel blockers could enhance the protection afforded the isolated, working rat heart by crystalloid cardioplegia against this type of injury at 37 degrees C. Hearts from 42 male rats in seven groups (n = 6) were studied in an isolated, working heart preparation measuring aortic flow (ml/min/gm dry wt), peak systolic pressure (mm Hg), coronary artery flow (ml/min/gm dry wt), and calculated coronary vascular resistance (dyne.sec.cm-5/gm dry wt). Creatine kinase and lactate dehydrogenase release were measured before ischemia and at various times during the postischemic reperfusion period. Time-matched control hearts (group 1) were perfused for 2 hours. After finding that 30 minutes of ischemia and 10 minutes of reperfusion (group 2) produced significant (p less than 0.01) functional impairment that was completely protected (group 3) by a preischemic bolus of St. Thomas' Hospital cardioplegic solution, we again found significant (p less than 0.01) functional impairment after 40 minutes of ischemia and 10 minutes (group 4) or 20 minutes (group 5) of reperfusion despite a preischemic bolus of St. Thomas' Hospital cardioplegic solution. Diltiazem (10 mg/L) plus St. Thomas' Hospital cardioplegic solution (group 6) did not significantly (p less than 0.01) enhance functional recovery. Addition of superoxide dismutase plus catalase (200 microns/ml) (group 7) produced marked improvement in functional recovery that did not differ significantly (p less than 0.01) from control results (group 1). The creatine kinase and lactate dehydrogenase data strongly supported the preceding functional data. Coronary flow and vascular resistance were not significantly (p less than 0.01) changed from control values in any group. We conclude that the addition of superoxide dismutase and catalase but not diltiazem to St. Thomas' Hospital cardioplegic solution can significantly enhance myocardial protection against normothermic ischemia/reperfusion injury. This implicates oxygen-derived free radicals as mediators of this type of injury.
 ...
PMID:Enhancement of crystalloid cardioplegic protection against global normothermic ischemia by superoxide dismutase plus catalase but not diltiazem in the isolated, working rat heart. 336 28

It has been reported that CoQ10, ubiquionone, may have a protective effect on the mitochondrial injury induced by myocardial ischemia and reperfusion during open heart surgery. The purpose of this study was to investigate whether CoQ10 may enhance myocardial protection when given before ischemia, during ischemia or during reperfusion in the isolated working rat heart. Hearts (n = 6-9/group) from male Wistar rats were aerobically (37 degrees C) perfused (20 min) with bicarbonate buffer. In the first series of studies, this was followed by a 3 min infusion of St. Thomas' Hospital cardioplegic solution containing various concentrations of CoQ10. Hearts were then subjected to 39 min of normothermic (37 degrees C) global ischemia and 35 min of reperfusion (15 min Langendorff, 20 min working). The percent recovery of aortic flow (%AF) was 50.5 +/- 3.3% in the CoQ10 free controls versus 55.9 +/- 4.4, 62.1 +/- 3.1*% (*p < 0.05) in the 29, 44 and 58 mumol/L CoQ10 groups, respectively. Creatine kinase (CK) leakage during Langendorff reperfusion had a tendency to decrease in the 58 mumol/L group. In the second series of studies, 3 min of cardioplegia without CoQ10 and 38 min of ischemia (37 degrees C) were followed by a 15 min Langendorff reperfusion with 0 or 58 mumol/L of CoQ10 and 20 min working reperfusion. %AF was 53.2 +/- 2.7 and 39.2 +/- 7.1% in the 0 and 58 mumol/L CoQ10 groups, respectively. CK leakage had a tendency to increase in the 58 mumol/L group.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of CoQ10 on myocardial ischemia/reperfusion injury in the isolated rat heart]. 760 95

Brief periods of ischemia have been suggested to protect against myocardial injury caused by a subsequent episode of prolonged ischemia and reperfusion. However, the protective effects of brief ischemic periods against myocardial dysfunction after prolonged myocardial ischemia are controversial. To examine whether the protective effects of brief ischemic episodes relate to the extent of prior ischemic events, isolated rat hearts were subjected to either no preischemia (group A); one 5-minute episode of preischemia and 10 minutes of reperfusion (group B); or two 1-minute episodes of ischemia, each followed by 5 minutes of reperfusion (group C). All hearts were then subjected to 15 minutes of total ischemia and 10 minutes of reperfusion. In group A, after 10 min of reperfusion coronary perfusion pressure (CPP) was 31% +/- 10% (mean +/- SEM) higher than the control value, peak force of cardiac contraction (FCC) was 64% +/- 5% lower, and heart rate was 18% +/- 3% lower. In group B, CPP increased 26% +/- 6%, FCC fell 58% +/- 7%, and heart rate decreased 22% +/- 8% (group B vs group A, P value not significant) after ischemia and reperfusion. In group C, CPP increased 23% +/- 7%, FCC decreased 57% +/- 8%, and heart rate fell 8% +/- 4% on reperfusion (group C vs groups A and B, P value not significant). Creatine kinase (CK) was measured in the hearts from different groups and was found to be similar. Release of the adenosine triphosphate (ATP) metabolites hypoxanthine, inosine, and adenosine was also not different in the coronary effluents of the three groups of hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Failure of brief ischemic episodes to protect against myocardial dysfunction caused by ischemia and reperfusion in isolated rat hearts. 798 1

Calcium release from sarcoplasmic reticulum (SR) may contribute to the intracellular calcium overload observed during myocardial ischemia and reperfusion. We have therefore investigated the ability of ryanodine to enhance myocardial protection when given before ischemia or during reperfusion in the isolated working rat heart. Hearts (n = 6-9/group) from male Wistar rats were aerobically (37 degrees C) perfused (20 min) with bicarbonate buffer (Ca2+ = 2.4 mM). In the first series of studies, this was followed by a 3 min infusion of St Thomas' Hospital cardioplegic solution containing various concentrations of ryanodine. Hearts were then subjected to 38 min of normothermic (37 degrees C) global ischemia and 35 min of reperfusion (15 min Langendorff, 20 min working). The recoveries of aortic flow (%AF) were 50.3 +/- 2.5% in the ryanodine free controls versus 55.2 +/- 5.8, 72.0 +/- 1.3 (p < 0.05), 61.0 +/- 4.3, 51.8 +/- 5.1 and 32.1 +/- 5.0 (p < 0.05)% in the 0.88, 1.75, 2.13, 2.50 and 10.00 nM ryanodine groups, respectively. Creatine kinase (CK) leakage during Langendorff reperfusion was reduced in the 1.75 nM group but was similar to control in all other groups. In the second series of studies, 3 min of cardioplegia without ryanodine and 38 min of ischemia (37 degrees C) were followed by 15 min of Langendorff reperfusion with 0, 0.09, 0.18, 0.88 or 1.75 nM ryanodine, %AF was 59.3 +/- 3.3%, 54.7 +/- 3.3, 53.8 +/- 3.5, 38.4 +/- 8.9 (p < 0.05) and 33.3 +/- 5.8 (p < 0.05)% in the 0, 0.09, 0.18, 0.88 and 1.75 nM ryanodine groups, respectively. CK leakage tended to increase dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Sarcoplasmic reticular calcium release and myocardial protection--effect of ryanodine on myocardial ischemia and reperfusion-induced injury]. 817 88

The time-related frequency of elevated results for the mass concentrations of the MB isoenzyme of creatine kinase and of troponin T were compared with that of creatine kinase and creatine kinase-MB activity in patients with acute myocardial infarction. Patients (322; 175 with and 147 without myocardial infarction) consecutively admitted for evaluation of possible acute myocardial infarction were investigated. Reference limits for troponin T (0.1 microgram/l) and creatine kinase-MB mass concentration (5.0 micrograms/l) were exceeded frequently in patients with unstable angina pectoris (troponin T 43%, creatine kinase-MB mass concentration 24%) in contrast to patients with no acute ischaemic heart disease (both < 5%). Within 4 and between 4-8 hours after onset of chest pain, the frequency of elevated results for creatine kinase-MB mass concentration and troponin T in patients with acute myocardial infarction was considerably higher (20-30%) than for creatine kinase and creatine kinase-MB activity. Creatine kinase-MB mass concentration and troponin T both allowed earlier diagnosis of acute myocardial infarction than creatine kinase and creatine kinase-MB activity, but troponin T was not elevated before the creatine kinase-MB mass concentration.
 ...
PMID:The mass concentrations of serum troponin T and creatine kinase-MB are elevated before creatine kinase and creatine kinase-MB activities in acute myocardial infarction. 830 15


1 2 3 Next >>