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)

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.
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PMID:Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations. 817 1

Caloric restriction (CR) is a novel dietary therapy that has a protective effect on myocardial ischemia. However, the mechanisms underlying the therapeutic effect of CR remain unclear. Transfer RNA-derived small RNAs (tsRNAs) are a novel type of short non-coding RNAs that have potential regulatory functions in various physiological and pathological processes. In this study, we explored new therapeutic targets of CR through tsRNA sequencing. Rats were randomly divided into three groups: a normal control group (norm group), isoproterenol (ISO)-induced myocardial ischemic group (MI group), and CR pretreatment plus ISO-induced myocardial ischemic group (CR + MI group). Triphenyl tetrazolium chloride staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, serum creatine kinase (CK) and lactic acid dehydrogenase activity detection kits, and creatine kinase isoenzyme 1 levels were used to measure the degree of myocardial ischemic injury. These indicators of myocardial ischemia were significantly improved in the CR + MI group compared with those in the MI group. In the ischemic myocardial tissue of the MI group, a total of 708 precisely matched tsRNAs were identified, and 302 tsRNAs (fold change >1.5, P < 0.05) were significantly changed when compared with those in the norm group. Furthermore, 55 tsRNAs were significantly regulated by CR pretreatment, among which five tsRNAs (tiRNA-His-GTG-004, tRF-Gly-TCC-018, tRF-Cys-GCA-022, tRF-Lys-CTT-026, tRF-Met-CAT-008) were randomly selected and verified by quantitative real-time polymerase chain reaction. In addition, predictions of target genes and bioinformatics analysis indicated that these tsRNAs may play a therapeutic role through the regulation of macromolecular metabolism. In conclusion, our findings reveal that tsRNAs are potential therapeutic targets for CR pre-pretreatment to improve myocardial ischemic injury. This study provides new ideas for future research on elucidating the mechanisms of CR pretreatment in ameliorating myocardial ischemic injury.
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PMID:Systematic Analysis of tRNA-Derived Small RNAs Discloses New Therapeutic Targets of Caloric Restriction in Myocardial Ischemic Rats. 3322 44