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

The effects of exogenous superoxide dismutase (SOD) on acute myocardial ischemia (MI) was investigated in isolated electrically-driven rabbit hearts (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37 degrees C). Acute regional ischemia (MI) was induced by occlusion of a coronary artery branch (CAO) and quantitated from epicardial NADH-fluorescence photography. SOD (48 U/ml) was applied either 30 min after CAO in a single coronary occlusion model (treatment) or 30 min before the 2nd CAO in a repetitive coronary occlusion model (pre-treatment). SOD had no significant influence on the left ventricular pressure or the global coronary flow (p > 0.05). MI was significantly diminished in hearts pre-treated with SOD before CAO (-25%)(p < 0.05), but remained unaffected when SOD was applied after CAO (p > 0.05). The results suggest that superoxide anion radicals contribute to ischemic tissue injury. SOD shows cardioprotective properties only if present in the ischemic zone, requiring the application of SOD before CAO in poorly collateralised rabbit hearts.
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PMID:Comparison of the cardioprotective efficacy of superoxide dismutase in a single and a repetitive coronary occlusion model in rabbit hearts. 859 59

Myocardium undergoes functional changes in the infarcted region primarily due to ischemia. Following myocyte functional alterations of the noninfarcted myocardium are caused by remodelling and hypertrophy. We have monitored and compared changes in the electrocardiographical (ECG) image after coronary artery occlusion (CAO, n=5) and intracoronary endothelin-1 (ET-1, n=3) administration during a 6-month period. In 3 dogs, the CAO was repeated 6 months after the first occlusion. Signal-averaged ECG (SA ECG) was recorded before the operation and 10 days, 1 month, 3 months and 6 months after myocardial infarction (MI). The modified Wigner distribution was used for spectrotemporal analysis of the SA ECG. Eight-hour Holter monitoring was performed in each dog before and after experimental MI. Spectrotemporal representations of the QRS complex were stabilized after the first 1-month period in the group of dogs after CAO. The same results were also observed after the repeated CAO. No arrhythmias were recorded 9 days after CAO. The spectrotemporal representations of the QRS complex after intracoronary ET-1 administration were not stabilized during the whole observed period. Very few arrhythmic events were recorded by Holter monitoring already 3 days after intracoronary ET-1 injection. Experimental MI induced by CAO caused a changed ECG image, which was stable from 1 month after MI induction till the end of the monitoring. However, the ECG image after ET-1 administration was not stable during the whole observed period. No arrhythmic events were recorded in either group 3 months postoperatively that could be caused by healthy myocardial status before the experimental MI induction. In clinical practice, however, ischemic heart disease usually precedes the MI. Arrhythmogenic substrate could thus be a consequence of combination of healthy status of the myocardium before MI and MI itself.
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PMID:Long-term monitoring of the changes in signal-averaged ECG after coronary artery occlusion and intracoronary endothelin-1 injection in dogs. 1585 64

Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO (n=5), 30 s CAR/30 s CAO (n=7), and 1 min CAR/1 min CAO (n=6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33+/-4 vs. 34+/-4%, 30+/-4 vs. 30+/-4%, and 33+/-4 vs. 32+/-4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39+/-7%, n=6 vs. 56+/-4%, n=7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.
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PMID:Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits. 1656 17

Evidence suggests that substance P (SP) participates in the pathology of acute myocardial ischemia and infarction but the profiles of the peptide in regulation of cardiac functions are still elusive. The aim of this study was to investigate the role of substance P in regulation of cardiac functions and its association with adrenergic mechanism in acute myocardial ischemia and infarction with rodent models. The experiments were carried out in Sprague-Dawley rats. SP and norepinephrine were significantly up-regulated in myocardium at 15min, 30min and 60min of coronary artery occlusion. Pretreatment of the rats with a specific antagonist of neurokinin-1 receptor, D-SP, significant increased+dp/dt and decreased -dp/dt, compared with the controls, pretreated with 0.9% saline. Pretreatment of the isolated CAO hearts with substance P (10(-7)mol/L) significantly increased left ventricular end diastolic pressure. SP producing no effects on cardiac functions when given alone to isolated (non-CAO) heart caused significant attenuation of the changes in the contractility and diastolic functions induced by norepinephrine, when given with norepinephrine. SP attenuated the increase in the activity of PKA provoked by norepinephrine in cultured myocytes. In conclusion, the findings may indicate SP regulates cardiac functions via modulation of adrenergic activity, through suppression of over-activation of PKA.
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PMID:Implication of Substance P in myocardial contractile function during ischemia in rats. 2125 75