Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiischemic effect of pirsidomine (CAS 936 (3-(cis-2,6-dimethylpiperidino)-N-(4-methoxybenzoyl))-sydnon imine), a new nitric oxide donor, was investigated in a model of myocardial infarction in the dog. Dogs were anaesthetised, thoracotomized, and the left descending coronary artery was occluded for 6 h. Pirsidomine was given intraduodenally (i.d.) at the dose of 1.0 mg/kg to 11 dogs 30 min prior to coronary occlusion. Eleven dogs received the solvent i.d. and served as controls. Pirsidomine administration completely prevented the increase in left ventricular end-diastolic pressure and pulmonary artery pressure induced by the coronary occlusion and resulted in a marked decrease in systolic and diastolic blood pressure, cardiac output, left ventricular contractility, left ventricular work and left ventricular oxygen consumption. Additionally, pirsidomine completely prevented the occlusion-induced increase in flow in the non-occluded circumflex coronary artery. Regional blood flow measurements (with radioactive microspheres) revealed that pirsidomine induced a significant reduction in blood flow in the non-ischemic areas (both epi- and endocardial) but in the course of the ischemia, significantly increased flow in the ischemic epicardial areas. Infarct-size (triphenyltetrazolium chloride technique) in control dogs was 45% of the area at risk, but only 26% (P < 0.05) in pirsidomine-treated dogs. Thus, pirsidomine had a marked antiischemic effect in this model. This was probably due to the hemodynamic unloading of the heart as well as to redistribution of blood from the non-ischemic to the ischemic areas of the myocardium.
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PMID:Antiischemic effects of pirsidomine, a new nitric oxide donor. 808 46

Ischaemic injury in a number of animal models is reduced by mivazerol (2-hydroxy-3-[(1-H-imidazol-4-yl) methyl]-benzamide, CAS 125472-02-8). This effect was accompanied by a reduction in heart rate. The effect of mivazerol on myocardial blood flow and lactate production in the ischaemic myocardium was examined at constant heart rate by right atrial pacing in an anaesthetised open-chest dog model. Three periods of ischaemic were induced by coronary occlusion for 5 min. The first (sham) and the second in the absence of the drug and the third 15 min after 10 nmol/kg i.v. Arteriovenous differences in plasma lactate using a local vein and coronary sinus draining the ischaemic and non-ischaemic myocardium, respectively, were measured before and after 4 min after coronary occlusion. Blood flow (microspheres) was determined at 3 min of ischaemia. Mivazerol reduced lactate production by the ischaemic area from 2.6 +/- 1.2 to 1.5 +/- 0.9 mmol/l (paired t-test, p < 0.01), but blood flow to the ischaemic sub-endocardium was not changed: 0.19 +/- 0.1 vs 0.21 +/- 0.12 ml.g-1.min-2. Mean ST segment elevation tended to be reduced 1.6 +/- 1.0 vs 3.8 +/- 3.0 mV (one-sided paired t-test, p = 0.05). Mivazerol exerts its anti-ischaemic effect at least in part by a reduction in ischaemic lactate production but not by increasing ischaemic blood flow.
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PMID:Effect of mivazerol on myocardial lactate production, blood flow and electrocardiographic signs of ischaemia induced by coronary artery ligation in the anaesthetised dog. 903 36