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)

Superoxide dismutase (SOD) has been documented to limit myocardial infarct size in the richly collateralized dog heart. This study was designed to explore this concept in a low-collateralized animal model. A blind, randomized, placebo-controlled protocol was used in 65 pentobarbital-anesthetized pigs subjected to closed-chest left anterior descending coronary artery occlusion for 30 (n = 22), 60 (n = 22), and 90 (n = 14) minutes followed by reperfusion up to 24 hours from the start of occlusion. Another seven control pigs were subjected to 24 hours of permanent occlusion. A total dose of 9 mg/kg bovine CuZn SOD was administered as a bolus injection immediately before reperfusion followed by a 1-hour infusion. Infarct size was assessed by tetrazolium staining. Myocardium at risk and collateral flow were determined by using cerium-141-labeled microspheres (15 microns) during the occlusion. After 30 minutes of occlusion, infarct sizes in placebo versus SOD-treated animals were 45.5 +/- 15.7% vs. 23.8 +/- 15.6% of myocardium at risk (p = 0.007). The corresponding values after 60 minutes of occlusion were 78.6 +/- 9.3% vs. 66.9 +/- 14.6% (p = 0.035). SOD administered after 90 minutes of occlusion did not limit infarct size (88.5 +/- 4.8% vs. 92.3 +/- 5.2%). Twenty-four hours of coronary occlusion resulted in infarction of 92.4 +/- 4.2% of myocardium at risk. (All values are mean +/- SD.) Ventricular fibrillation occurred in only nine pigs distributed equally between SOD and placebo. The results indicate that CuZn SOD has the potential to further improve the myocardial salvage established by reperfusion of an ischemic pig heart territory. However, the narrow time window for limiting infarct size in the pig by reperfusion is not much extended by SOD.
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PMID:Limitation of myocardial infarct size by superoxide dismutase as an adjunct to reperfusion after different durations of coronary occlusion in the pig. 233 28

The effects of a new thromboxane A2 synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180 min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100 mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30 min after coronary ligation (7 +/- 9 ms vs 32 +/- 17 ms, p less than 0.05). The dispersion at 30 min after coronary ligation, though, was not affected in the DP-1904 treated group (2 +/- 4 ms vs 10 +/- 9 ms, n.s.). The VFT (determined with pulse trains) decreased from 28 +/- 5 mA to 15 +/- 11 mA (p less than 0.05) 30 min after coronary ligation in the control group, but was not affected (30 +/- 0 mA vs 27 +/- 4 mA) in the DP-1904 group. The plasma concentration of thromboxane B2 decreased after DP-1904 administration (baseline vs 30 min after coronary ligation: 475 +/- 165 pg/ml vs 165 +/- 74 pg/ml, n = 3, p less than 0.05), while the concentration of 6-keto-prostaglandin F1 alpha increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.
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PMID:Effects of a thromboxane A2 synthetase inhibitor on ventricular fibrillation threshold during coronary artery occlusion and reperfusion. 233 49

In pentobarbital-anesthetized rats the left coronary artery was ligated for 5 or 30 min and then opened for reperfusion of the ischemic myocardial area. Twelve min prior to the coronary occlusion yohimbine stereoisomers, namely corynanthine and rauwolscine, or saline solution were given intravenously. In the saline controls both ischemia and reperfusion provoked severe tachyarrhythmias with ventricular fibrillation in 37.5% or 54.6%, respectively. Using corynanthine and rauwolscine a highly significant antiarrhythmic effect was observed. Corynanthine completely prevented ventricular fibrillation and delayed significantly the development of myocardial necrosis. The factors likely underlying the antiarrhythmic and antinecrotic effects are discussed.
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PMID:Antiarrhythmic and antinecrotic effects of yohimbine stereoisomers in rats during coronary occlusion and reperfusion. 235 Mar 27

To investigate the importance of local noradrenaline (NA) release in initiating early ventricular extrasystoles (VES) and primary ventricular fibrillation (VF) after acute myocardial ischemia, a special form of regional myocardial chemical sympathectomy (RMCS) has been performed in dogs. After RMCS the tissue content of NA within the denervated region was reduced below 1.5% of normal, whereas the residual myocardium retained its functional state almost unchanged. After acute left circumflex coronary artery (LCX) occlusion (30 min), all control animals with normal circumflex circulation and without functionally effective collaterals died of VF. In contrast, after RMCS none of the dogs had VF and very few had VES. After RMCS the rise in myocardial extracellular K+ activity ([K+]e) during coronary occlusion is slightly slower, but the same [K+]e are reached at 8 min of occlusion. Therefore, the effect of RMCS cannot be explained by changes in myocardial K+ liberation. These results, obtained from RMCS experiments, are supported by the preliminary results of experiments using a special perfusion technique to wash out blood from the acutely occluded myocardial region, and show an ischemia-induced raise of the locally released NA in the early arrhythmic phase 1a with a further increase in phase 1b.
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PMID:Antiarrhythmic effect of regional myocardial chemical sympathectomy in the early phase of coronary artery occlusion in dogs. 241 Jul 41

The effects of nifedipine against ischemia- and reperfusion-induced arrhythmias were investigated using anesthetized rats with transient coronary artery occlusion. Nifedipine (5 micrograms/kg i.v.) administered 10 min prior to occlusion significantly decreased the incidence of arrhythmias occurring during 20-min coronary occlusion. The incidence and duration of reperfusion-induced ventricular fibrillation and subsequent mortality following 5-min coronary occlusion were also significantly reduced by this intervention. However, administration of nifedipine 1 min prior to reperfusion afforded no protection against reperfusion arrhythmias. To investigate whether nifedipine possesses a true antiarrhythmic action or merely extends the ischemic duration prior to reperfusion resulting in maximal rhythm disturbances, reperfusion was initiated after 3, 5, 7, 10, 20, and 30 min of ischemia. Nifedipine reduced the incidence of reperfusion-induced ventricular fibrillation after all ischemic intervals, with no change in the time of peak vulnerability to reperfusion arrhythmias. Measurements of coronary flow with 153Gadolinium microspheres indicated that flow within ischemic tissue relative to that in normal tissue was significantly increased by nifedipine. Thus, administration of nifedipine prior to occlusion affords a protective effect against ischemia- and reperfusion-induced arrhythmias, and this action is not due to extension of the ischemic duration prior to reperfusion resulting in maximal rhythm disturbances.
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PMID:Ischemia- and reperfusion-induced arrhythmias: beneficial actions of nifedipine. 243 54

The effectiveness of verapamil in preventing ventricular fibrillation caused by coronary occlusion or reperfusion has been well demonstrated in animal studies, but these experimental data have not yet been confirmed in man. In this study we evaluated the prevalence of ventricular arrhythmias (fibrillation, sustained tachycardia and frequent extrasystoles) in patients hospitalized for myocardial infarction and treated with or without verapamil. The records of patients admitted to our Coronary Intensive Care unit during a 5-year period were analyzed retrospectively. Strict selection criteria enabled us to divide our patients into two homogeneous groups. The control group (group A) consisted of 106 patients who received only continuous infusions of heparin. The treated group (group B) comprised 89 patients who received exclusively verapamil by intravenous injections followed by continuous infusions. The prevalence of ventricular arrhythmia of all types was significantly lower in group B (22 p. 100) than in group A patients (71 p. 100; p less than 0.001). Episodes of ventricular fibrillation, in particular, were considerably less frequent in group B patients (1 p. 100) than in group A patients (13 p. 100; p less than 0.001). It would appear from these results that verapamil is highly effective in preventing death due to cardiac arrhythmia in the acute phase of myocardial infarction.
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PMID:[Efficacy of verapamil in the prevention of ventricular fibrillation in the acute phase of myocardial infarction]. 246 Nov 79

The effects of calcium channel antagonists and an agonist on susceptibility to ventricular fibrillation were investigated using chronically instrumented dogs with a healed anterior wall myocardial infarction. Three to 4 weeks after the infarction, a 2-min coronary occlusion was initiated during the last minute of exercise and continued for 1 min after cessation of exercise. Twenty-two dogs developed ventricular fibrillation (susceptible) whereas the remaining 14 animals did not (resistant) during this exercise plus ischemia test. The exercise plus ischemia test was repeated in the susceptible dogs after the following treatments: verapamil (n = 17, 250 micrograms/kg), nifedipine (n = 9, 10 and 100 micrograms/kg) and magnesium sulfate (n = 9, 100 mg/kg). Verapamil prevented ventricular fibrillation in all dogs whereas the high dose of nifedipine protected eight of nine animals; the low dose of nifedipine protected one of nine animals and magnesium sulfate protected seven of nine dogs. Finally, the calcium channel agonist Bay K8644 (n = 9, 30 micrograms/kg) was given to resistant animals. All resistant dogs developed ventricular fibrillation when the exercise plus ischemia test was repeated after Bay K8644. These data suggest that calcium entry may play a critical role in the development of arrhythmias during ischemia, with increased calcium entry provoking arrhythmias and calcium entry blockade preventing the lethal events.
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PMID:Effect of calcium channel antagonists on susceptibility to sudden cardiac death: protection from ventricular fibrillation. 246 81

In anesthetized open-chest pigs, DL- or D-propranolol (1 mg/kg i.v.) was administered 15 min prior to ligation of the left anterior descending coronary artery (LAD) about halfway from its origin. Sequential myocardial tissue samples were obtained before and after LAD occlusion. The samples were analyzed histofluorimetrically to determine the density of catecholamine containing neurons (quantified morphometrically), and radioenzymatically for total tissue noradrenaline content. The extracellular K+ concentration was measured using K+-sensitive polyvinyl chloride (PVC)-membrane electrodes on the surface of the ischemic myocardium. Under control conditions, ventricular arrhythmias (VA) occurred in a typical 1a and 1b phase. Pretreatment with propranolol diminished the number of VA generated in the 1b phase but not those in the 1a phase; however, these differences were statistically not significant. Neither pretreatment with DL- nor D-propranolol influenced the time course or probability of development of ventricular fibrillation (VF). Coronary artery occlusion led to a significant reduction in noradrenaline concentration of the ischemic myocardium in control animals (from an initial concentration of 526 +/- 65 ng/g w/w to 368 +/- 75 ng/g w/w) within the first 5 min of ischemia, whereas noradrenaline concentration remained nearly unchanged in drug-treated animals (from 838 +/- 86 to 811 +/- 61 ng/g w/w in the DL group and from 701 +/- 36 to 709 +/- 31 ng/g w/w in animals that received D-propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of propranolol on early postischemia arrhythmias and noradrenaline and potassium release of ischemic myocardium in anesthetized pigs. 246 34

In our earlier experiments prolonged administration of the stable PgI2 analogue: 7-oxo-PgI2 ephedrine salt to dogs afforded a long-lasting protection against coronary occlusion induced ischemia as well as against postocclusion and reperfusion arrhythmias. In the present experiments we wanted to clear, whether this prolonged protective action is present in other types of arrhythmia, which are not due to ischemia. The ouabain-arrhythmia seemed to be suitable for elucidation of this question. Therefore guinea pigs were pretreated with 50 micrograms/kg i.p. 7-oxo-PgI2 and 24, 48, 72 and 96 hrs after treatment anesthetized with 35 mg/kg sodium pentobarbitone. To prevent ouabain bradycardia, 0.4 mg/kg atropine was administered i.p. Ouabain was applied by intermittent infusion technique i.e. an initial infusion for 5 minutes of a total dose of 60 micrograms/kg into the right jugular vein was followed after a 25 minutes interval by infusions of 30 micrograms/kg for 2.5 minutes every 10 minutes until cardiac arrest. The ouabain induced rhythm disturbances appeared in the following order: Anomalies in T wave morphology, ventricular or nodal extrasystoles, atrio-ventricular and intraventricular conduction disturbances, ventricular tachycardia, ventricular fibrillation and finally cardiac arrest. If 50 micrograms/kg i.p. 7-oxo-PgI2 was given to ouabain-intoxicated animals at the appearance of the first extrasystole a transient aggravation of this arrhythmia developed. In 7-oxo-PgI2 pretreated animals the total amount of ouabain necessary to induced rhythm disturbances was markedly elevated, the appearance of the various arrhythmias significantly delayed. Maximal protective effects were seen 48 hrs after the administration of 50 micrograms/kg 7-oxo-PgI2.
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PMID:On the 7-oxo-PgI2 induced lasting protection against ouabain arrhythmias in anesthetized guinea pigs. 247 Mar 57

The effect of anipamil pretreatment on ischemic electrocardiogram changes and loss of creatine kinase (CK) after 3 h of left anterior descending coronary artery (LAD) occlusion (group I) and, in a second set of experiments, on reperfusion arrhythmias after 5 min of coronary occlusion (group II) in closed-chest rats was investigated. An LAD occluder was implanted in animals under anaesthesia 8 days before coronary occlusion. Rats in group I were orally treated for 8 days with 6.0 mg/kg anipamil once daily; LAD occlusion was performed 4 h after the last treatment. Group II animals received a single injection of 0.5 or 1.0 mg/kg anipamil intravenously 30 min before coronary occlusion. Oral anipamil significantly reduced CK loss compared with untreated controls. Three hours after occlusion, plasma CK was 99 +/- 37 U/L in the anipamil group compared with 257 +/- 47 U/L in controls. During the first 10 min after occlusion anipamil delayed the increases of the R wave and of the ST segment. In the reperfusion experiments all control rats showed polymorphous ventricular tachycardia (VT) immediately after restoration of coronary flow; 77% degenerated to ventricular fibrillation (VF). After 0.5 mg/kg anipamil i.v. VT was observed in 61% of the rats, VF only in 14%; pretreatment with 1.0 mg/kg totally prevented reperfusion arrhythmias in all animals. We conclude that pretreatment with anipamil reduces the functional and biochemical damage after acute myocardial ischemia and totally prevents reperfusion-induced arrhythmias in closed-chest rats.
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PMID:Effects of anipamil on electrocardiogram, plasma creatine kinase, and reperfusion arrhythmias after coronary occlusion in closed-chest rats. 247 96


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