UMLS:C0151814 - FACTA Search

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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of coenzyme Q9 (25 mg/kg), N6-cyclohexyl adenosine (CHA, 100 micrograms/kg) and their combination were compared in rats with short-term or permanent ligation of the left coronary artery. The following parameters were evaluated in three series of experiments: 1) incidence and duration of ventricular fibrillation and tachycardia during coronary occlusion (10 min) and consecutive reperfusion (5 min); 2) contractility and electrical stability of the heart (ventricular fibrillation threshold) in animals with 2-day myocardial infarction; 3) ischemic myocardial mass after coronary occlusion (5 min) and necrotic tissue mass in 2-day myocardial infarction. The rats were given oral drugs 5 days and 2 hours before the study. All the experiments were performed in open-chest anesthetized (nembutal, 50 mg/kg) rats exposed to ventilation at room air. Both the coenzyme Q9 and CHA significantly reduced the incidence and duration of coronary occlusion and reperfusion arrhythmias, prevented cardiac contractile depression (heart rate.developed pressure) and increased ventricular fibrillation threshold). The effect of coenzyme Q9 was more marked than that of CHA. Coenzyme Q9 substantially reduced necrotic tissue mass while CHA diminished ischemic tissue mass. At the same time the total cardioprotective action of the Q9 + CHA combination was more pronounced than that of them used alone.
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PMID:[Cardioprotective effect of combined use of coenzyme Q9 and cyclohexyladenosine in ischemia, reperfusion and acute myocardial infarction]. 192 Nov 36

The effects of drugs on ischemia and reperfusion-induced arrhythmias were studied in vivo in anesthetized rats. The chest was opened under artificial respiration and the heart was exposed. The left anterior descending coronary artery was occluded, followed by reperfusion for 10 min each. The drugs (mannitol 10-50 mg/kg, aspirin 0.25-5 mg/kg, verapamil 5-50 micrograms/kg and propranolol 1 mg/kg iv) were tested in the vagotomized animals. The test agent was dissolved in saline and 0.5 ml infused 15 min before the coronary occlusion. The results indicated that mannitol and aspirin reduced the incidence and duration of arrhythmias (ventricular premature contraction, ventricular tachycardia and ventricular fibrillation) during ischemia and reperfusion, while verapamil and propranolol reduced the incidence of arrhythmias during ischemia.
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PMID:Drug effects on myocardial ischemia- and reperfusion-induced arrhythmias in anesthetized rats. 194 22

Severe arrhythmias occur predictably on reperfusion after 5 minutes of coronary occlusion in the rat. There is little data available on whether ischemic preconditioning (PC) of hearts can reduce the incidence of such arrhythmias. The effect of PC (three cycles of 2 minutes of coronary occlusion and 5 minutes of reperfusion) on development of arrhythmias after a subsequent 5-minute coronary artery occlusion and reperfusion was studied. Rats (n = 16 each group) underwent 5-minute occlusion and reperfusion alone or preceded by PC; arrhythmias were monitored during ischemia and for 10 minutes of reperfusion, and biopsies were taken for creatine phosphate and adenosine triphosphate in ischemic and nonischemic zones of the left ventricle. PC reduced the incidence of ventricular tachycardia (VT) during occlusion (81% control versus 13% PC, p less than 0.001). On subsequent reperfusion, ventricular fibrillation (VF) developed in zero PC animals versus 13 (81%) of controls (p less than 0.001), and irreversible VF in zero of PC versus seven (44%) of controls (p = 0.007). VT occurred in four (25%) of PC versus all (100%) of controls (p less than 0.001). PC reduced mean duration of VT plus VF from 320 +/- 54 to 5 +/- 1 seconds (p less than 0.001) and delayed arrhythmia onset from 8 +/- 2 to 85 +/- 35 seconds after reperfusion. There was no difference in creatine phosphate levels in the ischemic zone at the end of reperfusion in PC animals compared with controls without irreversible VF (16.2 +/- 4.1 versus 15.5 +/- 3.9 nmol/mg protein, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of preconditioning ischemia on reperfusion arrhythmias after coronary artery occlusion and reperfusion in the rat. 198 72

This study tested the hypothesis that sympathetic neural stimulation increases the prevalence of reperfusion-induced ventricular fibrillation and explored the mechanisms by which this occurs and how it may be prevented. In anesthetized, autonomically denervated dogs, we examined the effects of bilateral ansae subclaviae stimulation (SS) and of induction of pericardial biosynthesis of prostaglandins, an intervention that reduces SS effects by acting at presynaptic sites. A 5-minute occlusion of the left anterior descending coronary artery distal to the first or second diagonal branch was performed during SS. Heart rate was maintained constant by atrial pacing. In the absence of SS, one of 23 dogs developed ventricular fibrillation during occlusion, and three of the remaining 22 dogs developed ventricular fibrillation upon reperfusion. SS did not increase the prevalence of occlusion-induced ventricular fibrillation (four of 23 dogs) but increased the prevalence of reperfusion-induced ventricular fibrillation (12 of the remaining 19 dogs, p = 0.01). SS did not affect occlusion-induced decrease in local electrogram amplitude recorded from the ischemic myocardium or myocardial blood flow to the ischemic myocardium during occlusion or reperfusion. SS, however, prevented occlusion-induced increase in diastolic excitability threshold. Instillation into the pericardial cavity of arachidonic acid solution (3 micrograms/ml) resulted in release of prostacyclin, measured by radioimmunoassay as a stable metabolite 6-ketoprostaglandin F1 alpha (63.1 +/- 11.3 ng/ml, n = 11, mean +/- SEM), and of prostaglandin E2 (7.0 +/- 0.9 ng/ml, n = 11). This pericardial solution blunted SS-induced increase in mean arterial blood pressure and reduced the prevalence of ventricular fibrillation during reperfusion (six dogs to one dog, p less than 0.05). Blood flow to the ischemic myocardium remained unaffected. Indomethacin, when added to the solution (3 micrograms/ml), reversed the effects of prostaglandin release and arrhythmia development. These data indicate that efferent sympathetic stimulation during a coronary occlusion and reperfusion sequence increases the prevalence of reperfusion-induced ventricular fibrillation that is reduced by pericardial biosynthesis of prostaglandins. Pericardial prostaglandin synthesis may serve as a unique antiarrhythmic function by regulating efferent cardiac sympathetic nerve effects.
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PMID:Pericardial prostaglandin biosynthesis prevents the increased incidence of reperfusion-induced ventricular fibrillation produced by efferent sympathetic stimulation in dogs. 211 29

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.
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PMID:Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy. 214 98

The N-terminus consisting of amino acids (a.a.) 1-98 (i.e., proANF 1-98), C-terminus (i.e., ANF; a.a. 99-126) and midportion of N-terminus consisting of a.a. 31-67 (proANF 31-67; Vessel Dilator) of the 126 a.a. ANF prohormone were present in the urine in 5-to-8-fold increased concentrations versus their plasma concentrations in 6 dogs under basal conditions. With acute coronary occlusion the right atrial plasma concentrations of these peptides increased two-to-three-fold, while in the urine only proANF 31-67 increased (3.5-fold). Ventricular fibrillation caused a 4-to-10-fold increased secretion into the right atrial chamber with a simultaneous 3-to-4.7-fold increase in the urine of proANF 1-98, proANF 31-67, and ANF. This investigation demonstrates that proANF 1-98, proANF 31-67 and ANF are normally present in urine and increase in the urine with cardiac stimuli that cause their release from the heart.
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PMID:The N-terminus, C-terminus, and vessel dilator of the ANF prohormone are present in the urine and increase with ventricular fibrillation. 214 74

Reductions in cardiac vagal tone have been shown to correlate with increased susceptibility to ventricular fibrillation (VF). If these reductions in vagal tone contribute to VF, one would predict that interventions that increase vagal tone should protect against these lethal arrhythmias. Therefore, VF was induced in 17 mongrel dogs with healed myocardial infarctions by a 2-min coronary occlusion during exercise. On a subsequent day, the cholinergic agonist carbachol (20 micrograms/kg, i.v.) was given before the exercise plus ischemia test (n = 14). Carbachol elicited significant reductions in heart rate (control 204.5 +/- 27.7 vs. carbachol 147.0 +/- 49.6 beats/min) and prevented VF in 11 of 14 animals. When the decline in heart rate was prevented by ventricular pacing, carbachol prevented VF in five of six animals. Cyclic GMP may act as an intracellular messenger of cholinergic activation; therefore, 8-bromo cyclic GMP (n = 9) was infused (100-150 micrograms.kg-1.min-1, i.v.) throughout the exercise beginning 45 min before onset of exercise. Heart rate increased but VF was prevented in eight of nine animals. Similar results were noted for dibutyryl cyclic GMP (n = 5). These data suggest that cholinergic agonists and cyclic GMP can prevent VF in susceptible animals independently of heart rate changes.
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PMID:Effect of carbachol and cyclic GMP on susceptibility to ventricular fibrillation. 215 44

To study the effects of pharmacologic interventions on reperfusion-induced arrhythmias, open chest anesthetized dogs were subjected to occlusion of a coronary artery for 3 hours followed by reperfusion for 3 hours. Electrocardiograms were recorded with a two-channel monitor with the subsequent recordings submitted to computer-assisted analysis. The extent of myocardial infarction was measured by staining with triphenyl tetrazolium chloride. Mexiletine (12 mg/kg) and verapamil (0.9 mg/kg) were given, starting at 120 min of coronary occlusion and continued until the end of experiments. Dibunol (60 mg/kg) was administered at 120 min of ischemia. Dibunol and dibunol together with verapamil reduced the extent of infarction (to 62 +/- 6% and 53 +/- 4% of the zone at risk, respectively; compared to 77 +/- 3% of the zone at risk in the control group, P less than 0.05) while verapamil alone and mexiletine did not. There were 5 fatal episodes of ventricular fibrillations in 23 dogs, together with other malignant arrhythmias when occlusion was released in the control group. Mexiletine and verapamil prevented these episodes of ventricular fibrillation during reperfusion while dibunol, and dibunol together with verapamil, did not. Apart from fibrillations, mexiletine eliminated ventricular tachycardias, in contrast to the other drugs, which did not. Mexiletine and verapamil alone prevented ventricular premature beats while dibunol, and dibunol with verapamil, exacerbated their generation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacologic modifications of reperfusion arrhythmias in the dog in vivo: possible relation to limitation of the extent of infarction. 221 Aug 95

The changes of monophasic action potential (MAP) in ischemic and reperfused feline ventricle in situ were studied. When the feline coronary artery was ligated the MAPD50 was found to be markedly shortened, the T wave and S-T segment were elevated evidently. Within seconds of releasing the coronary occlusion ventricular fibrillation and death occurred in all animals. Intravenous injection of BTHP markedly prolonged the MAPD50 and MAPD90 and reduced the heart rate, while no influence on T wave and S-T segment were observed. After occlusion of the coronary artery, the T wave and S-T segment only increased slightly and the MAPD50 recovered to its control level. During reperfusion the occurrence of ventricular fibrillation was significantly reduced. In contrast, prazosin, verapamil and propranolol did not show significant effect on changes of MAP, but BTHP and Pra, Ver and Pro all showed protective effect on feline ischemic and reperfused myocardia by ligation and reperfusion of the coronary artery with decrease of the number of arrhythmia, ventricular fibrillation and death. The order of antiarrhythmic action of these agents was BTHP = Pra greater than Ver greater than Pro. The total incidence of ventricular fibrillation reduced from the control values of 100% in ischemia/reperfusion heart to 0% (BTHP and Pra), 20% (Ver) and 40% (Pro).
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PMID:[Effects of benzyltetrahydropalmatine on ischemia reperfusion with monophasic action potential]. 228 90

STUDY OBJECTIVE - The aim of the study was to investigate the influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a model of myocardial ischaemia. DESIGN - Myocardial ischaemia was induced in an open chest canine model by occluding the left coronary artery for 2 h. This was followed by 6 h reperfusion. The influence of reflow fibrillation and internal electric defibrillation on infarct size was investigated and compared to dogs which did not develop fibrillation. Infarct size and its major determinants, rate-pressure product (RPP), area at risk (AR), and collateral flow (MBF), were measured and their relationships studied in the two situations, using uni- and multilinear regression analysis. SUBJECTS - 21 adult mongrel dogs of either sex were used in the studies, which were done under pentobarbitone anaesthesia. Two were excluded because they developed ventricular fibrillation soon after coronary occlusion, and one did not survive reflow ventricular fibrillation. Of the remaining 18 dogs, six developed reflow ventricular fibrillation and were compared to the control group of 12 which did not develop fibrillation. MEASUREMENTS and RESULTS - A mean of 70.8(SEM 18.7) joules was required to revive the six dogs with reflow ventricular fibrillation. Difference in mean infarct size in the two groups did not reach significance [49.1(4.4) in fibrillation group v 38(6.2) in the controls]. The multiple linear regression model in the control group accounted for 91% of the variation in infarct size (IS): IS = -3.4 + 0.49 (AR) -21.8 (MBF) + 0.025 (RPP). The equation was not modified by including the reflow fibrillation dogs: IS = -3.1 + 0.52 (AR) - 19 (MBF) + 0.02 (RPP). Ischaemic determinants of infarct size in the reflow fibrillation dogs were computed in the control group equation to compare the infarct size predicted by the model to the measured infarct size in each individual dog in the reflow fibrillation group. There was no significant difference between the means: 12.9(2.9)% (predicted) v 14.9(2.5)% (measured). CONCLUSIONS - In this model of myocardial infarction, reflow ventricular fibrillation and low energy internal electric shocks do not damage the myocardium at risk significantly.
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PMID:Influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a canine preparation of myocardial infarction. 232 19

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