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)

1. The aim of this study was to compare the effects of the non-selective phosphodiesterase (PDE) inhibitor, isobutylmethylxanthine (IBMX) and the selective PDE III inhibitor, milrinone, in a rabbit model of acute myocardial ischaemia. 2. Coronary artery occlusion caused changes in the ST-segment of the ECG and ectopic activity in all control rabbits. Ventricular fibrillation occurred in 10 out of 14 (71%) of these animals. Pretreatment with IBMX 100 micrograms kg-1 plus 10 micrograms kg-1 min-1, starting 10 min before coronary artery occlusion, reduced ischaemia-induced ST-segment changes and ventricular fibrillation occurred in only 10% of this group (n = 10). A similar dose of milrinone had no antiarrhythmic activity, whereas with a lower dose of milrinone, 30 micrograms kg-1 plus 3 micrograms kg-1 min-1 (n = 10), only 30% of rabbits fibrillated and ST-segment changes were attenuated. 3. Acute administration of both IBMX and milrinone reduced arterial blood pressure. With the higher dose of milrinone a significant effect was still present after 10 min of drug infusion. A greater hypotensive response to the higher dose of milrinone was observed in the rabbits which subsequently fibrillated during ischaemia. A marked tachycardia was also observed after administration of the higher dose of milrinone. 4. At the end of the experiment platelet aggregation was studied ex vivo. ADP-induced aggregation was reduced by pretreatment of the rabbits with milrinone but not IBMX. Both PDE inhibitors enhanced the ability of isoprenaline to inhibit ADP-induced platelet aggregation but milrinone was more effective, particularly at the higher dose. The results demonstrate that IBMX was antiarrhythmic but that this activity was not directly related to inhibition of platelet aggregation. Adverse haemodynamic effects may explain the failure of milrinone to have similar activity during myocardial ischaemia.
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PMID:Comparison of the effects of isobutylmethylxanthine and milrinone on ischaemia-induced arrhythmias and platelet aggregation in anaesthetized rabbits. 247 45

To investigate the influence of local cardiac converting enzyme (CE) inhibition on the effects of angiotensin I (ANG I), ANG II, and bradykinin (BK), experiments were performed in ischemic isolated perfused working rat hearts. Acute regional myocardial ischemia was induced by 15 min occlusion of the left coronary artery followed by reperfusion. In ischemic isolated rat hearts, perfusion with ramiprilat (100 ng/ml, 2.58 x 10(-7) mol/l), the active moiety of the CE inhibitor ramipril, after coronary occlusion protected against ventricular fibrillation that invariably occurred in untreated control hearts in the reperfusion period. Addition of ANG I and ANG II to the perfusate enhanced, whereas BK reduced postischemic reperfusion arrhythmias, which were almost abolished in the hearts from ramipril (1 mg/kg p.o.) pretreated rats. Perfusion with ANG I and ANG II reduced cardiac function and coronary flow, increased the activities of lactate dehydrogenase and creatine kinase in the perfusate, and decreased high-energy-rich phosphates and glycogen in the myocardium. In contrast, BK reduced the enzymatic activities in the perfusate and improved the metabolic parameters in the myocardium. In hearts from ramipril pretreated animals, the ANG I effects were abolished, whereas the ANG II actions remained unchanged. The results of these experiments are consistent with the hypothesis that the beneficial effects of CE inhibitors on ventricular arrhythmias, cardiac function, and metabolism are due to local interference with CE in the coronary vascular wall or heart tissue and subsequent reduction of local ANG II generation and BK degradation.
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PMID:Influence of local converting enzyme inhibition on angiotensin and bradykinin effects in ischemic rat hearts. 248 67

We performed coronary angiography within 95 minutes of the onset of symptoms in seven patients with an acute coronary event after an exercise stress test. The test was normal in six patients. Previous angiography in four patients revealed no evident or moderate obstructive coronary arterial disease. After the test, unstable angina developed in two patients, acute myocardial infarction in four and ventricular fibrillation in one, who was successfully resuscitated. At acute angiography the coronary artery involved was occluded in four and sub-totally obstructed in three. In three cases, coronary occlusion was due to thrombosis, vasospasm, or both. In six vessels there was an eccentric lesion, which is consistent with a ruptured plaque. These findings show that physical exercise can unexpectedly provoke an acute coronary event with sub-total or total occlusion of a previous angiographically normal or moderately obstructed coronary artery. The mechanism is probably related to exercise-induced plaque rupture which can produce coronary (sub)occlusion by coronary thrombosis, spasm, or both.
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PMID:Unstable angina, myocardial infarction and sudden death after an exercise stress test. 250 74

By means of Langendorff method and standard microelectrode techniques the effects of Ciwujia on reperfusion induced arrhythmias and action potential alterations were studied in isolated rat heart with transient coronary occlusion. Inclusion of Ciwujia extract (equivalent to 1.2 and 2.4 mg crude drug/ml) was found helpful in reducing reperfusion induced ventricular fibrillation and ventricular tachycardia. Associated with this reduction in rhythm disturbances was an increase in the total duration of normal sinus rhythm during the 3 min reperfusion period. With the administration of Ciwujia the number of cells with abnormal action potential configurations was significantly reduced. This confirms that Ciwujia can protect myocardium from electrophysiological abnormalities, and therefore reduces the incidence of malignant arrhythmias.
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PMID:[Effects of ciwujia (Acanthopanax senticosus Harms) on reperfusion-induced arrhythmia and action potential alterations in the isolated rat heart]. 250 75

Cicletanine is a new antihypertensive agent. In view of its various pharmacological properties and of the different factors involved in sudden death, cicletanine was tested on an ischaemia-reperfusion model in anaesthesized dogs. In these experiments myocardial reperfusion induced ventricular fibrillation in 87 p. 100 of the cases, where as only 20% of those animals who received cicletanine 20 mg/kg intravenously 15 minutes before the 30 minute coronary occlusion developed ventricular disorders (p less than 0.001 vs controls). Moreover, cicletanine showed good antiarrhythmic activity during occlusion (total number of arrhythmias: 73.0 +/- 23.15 in treated animals, as against 293.4 +/- 40.03 in controls; p less than 0.05). Thus, antihypertensive treatment with cicletanine may prevent some of the cardiovascular risks associated with arterial hypertension.
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PMID:[Effect of cicletanine on a sudden death model in dogs]. 251 57

Using anaesthetised rats we have assessed (1) whether the density of alpha 1 adrenergic receptors increases during coronary artery occlusion, (2) whether any change in density can be associated with the onset of reperfusion induced ventricular fibrillation, and (3) whether alpha 1 blockade with prazosin modifies the incidence of reperfusion induced ventricular fibrillation. The incidence of fibrillation upon reperfusion after 3, 5, 10, 20 and 30 min occlusion was 20, 75, 50, 16 and 10% (n = 10-12 in each group) respectively. alpha 1 Receptor density was measured using [3H]-prazosin in non-ischaemic and ischaemic tissue obtained after 0, 5 and 30 min ischaemia. Receptor density was not significantly altered at the time of maximum incidence of reperfusion induced ventricular fibrillation (5 min occlusion) but did significantly increase in both non-ischaemic and ischaemic tissue after 30 min occlusion, when the incidence of fibrillation upon reperfusion was very low (8%). At this time the values were 17.0(SEM 2.3) and 18.4(0.6)fmol.mg-1 protein in non-ischaemic and ischaemic zones as compared to 10.7(0.6) and 12.8(1.0)fmol.mg-1 protein in sham operated control animals (p less than 0.05 in both cases). Prazosin (0.1 or 1.0 mg.kg-1 body wt intravenously, 5 min prior to coronary occlusion) did not alter the incidence of ventricular fibrillation, ventricular tachycardia or total number of premature ventricular complexes upon reperfusion. We conclude that ischaemia induced changes in alpha 1 receptor density do not parallel changes in vulnerability to reperfusion induced arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation between reperfusion induced arrhythmias and increases in ventricular alpha 1 receptor density in the anaesthetised rat. 255 4

Periodic fluctuations in the R-R interval have been used as noninvasive measures of cardiac autonomic tone. For example, a reduced heart rate variability has been shown to correlate with an increased mortality in patients recovering from myocardial infarction. The effects that physiologic perturbations such as exercise have on this heart rate variability have not been investigated. Therefore, heart rate variability was measured throughout a submaximal exercise test in 36 mongrel dogs with healed anterior myocardial infarctions. The amplitude of the respiratory component (0.24-1.04 Hz) was determined by time-series analysis techniques and was used as an index of cardiac vagal tone. On a subsequent day, a 2-minute coronary occlusion was initiated during the last minute of exercise. Twenty-two animals developed ventricular fibrillation (susceptible), whereas 14 animals did not (resistant). Exercise elicited a significantly greater increase in heart rate (resistant, 205.4 +/- 7.1; susceptible, 227.0 +/- 5.4 beats/min) in susceptible animals, which was accompanied by a greater reduction in the cardiac vagal tone index (resistant, 2.7 +/- 0.3; susceptible, 1.1 +/- 0.2 ln msec2) as compared with resistant animals. Conversely, atropine sulfate (50 micrograms/kg) given during exercise elicited a greater heart rate increase in the resistant dogs (heart rate change: resistant, 54.2 +/- 7.0; susceptible, 18.7 +/- 4.4 beats/min). Taken together, these data suggest that exercise elicited a greater reduction in cardiac vagal tone in animals known to be susceptible to ventricular fibrillation.
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PMID:Time-series analysis of heart rate variability during submaximal exercise. Evidence for reduced cardiac vagal tone in animals susceptible to ventricular fibrillation. 256 40

Although the incidence of ventricular arrhythmias following myocardial ischaemia lessens as ischaemia improves, it is not clear whether this is correlated with a reduction in the degree of ST segment elevation. To explore this further we examined the effects of change in heart rate and the administration of the calcium antagonist diltiazem, 0.02 mg.kg-1.min-1, on ST segment elevation and the alternans of ST segment elevation (STA) and on serious ventricular arrhythmia induced by 10 min occlusion of the left anterior descending coronary artery in 86 mongrel dogs. The dogs were divided into three groups: 26 dogs paced at a rate of 180 beats.min-1 (group A); 44 dogs paced at a rate of 120 beats.min-1 (group B); and 16 dogs paced at a rate of 180 beats.min-1 and given diltiazem intravenously from 25 min before the coronary occlusion (group C). The degree of ST segment elevation and STA within 3 min of ischaemia was significantly lower in group B than in group A. There was no marked difference in the degree of ST segment elevation between groups A and C, but the STA was lower in group C than in group A. Incidence of ventricular tachycardia and ventricular fibrillation was significantly lower in groups B and C than in group A, and the timing of their first appearance was 4.5 (SEM 0.6), 4.2(0.9) and 3.0(0.4) min, respectively. We suggest that the reduction in serious ventricular arrhythmias associated with the decrease in heart rate was caused by the improvement of STA secondary to the improvement of ST segment elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of heart rate and diltiazem hydrochloride on alternans of ST segment elevation and ventricular arrhythmia during acute myocardial ischaemia in dogs. 259 Sep 25

Disturbances in autonomic control during myocardial ischemia may contribute significantly to the development of malignant cardiac arrhythmias. Therefore acute ischemia was induced in 29 mongrel dogs with healed myocardial infarctions during an exercise test. Seventeen animals developed ventricular fibrillation (susceptible, S), whereas 12 dogs did not (resistant, R). Before the exercise plus ischemia test a coronary occlusion was made at rest. The amplitude of respiratory sinus arrhythmia (0.24- to 1.04-Hz component of R-R interval fluctuation) was used as an index of cardiac vagal tone. Acute ischemia elicited a significantly larger heart rate increase in susceptible animals (S: control 115.6 +/- 0.8, occlusion 176.4 +/- 8.2 beats/min vs. R: control 114.6 +/- 8.9, occlusion 145.7 +/- 7.5 beats/min). Accompanying the heart rate increase were significantly greater reductions in the cardiac vagal tone index in the susceptible animals. (S: control 6.4 +/- 0.3, occlusion 2.2 +/- 0.6 ln ms2 vs. R: control 6.6 +/- 0.4, occlusion 5.1 +/- 0.5 ln ms2). beta-Adrenergic receptor blockade reduced the heart rate increases but exacerbated the reductions in the cardiac vagal tone index. These data suggest that coronary artery occlusion elicits a significantly greater increase in sympathetic activity coupled with a greater reduction in parasympathetic activity in animals subsequently shown to be susceptible to ventricular fibrillation.
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PMID:Autonomic response to coronary occlusion in animals susceptible to ventricular fibrillation. 260 74

The effect of (+/-)-sotalol (a beta-blocker with class III antiarrhythmic activity) against reperfusion-induced arrhythmias was studied in artificially ventilated, open-chest, Sprague-Dawley and Wistar rats. Coronary artery occlusion was produced for 5 min and reperfusion allowed for 10 min. A somewhat different arrhythmic profile was observed between saline-treated rats of the 2 strains studied, with more Sprague-Dawley rats experiencing an irreversible ventricular fibrillation (VF) upon reperfusion, compared to Wistar rats, in whom a combination of reversible ventricular tachycardia (VT) and VF was more frequently observed. No difference in action potential characteristics and ventricular effective refractory period determined in vitro, nor in myocardial noradrenaline content, was found between the 2 strains of rats. (+/-)-Sotalol (5 and 10 mg/kg, IV) showed marked beta-blocking activity and reduced the mean duration of VT-VF in both strains studied. It also produced similar increases in action potential duration and refractory period in vitro in these 2 strains. In a different series of experiments, the antiarrhythmic action of the racemic form was compared to that of (+)-sotalol using Wistar rats. (+)-Sotalol had much less beta-blocking activity, and was found to be similarly effective against reperfusion-induced VT-VF. It is concluded that the antiarrhythmic effect of sotalol against reperfusion-induced arrhythmias may not be related to beta-adrenergic blockade but probably to class III type activity. Despite differences in the profile of reperfusion-induced arrhythmias between Sprague-Dawley and Wistar rats, both strains were sensitive to the antiarrhythmic action of (+/-)-sotalol.
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PMID:Effect of sotalol against reperfusion-induced arrhythmias in Sprague-Dawley and Wistar rats. 261 63


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