Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Encainide is a potent sodium channel antagonist. It dissociates slowly from blocked, repolarized channels (time constant of recovery greater than 20 seconds). It markedly slows myocardial and His Purkinje conduction in vitro, in animal models and in humans. In vitro the parent compound and its major metabolites, O-demethyl and 3-methoxy-O-demethyl encainide, have variable effects on action potential duration and refractoriness. In man the parent compound has relatively little effect on refractoriness and QT interval, but its metabolites may increase refractoriness moderately. Encainide has no significant effect on the normal sinoatrial node, and only its metabolites significantly depress atrioventricular nodal conduction and refractoriness. In models of ischemia, all of encainide's actions are more pronounced in ischemic than in normal tissue. Encainide is similar in its basic and clinical electrophysiologic profile to flecainide and lorcainide although its constellation of electrophysiologic properties is unique. It differs from quinidine, procainamide and disopyramide by slowing conduction more and affecting refractoriness less, and by absence of anticholinergic side effects.
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PMID:Basic and clinical cardiac electrophysiology of encainide. 242 30

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

Adenosine is a potential cardioplegic agent by virtue of its specific inhibitory properties on nodal tissue. We tested the hypothesis that adenosine could be more effective than potassium in inducing rapid cardiac arrest and enhancing postischemic hemodynamic recovery. Isolated rat hearts were perfused with Krebs-Henseleit buffer or cardioplegic solutions to determine the time to cardiac arrest and the high-energy phosphate levels at the end of cardioplegia. Cardioplegic solutions contained adenosine 10 mmol/L, potassium 20 mmol/L, or adenosine 10 mmol/L + potassium 20 mmol/L and were infused at a rate of 2 ml/min for 3 minutes at 10 degrees C. Both time taken and total number of beats to cardiac arrest during 3 minutes of cardioplegia were reduced by adenosine 10 mmol/L and adenosine 10 mmol/L + potassium 20 mmol/L when compared with potassium 20 mmol/L alone (p less than 0.001). Tissue phosphocreatine was conserved by adenosine 10 mmol/L when compared with potassium 20 mmol/L, being 7.1 +/- 0.2 (mumol/gm wet weight (n = 7) and 6.0 +/- 0.3 mumol/gm wet weight (n = 5), respectively (p less than 0.05). Postischemic hemodynamic recovery was tested in isolated working rat hearts. After initial cardiac arrest, the cardioplegic solution was removed with Krebs-Henseleit buffer at a rate of 2 ml/min for 3 minutes at 10 degrees C, and thereafter total ischemia was maintained for 30 or 90 minutes at 10 degrees C before reperfusion. Adenosine 10 mmol/L enhanced recovery of aortic output when compared with potassium 20 mmol/L or adenosine 10 mmol/L + potassium 20 mmol/L, the percentage recovery after 30 minutes of ischemia being 103.0% +/- 4.4% (n = 6), 89.0% +/- 5.8% (n = 6), and 86.6% +/- 4.3% (n = 6), respectively (p less than 0.05 for comparison between adenosine 10 mmol/L and potassium 20 mmol/L). Thus adenosine cardioplegia caused rapid cardiac arrest and improved postischemic recovery when compared with potassium cardioplegia and with a combination of these two agents.
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PMID:Adenosine cardioplegia. Adenosine versus potassium cardioplegia: effects on cardiac arrest and postischemic recovery in the isolated rat heart. 184 75

Exogenous adenosine has been shown to have potent electrophysiologic effects and antiarrhythmic properties within the atrioventricular (AV) node. Endogenous adenosine, a nucleoside with an increased release signaled by ischemia and hypoxia, is not believed to exert significant effects during homeostatic conditions. Recent experimental evidence suggests, however, that under normoxic conditions, the amount of adenosine released may be sufficient to mediate some of its physiologic effects. This study was designed to test the hypothesis that in humans the electrophysiologic effects of endogenously released adenosine on AV nodal conduction can be demonstrated under normoxic conditions by inhibiting uptake and degradation of the nucleoside. In the first protocol, the effects of intravenous dipyridamole (0.56 mg/kg bolus i.v., 5 micrograms/kg/minute infusion), a nucleoside-transport blocker that elevates endogenous plasma levels of adenosine, on AV nodal conduction were evaluated in seven patients. At a constant atrial paced cycle length, dipyridamole increased the AH interval from 110 +/- 19 to 164 +/- 26 msec, p = 0.002 (+/- SEM). Aminophylline (5.6 mg/kg i.v.), a competitive antagonist of adenosine, completely reversed the effects of dipyridamole on AV nodal conduction. Similarly, dipyridamole increased the cycle length at which pacing-induced AV nodal Wenckebach occurred, from 348 +/- 31 (control) to 388 +/- 33 msec (dipyridamole) (p = 0.002). In a second protocol, the effects of intravenous dipyridamole were evaluated in another group of six patients who had supraventricular tachycardia (SVT) in which the AV node was part of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine. 259 20

Calcium antagonists such as verapamil/diltiazem predominantly delay av-nodal conduction. Thus, the most important clinical indications for their application are the av-nodal-reentrant-tachycardia as well as the slowing of rapid ventricular response in intraatrial tachyarrhythmias. To reestablish sinus rhythm in atrial fibrillation, verapamil should be combined with chinidin. Usually, ventricular arrhythmias cannot be suppressed by calcium antagonists, but they may be indicated in exercise-induced ventricular arrhythmias and tachycardias arising from the right ventricular outflow tract. Verapamil/diltiazem are effective in ischemia-induced tachyarrhythmias, especially ventricular fibrillation, because of the reduction of ischemia-related conduction delay in the ischemic zone. The effectiveness of calcium antagonists in the secondary prevention of myocardial infarction can not yet be definitively defined.
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PMID:[Anti-arrhythmia effects of calcium antagonists]. 269 64

The dose-response characteristics for the effect of ATP upon cardiac function and vascular tone have been investigated in the isolated perfused rat heart. Vasodilation was observed with low ATP concentrations (0.01-0.1 mM) whereas severe vasoconstriction occurred with high concentrations (1.0-10.0 mM). At all doses studied, heart rate and pressure-rate product were reduced in a dose-dependent manner, with 10 mM ATP almost complete cardiac arrest was observed. Analysis of epicardial electrograms revealed that ATP induced arrhythmias, prolonged the P-R interval and induced partial blockade of S-A nodal activity and A-V conduction. Investigating possible mechanisms for the vascular and contractile effects of ATP, it was possible to exclude the calcium chelating properties of ATP and the effects of coincident ischemia arising as a consequence of ATP-induced vasoconstriction. Pharmacological studies revealed the ATP-induced vasoconstriction to be unresponsive to a range of coronary vasodilators and also allowed exclusion of prostaglandins, catecholamines and adrenergic receptors in the mediation of ATP effects. Investigations with acetylcholine revealed remarkably similar effects upon both contractile and vascular activity but studies with atropine suggested that the muscarinic receptor was not involved. Studies with theophylline allowed a dissociation of the vascular and contractile effects of ATP and indicated a possible involvement of the adenosine receptor in the cellular response to both high and low concentrations of ATP.
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PMID:Vascular and contractile responses to extracellular ATP: studies in the isolated rat heart. 299 28

Sinus node and atriventricular (A-V) nodal functions were evaluated by right atrial pacing in 220 consecutive patients recovering from acute myocardial infarction (AMI), 10-28 days after the infarct (mean = 14 days). In the 188 patients in whom a pacing rate of 120 beats/min could be achieved, sinus node recovery time, corrected sinus node recovery time (CSNRT) and total recovery time were correlated to infarct site and the presence or absence of myocardial ischemia. Sinus node recovery time and total recovery time were significantly longer in patients with inferior (1,153 + 28 and 3,129 + 179 ms, respectively) or non-Q-wave infarct (1,112 + 28 and 3,730 + 266 ms, respectively), than in patients with anterior infarct (1,044 + 20 and 1,153 + 28 ms, respectively). The parameters were within the reported normal range. When corrected for heart rate (CSNRT), these differences were no longer present. The presence or site of residual ischemia during right atrial pacing did not affect the sinus nodes parameters. A-V nodal function, studied in all 220 patients, was assessed by the appearance of second-degree A-V block at pacing rates below 120 beats/min and by measuring the shortest atrially paced cycle length with 1:1 A-V conduction. Second-degree A-V block appeared at a similar frequency in different AMI locations. Thus, sinus and A-V node functional status in patients recovering from AMI are not affected by infarct site or by the presence or absence of residual myocardial ischemia.
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PMID:Sinus node and atrioventricular nodal function in 220 patients recovering from acute myocardial infarction. 316 17

The hypothesis that production of ischemia or cooling of an arrhythmogenic area or pathway could interrupt tachycardias was tested by subselective catheterization of the coronary artery supplying the site of origin of ventricular tachycardia (9 patients), the accessory pathway (2 patients) and the site of origin of atrial tachycardia (1 patient). Ventricular tachycardia was reproducibly terminated and reinduction temporarily prevented in 8 of the 9 patients by occlusion of the artery or administration of iced isotonic saline. Block in the accessory pathway was obtained in 1 of the 2 patients with Wolff-Parkinson-White syndrome. Selective cooling through the atrioventricular nodal artery in 1 patient terminated his circus movement tachycardia. Reproducible termination of a continuous atrial tachycardia was obtained by cooling of the atrial branch supplying the site of origin of the arrhythmia. These data demonstrate the feasibility of identification and selective catheterization of the coronary artery branch supplying blood to an arrhythmogenic area or pathway and suggest a new possibility for treatment of tachycardias by permanently blocking the blood supply to the site of origin or pathway of a tachycardia.
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PMID:Termination of tachycardias by interrupting blood flow to the arrhythmogenic area. 341 15

Ischaemia of the sinoatrial node (SAN) region was produced in 57 dogs by obstructing the sinoatrial nodal artery by injecting it with various media. In the light microscope ischaemia of the nodal cells resulted in myocytolysis. The cells were oedematous, with a distinctly cleared cytoplasm and cytoplasmic vacuolization. Macrophages penetrated into the nodal cells. Myocytolysis resulted either in disintegration of the cell membrane and the nucleus or in atrophy of nodal cells. The damaged cells were gradually replaced with collagenous connective tissue. Ischaemic changes in the light microscope appeared between hours 3 to 24 after the onset of ischaemia and continued to develop for a period of 4 to 5 weeks showing a variable intensity in different areas of the SAN region. The process became virtually stabilized between months 1 to 7. The degree of ischaemia was most probably responsible for the fact that changes of various degree--myocytolysis, atrophy and fibrosis--were present simultaneously. The preservation of ganglion cells in ischaemic tissue is discussed.
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PMID:Light microscopy of sinoatrial node ischaemia. 367 19

During diagnostic cardiac catheterization for the evaluation of chest pain, His bundle electrograms were obtained in 32 male patients before and 2 to 5 minutes after each of two interventions known to acutely affect left ventricular volume and left ventricular end-diastolic pressure (the injection of 40 to 60 cc of contrast medium during left ventriculography and the administration of 0.4 mg of sublingual nitroglycerin). Changes in left ventricular end-diastolic pressure (18 +/- 6 vs 30 +/- 7 mm Hg, p less than 0.001 following ventriculography and 32 +/- 8 vs 19 +/- 8 mm Hg, p less than 0.005 following nitroglycerin administration) were accompanied by parallel alterations in HQ (48 +/- 8 vs 54 +/- 10 msec, p less than 0.005 following ventriculography and 57 +/- 10 vs 53 +/- msec, p less than 0.005 following nitroglycerin administration), but there were no significant changes in atrioventricular (AV) nodal conduction (AH). Significantly greater changes in HQ were seen in patients with triple-vessel coronary artery disease than in the remainder of the population, although there was clinical and/or ECG evidence of ischemia in only one patient. We conclude that factors other than progression of intrinsic conduction system disease may affect infranodal conduction. HQ should be interpreted cautiously in situations with rapidly changing hemodynamics, especially in patients with severe coronary artery disease.
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PMID:Acute changes in infranodal conduction time following left ventriculography and sublingual nitroglycerin administration in man. 641 Aug 92


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