Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged (greater than 152 msec) calculated sinoatrial conduction times (SACT) were found in 24 of 470 patients studied by the atrial extrastimulus technique, ranging from 155 to 220 msec (180+/-4.4; mean+/-SEM). There were 18 males and six females with ages of 29 to 85 (mean 65+/-2.6). Electrocardiographic monitoring revealed significant sinus or atrial dysrhythmias in 19 (79%) patients. Of these 19, 15 had persistent sinus bradycardia and/or sinoatrial block, three had sinus bradyarrhythmia with paroxysmal atrial tachycardia, and one had isolated atrial tachycardia. Additional electrophysiological evidence of sinus node or atrial dysfunction was present in 11 patients. Four patients needed permanent pacing during follow-up (mean follow-up period of 427+/-39 days) because of symptomatic bradyarrhythmia. Three patients died, none suddenly. In conclusion, prolonged calculated SACT was associated with a high incidence of electrocardiographic and electrophysiologic abnormalities of sinus node and/or atrium. Despite this, bradyarrhythmic morbidity was relatively low, suggesting that prolonged sinoatrial conduction time in the absence of symptoms is not an indication for prophylactic pacing.
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PMID:Clinical significance of prolonged sinoatrial conduction time. 83 Feb 23

In halothane-nitrous oxide-anesthetized pigs, the effect of the competitive adenosine antagonist, BW-A1433U (a derivative of 1,3-dipropyl-8-phenylxanthine), on postdefibrillation bradyarrhythmia and hemodynamic depression was investigated. In protocol 1, repetitive episodes of ventricular fibrillation lasting 15 seconds before transthoracic DC shock were performed in five animals, before (control) and after the administration of BW-A1433U (5 mg/kg i.v.). An unsuccessful initial shock was immediately followed by a rescue shock of 40 A. In ventricular fibrillation episodes requiring rescue shocks, nine of 19 episodes (47%) exhibited second- or third-degree atrioventricular block at 15 seconds postdefibrillation compared with only one of 16 BW-A1433U episodes (6%). In protocol 2, the effect of BW-A1433U was determined in the presence of dipyridamole, a nucleoside uptake blocker known to potentiate the cardiac actions of adenosine. To counter the hypotensive effect of dipyridamole, methoxamine was continuously infused at 0.015 mg/kg/min i.v. Sequential episodes of ventricular fibrillation lasting 45 seconds were terminated by shocks of 40 A in the presence of methoxamine alone, after dipyridamole (1.5-7.5 mg i.v.), and after BW-A1433U (5 mg/kg i.v.). Over the first 15 seconds postdefibrillation, BW-A1433U significantly (p less than 0.05) increased the number of spontaneous beats (31 +/- 2) and systolic/diastolic blood pressure (111 +/- 4/67 +/- 5 mm Hg; mean +/- SEM; n = 9) compared with both methoxamine (16 +/- 2 beats; 98 +/- 14/52 +/- 12 mm Hg; n = 5) and dipyridamole (8 +/- 3 beats; 58 +/- 11/27 +/- 6 mm Hg; n = 9), respectively. Rapid infusion of BW-A1433U during dipyridamole postdefibrillation periods raised heart rate and blood pressure to preventricular fibrillation levels within 30 seconds. Thus, BW-A1433U can reverse and prevent postdefibrillation bradyarrhythmia and hemodynamic depression. Endogenous adenosine may be an important mediator of postdefibrillation cardiovascular collapse.
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PMID:Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. 273 45