Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventricular fibrillation (VF) is a life-threatening arrhythmia that leads to death unless electrical defibrillation is applied in time. Recent publications indicate that VF can be either sustained (SVF), requiring electrical defibrillation, or transient (TVF), reverting spontaneously into sinus rhythm. Since VF cannot be totally prevented by drugs, a new antiarrhythmic therapeutic approach has been proposed: drug-induced enhancement of the ability of the heart to defibrillate by itself. In this study we examined the defibrillating potency of two antiarrhythmic phenothiazines, ethmozine (ETM) and ethacizine (ETA), as well as their effects on catecholamine uptake and on the electrophysiological properties of the myocardial cell membrane. The antiarrhythmic-defibrillatory activity was examined in cats; the inhibitory effect on [3H]-norepinephrine (NE) uptake was examined in rat brain synaptosomes, and the electrophysiological membrane effects were examined by microelectrode recordings in perfused strips of heart ventricle from guinea-pigs. The results indicate that: 1. ETA exhibits similar but stronger antiarrhythmic-defibrillating and NE reuptake inhibitory effects than ETM; 2. ETA at 10-6 M decreases ventricular conduction time and increases Vmax while ETM at this concentration does not change them; 3. The defibrillating ability of the drugs can be related to their inhibitory potency on NE reuptake. We suggest that the risk of sympathomimetic arrhythmogenicity is prevented by the previously described, membrane stabilizing Class 1 antiarrhythmic properties of these drugs.
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PMID:Ethmozine and ethacizine--new antiarrhythmic drugs with defibrillating properties. 866 47

Selected metabolites, hormones and cardiovascular variables were measured in halothane anesthetized horses during 1 hour of dopamine infusion at a rate of 5 micrograms/kg/min (low) and 10 micrograms/kg/min (high), and for 1 hour after infusion. Plasma cortisol increased twofold in the low-infusion group but did not change significantly in the high-infusion group. Plasma nonesterified fatty acids, blood glucose, blood lactate, and plasma insulin increased in the high-infusion group. There was little difference in heart rate, systolic, diastolic, and mean arterial blood pressure between the two groups. The high infusion was associated with arrhythmias in several horses, and one horse showed ventricular fibrillation and died. If metabolic and hormonal changes are used as markers of a "stress response" in anesthetized horses the results must be carefully interpreted if a sympathomimetic agent such as dopamine is administered to maintain cardiovascular stability.
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PMID:Metabolic, hormonal, and hemodynamic changes during dopamine infusions in halothane anesthetized horses. 871 91

Ventricular fibrillation (VF) in conscious rats with coronary artery ligation occurs in two phases, before (phase 1) and after (phase 2) 90 min of ischaemia respectively. The mechanisms of phase 2 VF are not established. Interestingly, phase 2 VF is absent in isolated (denervated) buffer-perfused rat hearts. We investigated whether catecholamine supplementation (to mimic sympathetic drive) was sufficient to restore phase 2 VF in such hearts. Isolated rat hearts (n=10 per group) underwent coronary ligation for 240 min. At 90 min, during a period of relative electrical stability, the perfusion solution was switched from standard (Krebs) to identical solution or Krebs containing catecholamines (313 nM noradrenaline and 75 nM adrenaline) with or without 10 microM trimazosin (an alpha(1)-adrenoceptor antagonist) or 10 microM atenolol (a beta(1)-adrenoceptor antagonist). Although in all groups the incidence of phase 1 VF was high (80 - 100%), the temporal distribution of VF was monophasic, i.e. only one heart in one group developed phase 2 VF (P=NS). Other ventricular arrhythmias (e.g., tachycardia; VT) exhibited a similar temporal distribution. Nevertheless, haemodynamic changes confirmed sympathomimetic effects of catecholamines, e.g., heart rate was increased from 278+/-7 beats min(-1) in controls to 335+/-8 beats min(-1) (P<0.05) by catecholamines, an effect that could be blocked by atenolol (285+/-7 beats min(-1)) but not by trimazosin (342+/-12 beats min(-1)). Coronary flow was correspondingly increased from 7.7+/-0.7 ml min(-1) g(-1) to 16.5+/-1.3 ml min(-1) g(-1) (P<0.05); this effect could be blocked by atenolol (8.1+/-0.6 ml min(-1) g(-1)) and was enhanced by trimazosin (20.7+/-2.4 ml min(-1) g(-1)). In conclusion, despite evidence of adequate alpha- and beta-adrenoceptor activation, catecholamine supplementation to isolated buffer-perfused rat hearts was insufficient to restore phase 2 VF. It therefore appears unlikely that catecholamines alone mediate phase 2 VF.
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PMID:Independent contribution of catecholamines to arrhythmogenesis during evolving infarction in the isolated rat heart. 1183 29

New class III antiarrhythmic/defibrillating compound tedisamil was shown to facilitate termination of atrial and ventricular fibrillation in experimental as well as clinical conditions. However, class III-related inhibition of K(+) current associated with prolongation of repolarization can not solely explain its defibrillating ability. Following recent findings it was hypothesized that defibrillating effect of tedisamil is likely due to its sympathomimetic feature linked with modulation of intracellular calcium. Results of this study obtained in isolated heart preparation showed that elevated intracellular Ca(2+) free concentration was decreased by administration of tedisamil in concentration that did not induce Q-T interval prolongation. Due to species differences the effective concentration was in rat 10(-7) M, while in guinea pig 10(-5) M. On the contrary, further dramatic increase of elevated Ca(2+) was detected upon administration of tedisamil in concentration that markedly prolonged Q-T interval (10(-5) M in rat). It is concluded that defibrillating ability of tedisamil is most likely associated with attenuation of abnormal and harmful intracellular Ca(2+) elevation (that is highly arrhythmogenic) than with prolongation of APD or Q-T interval.
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PMID:Modulation of intracellular Ca(2+) concentration by tedisamil, a class III antiarrhythmic agent, in isolated heart preparation. 1288 19

With increasing drug abuse of cocaine, the chances are growing that an anaesthetist comes into contact with an acutely intoxicated patient or chronic cocaine user while on call or during his daily routine. In South America chewing coca leaves is daily practise, while in the industrialised world the drug is sniffed, smoked or injected intravenously. Clinically, cocaine is used topically in ENT and ophthalmology due to its local analgesic and strong vasoconstrictive properties. Cocaine has a similar effect on the CNS as amphetamines and produces euphoria and hallucinations. Cocaine acts indirectly on sympathetic stimulation, release of dopamine and inhibition of catecholamine metabolism. It is metabolised in the liver and by serum esterases. Intoxication with cocaine leads to respiratory depression, arrhythmias, ventricular fibrillation and death. If an emergency operation during acute cocaine intoxication is necessary, all sympathomimetic anaesthetic drugs must be avoided. A deep anaesthesia must be provided to reduce the risk of cardiovascular complications. In the literature, anaesthesia is regarded as safe for patients with chronic cocaine misuse after abstinence of 24 hours. This case report shows that, even without acute intoxication, severe cardiovascular problems are possible in patients with chronic cocaine abuse. Hence, we recommend a cocaine-free interval of at least one week before elective surgical procedures.
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PMID:[Intraoperative ventricular fibrillation in a patient with chronic cocaine abuse--a case report]. 1503

The syncopal attacks of complete heart block may be due either to ventricular standstill or to ventricular acceleration including fibrillation. As treatment may be harmful unless the underlying mechanism in each case is determined, it is important to apply the available methods for differentiation. Epinephrine and certain related compounds (sympathomimetic amines) are the only effective substances in the therapy of ventricular arrest. Isopropyl nor-epinephrine is a most potent drug in the prevention and treatment of ventricular arrest and has the advantage that it does not dispose to fibrillation. Quinidine is unreliable and probably hazardous in the control of ventricular fibrillation in heart block as it appears to precipitate this arrhythmia.Preliminary observations indicate that ectopic ventricular rhythms are also induced by procaine amide in complete heart block.Isuprel(R) may be of value in the therapy of ventricular acceleration, by preventing the ventricular arrest which frequently follows the initial acceleration.
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PMID:MECHANISM OF SYNCOPE AND ACTION OF DRUGS IN COMPLETE HEART BLOCK. 1873 18


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