ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01307.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Manifest Fast and Slow AV Nodal Conduction Patterns and Reentry.A 52‐year‐old woman with paroxysmal supraventricular tachycardias (PST) showed short and long PR intervals during sinus rhythm. Repetitive episodes of PST due to simultaneous anterograde conduction through fast and slow conduction pathways (one P‐two QRS) were recorded. A self‐limited episode of non‐paroxysmal AV nodal reentry with anterograde slow and retrograde fast pathway conduction was initiated by a single atrial premature beat. Each pathway depicted distinct refractory periods, conduction velocities, unidirectional block, and Wenckebach‐type block suggesting the possibility of a well‐defined anatomic

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01308.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Subcutaneous Lidocaine Affects Inducibility.A prospective study of 99 patients undergoing invasive electrophysiologic testing was conducted to determine whether the administration of lidocaine for local anesthesia influenced the inducibility of arrhythmias. Of the 99 patients, 42 had inducible arrhythmias. Multiple stepwise discriminant analysis indicated that the most important factor influencing inducibility was lidocaine dosage per weight, with a calculated cutoff of 3.2 mg/kg. There were 26/54 (48%) of patients who had no inducible arrhythmias below the cutoff, compared with 31/45 (69%) above the cutoff (P3.2 mg/kg and serum concentration above 1.4μg/mL (therapeutic range 1‐5μg/mL) 1 hour after administration, 18 had no inducible arrhythmias (86%). Younger, smaller patients were more affected (P1.4μg/mL, failure to induce may be sus

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01309.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Autonomic Modulation of Lethal Arrhythmias.Susceptibility to sudden death in dogs with healed myocardial infarction can be defined by the response to transient ischemia during treadmill exercise and can often be predicted by the baroreceptor slope, which is determined from least squares regression of the RR interval, or heart rate, response to increasing systolic pressure during a phenylephrine infusion. We used standard microelectrode techniques to study isolated Purkinje fiber bundles as well as subendocardial Purkinje fibers overlying the infarcted myocardium of dogs classified by treadmill testing as resistant or susceptible to sudden death. We determined the response to isoproterenol (Iso) alone and in the presence of acetylcholine (ACh). Control action potential (AP) characteristics for both groups were similar except for the following: in normal Purkinje fibers, susceptible dogs had a significantly lower AP overshoot and Vmaxthan resistant dogs. In addition, fibers from the in arct zones of susceptible dogs had lower maximal diastolic potentials than those from the normal Purkinje fibers of susceptible dogs. Iso significantly shortened AP duration in normal and infarct zone fibers of both groups. ACh alone had no effect on AP duration. In the infarct zone, ACh 10−7M did not antagonize Iso‐induced shortening of AP duration in susceptible or resistant dogs; but ACh 10−5M completely blocked Iso effects in resistant dogs. In normal Purkinje fibers, ACh antagonism of Iso effects was seen in susceptible and resistant animals. Iso and ACh had no significant effect on other transmembrane potential characteristics. The differences between resistant and susceptible dogs in control transmembrane characteristics and accentuated antagonism may contribute to the substrate that increases the likelihood of sudden death in this

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01310.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Antiarrhythmic Properties of UK‐ 66,914.UK‐66,914 is a potent Class III antiarrhythmic agent that has no effect on conduction velocity in normal tissue in vitro. The present study was performed to evaluate the influence of UK‐66,914 on conduction velocity in vivo in canine hearts with a previous myocardial infarction. Detailed three‐dimensional mapping of the heart in vivo was obtained using simultaneous recordings from 232 transmural sites. In dogs with a chronic anterior myocardial infarction, UK‐66,914 (50μg/kg) did not alter conduction velocity in regions exhibiting normal conduction (gt; 50 cm/sec) or regions with slowed conduction (30 cm/sec, 15‐30 cm/sec, or<15 cm/sec, whereas procainamide significantly decreased conduction velocity at all three levels. Evaluation of the hemodynamic profile of UK‐66,914 revealed no negative ionotropic effects in conscious dogs even at doses twentyfold those required to elicit increases in the effective refractory period. Therefore, UK‐66,914 is a potent and specific Class III antiarrhythmic agent, which does not alter conduction velocity in hearts with a previous myocardial infarction and exer

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01311.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Contraction and Intracellular Sodium.Intracellular sodium activity (aiNa) and contraction were simultaneously recorded in voltage‐clamped sheep Purkinje fibers while the sodium‐potassium pump was inhibited with strophanthidin or low potassium. Exposures to low (1.5×10−7M) and high (10−5M) doses of strophanthidin resulted in aiNaand contraction increasing together. However, when strophanthidin was washed off, aiNarecovered more slowly than contraction. Due to this lag of aiNabehind contraction, there was hysteresis in the relation between contraction and aiNa. We compared strophanthidin exposures in voltage‐clamped fibers to those in unclamped fibers with action potentials. The lack of association between contraction and aiNawas less when fibers were clamped. We conclude that some of the dissociation previously reported in unclamped fibers was due to changes of membrane potential with strophanthidin. Using voltage clamp, we also compared the effect of different doses of strophanthidin applied to the same fiber. Higher doses of strophanthidin caused a larger rise of contraction for a similar increase of aiNa. Higher doses, which inhibit the Na‐K pump to a greater extent, also resulted in a faster rate of rise of aiNa. Inhibition and reactivation of the Na‐K pump with bathing potassium (or rubidium) also resulted in hysteresis between contraction and aiNa. A greater reduction of potassium caused a larger rise of contraction for a similar rise of aiNa. Lower potassium inhibits the Na‐K pump more completely and results in a faster rate of rise of aiNa. Although the absolute rise of aiNawith strophanthidin or low potassium is related to the increase of contraction, we conclude that this is not the only factor. The inotropic effect of these agents is also related to the rate at which aiNarises; when the rate of rise is large, a given level of aiNais associated with a larger contraction. Such behavior may be compatible with the presence of aiNagradients from the subsarcolemmal space to the bulk cytoplasm during

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01312.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Use‐Dependent Effects of Amiodarone.Amiodarone is a highly effective antiarrhythmic agent. However, its exact mechanism of action remains uncertain. Prior studies suggest that intravenous amiodarone produces different electrophysiologic effects than chronic amiodarone administration. In addition, the effects of other antiarrhythmic agents andβ‐adrenergic stimulation on the electrophysiologic effects of amiodarone have not been well defined. In this study, we sought to evaluate the use‐dependent effects of intravenous (acute) versus oral (chronic) amiodarone administration on His‐Purkinje conduction in a closed‐chest canine model. We also sought to evaluate the effects of intravenous lidocaine and isoproterenol on the use‐dependent effects of chronically administered oral amiodarone. We found: (1) Acutely administered intravenous amiodarone (5 mg/kg bolus, followed by a 0.05 mg/kg/min infusion) does not produce a significant use‐dependent effect on His‐Purkinje conduction (serum amiodarone level 2.7 ± 1.1 mg/L), and acute beta blockade did not enhance use‐dependent effects of amiodarone; (2) Chronically administered oral amiodarone (1,000 mg/day ± 2 weeks) produced significant use‐dependent effects on His‐Purkinje conduction at similar serum drug concentrations (mean level 2.6 ± 1.5 mg/L; (3) Intravenous lidocaine (10 mg/kg bolus, 0.2 mg/kg/min infusion) produced significant additional use‐dependent effects to that of chronic oral amiodarone but only at rapid paced rates (cycle length 300‐210 msec); and (4) Isoproterenol (5μg/min infusion) significantly attenuated the use‐dependent effects of chronically administered amiodarone. The mechanism of action of acutely administered intravenous amiodarone appears to be different from that of chronic oral amiodarone. In addition, the marked use‐dependent effects observed after chronic amiodarone administration were reversed after catecholamine administration suggesting that attenuation of use dependence by sympathetic stimulation may negate some

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01314.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Cardiac Gap Junction Channel Regulation.Synchronization of pacemaker activity and cardiac action potential propagation is dependent upon the maintenance of electrical communication via gap junctions. Gap junction channels in mammalian heart are formed by a 43‐kilodalton (kD) protein, connexin43, and have a unitary conductance of 50 picosiemens (pS). In embryonic chick heart, three gap junction proteins of 42, 43, and 45 kD have been cloned, the functional properties of which have not been individually identified. Unitary channel conductances ranging from 40‐240 pS have been reported, but conductances of 40‐80 and 160 pS are most frequently observed in embryonic chick heart. Developmental changes in transjunctional voltage dependence are known to occur and may be correlated with differential expression of the three chick connexins during development. Gap junction conductance (gj) is highly regulated, being maintained or increased by ATP and cAMP‐dependent pathways. Conversely, gjis reduced by treatment with various lipophilic agents (e.g., n‐alkanols, arachidonic acid, halothane), large transjunctional potentials, increasing intracellular cation (e.g., H+, Ca2+) concentrations, and tyrosine phophorylation of rat connexin43. It is unclear at this time if any of the regulatory mechanisms can mediate beat‐to‐beat fluctuations in gjof normal myocardium. Most available evidence indicates that this modulation occurs by the open‐closed gating of individual channels rather than effects on the unitary channel conductance. The precise molecular mechanisms are not yet known, but the functional expression of gap junction proteins should allow for determination of the functional domains responsible for direct and indirect modulation of the cardiac gap ju

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01315.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01316.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Book Review in This Article:Progress in Cardiology, Volume 3, Number 2. Edited by Douglas P. Zipes and Derek J. Rowlands.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01317.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY