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PubMed1982

Growth of nosocomial pathogens in multiple-dose parenteral medication vials.

The extent to which microbial contamination of medications dispensed in multiple-dose vials might serve as a source of infection to patients has not been fully investigated. To characterize the effects of microbial contamination, we studied the growth-supporting properties of eight medications dispensed in multiple-dose vials. Two medications, procainamide and methohexital, demonstrated no survival of any microbes 24 h after inoculation. Succinylcholine chloride, regular insulin, potassium chloride, heparin, and thiopental slowly killed or allowed limited survival of several of the microorganisms used as contaminants. Lidocaine allowed survival or proliferation of several microbial strains suspended in 0.25% peptone water in saline, but slowly killed all strains except Pseudomonas cepacia suspended in 0.9% saline. Endotoxin, measured by the Limulus amebocyte lysate assay, was found in the two medications tested, lidocaine contaminated with Pseudomonas cepacia and insulin contaminated with enterococci. Inadvertent microbial contamination of at least some parenteral medications in multiple-dose vials may result in the exposure of patients to viable organisms. The potential, however, for medications such as lidocaine to support growth of organisms under selected circumstances should be noted by those responsible for preparing and administering these drugs. The potential hazard to patients from endotoxin in contaminated medications under these circumstances has not been assessed. Additional studies of this type should be pursued to provide more complete information about the risk of microbial contamination of products for parenteral use.

Bacteria↗

PubMed1970

Maintenance of sinus rhythm after atrial defibrillation.

The long-term results of 356 episodes of atrial defibrillation by DC shock carried out in 250 patients are reviewed. In 78 per cent of the cases, atrial fibrillation recurred by the end of 12 months in spite of the administration of quinidine or procainamide or propranolol, singly or combined. However, when no antidysrhythmic drugs were used the recurrence rate was higher at all periods of observation and 100 per cent at the end of 12 months. The difference in the overall results between the untreated group and the treated groups with the exception of the propranolol group is significant (p less than 0.05). In addition, the propranolol group showed an obviously reduced recurrence rate at 1 month, but afterwards the results tended to approximate those in the untreated group. The period during which sinus rhythm could be maintained in patients who underwent valve operations was on the whole the same as in patients who did not have heart surgery. However, in a small number of patients sinus rhythm was maintained for longer periods after mitral valve replacement than before it. Sinus rhythm was maintained for significantly longer periods when atrial fibrillation lasted less than 1 year than when it had been present for more than 1 year (p less than 0.001). It is concluded that there is justification for a judicious antidysrhythmic prophylaxis after atrial defibrillation.

Atrial Fibrillation↗

PubMed1973

Malignant hyperpyrexia. Further muscle studies in asymptomatic carriers identified by creatinine phosphokinase screening.

The history, clinical presentation, and management of malignant hyperpyrexia are presented. The aetiology seems to be associated with some inherited abnormality which affects the movement and binding of calcium ions in the sarcoplasmic reticulum, sarcoplasm, and mitochondria. Whether this is a primary muscular defect or secondary to some trophic neural influence is yet to be established. The subjects carrying the abnormal trait show evidence of a myopathy which is subclinical in most instances and revealed only by estimation of serum CPK or biopsy. In some families where the myopathy is clinically obvious there may be, in addition, a variety of musculoskeletal abnormalities. A plea is made for routine monitoring of temperature during anaesthesia and for procainamide or procaine to be readily available in all operating theatres. A history of anaesthetic deaths in a family calls for special care, and, if the serum CPK is elevated, suxamethonium and halothane are to be avoided. Families with orthopaedic and muscular abnormalities are at increased risk and should have estimation of serum CPK before surgery. As a bonus of this study it is suggested that serum CPK estimations be used to screen pigs for selective breeding and so eliminate the disease, which causes soft exudative pork.

Adolescent↗

PubMed1984

Progress and problems in understanding the involvement of calcium in heart function.

In this article we have briefly reviewed the role of Ca2+ in the excitation contraction coupling in the myocardium and have indicated that cardiac contraction and relaxation are initiated upon raising and lowering the intracellular concentration of free Ca2+, respectively. Different mechanisms for the entry of Ca2+ through sarcolemma as well as release of Ca2+ from sarcoplasmic reticulum and possibly mitochondria have been outlined for initiating cardiac contraction. Relaxation of the cardiac muscle appears to be intimately dependent upon efflux of Ca2+ through sarcolemma as well as sequestration of Ca2+ by the intracellular storage sites, particularly sarcoplasmic reticulum and possibly mitochondria. The actions of some pharmacological and pathophysiological interventions have been explained on the basis of changes in subcellular Ca2+ movements in myocardium. Quinidine, which produced an initial positive inotropic action on rat heart was also found to increase sarcolemmal Ca2+-ATPase activity without any changes in the Na+-K+ ATPase. Other antiarrhythmic agents, procainamide and lidocaine, also increased sarcolemmal Ca2+-ATPase activity without affecting the Na+-K+ ATPase. On the other hand, both Ca2+-ATPase and Na+-K+ ATPase activities were increased in heart sarcolemma obtained from cardiomyopathic hamsters. In this model the increased Ca2+-ATPase activity may promote the occurrence of intracellular Ca2+ overload in the cardiac cell whereas the increased Na+-K+ ATPase activity may increase Ca2+ efflux through Na+-Ca2+ exchange systems as an adaptive mechanism. It has been suggested that some caution should be exercised while interpreting the data from in vitro experiments in terms of functional changes in the myocardium. Furthermore, it has been proposed that the pathophysiology and pharmacology of Ca2+ movements at different membrane sites be understood fully in normal and diseased myocardium in order to improve the therapy of heart disease.

Adenosine Triphosphate↗

PubMed1995

Organic cation transport by rat liver lysosomes.

Hepatic organic cation transport has been characterized in rat liver plasma membrane vesicles, using the quaternary amine tetraethylammonium (TEA) as a model substrate. Sinusoidal TEA uptake is stimulated by an inside-negative membrane potential; TEA transport across the canalicular membrane is mediated by electroneutral organic cation-H+ exchange. Substrates for these transport processes include procainamide ethobromide (PAEB) and vecuronium, cationic drugs that undergo biliary excretion. Given the apparent absence of sinusoidal transport mechanisms able to generate high hepatocyte-to-blood organic cation concentration ratios, intracellular transport of organic cations may involve sequestration and concentration within acidified organelles. Therefore, the characteristics of TEA uptake were examined in isolated rat liver lysosomes that are acidified by a well-described H(+)-adenosinetriphosphatase (ATPase). Lysosomal uptake of [14C]TEA was a time- and ATP-dependent process, reaching steady state after 30-60 min. Steady-state [14C]TEA uptake was significantly reduced by omission of ATP and by addition of monensin, conditions that alter lysosomal pH and membrane potential gradients, and by the H(+)-ATPase inhibitors, N-ethylmaleimide and bafilomycin A. ATP-dependent lysosomal [14C]TEA uptake was significantly inhibited by PAEB, vecuronium, and other organic cationic substrates of canalicular TEA/H+ exchange. These findings demonstrate that rat liver lysosomes sequester certain organic cationic drugs, most likely via organic cation/H+ exchange driven by H(+)-ATPase. Canalicular organic cation/H+ exchange may reflect, in part, the exocytic insertion of this transporter from an intracellular compartment to this membrane domain.

Adenosine Triphosphate↗

PubMed1990

Mechanism of organic cation transport in rabbit renal basolateral membrane vesicles.

The transports of [3H]tetraethylammonium (TEA), [3H]procainamide (PCA), and N1-[3H]methylnicotinamide (NMN) were studied in rabbit renal basolateral membrane vesicles (BLMVs) by use of a rapid filtration assay. All three compounds exhibited a similar uptake profile into the BLMVs and reached equilibrium by 1 h. In the presence of valinomycin, a K+ ionophore and K+ gradients (in to out), an inside-negative potential difference (PD) was generated that stimulated the uptake of TEA, PCA, and NMN by 1.9-, 1.9-, and 2.1-fold, respectively. The effect of PD could be blocked by the organic cation transport inhibitor mepiperphenidol. An inside-negative PD was also generated by a pH gradient (inside acidic). An overshoot of TEA uptake was produced, which was blocked by a valinomycin voltage clamp. Counterflow studies revealed that 1 mM TEA was capable of trans-stimulating 50 microM [3H]TEA uptake and producing a peak overshoot of nearly three times the equilibrium value, which was not abolished in the presence of a valinomycin voltage clamp or a gramicidin pH clamp. When an inside-negative PD was imposed on 1 mM TEA-loaded BLMVs, the uptake of [3H]TEA was 33% less. In contrast, neither NMN nor PCA produced a trans-stimulation of [3H]NMN or [3H]PCA transport, respectively. In addition, the effect of several organic cations on the TEA-TEA exchange mechanism was studied. Mepiperphenidol, PCA, choline, cimetidine, and NMN all demonstrated cis inhibition (82, 81, 58, 51, and 20%, respectively). Arginine, a basic amino acid, and probenecid, an organic anion transport inhibitor, had no effect. Choline was capable of trans-stimulating TEA uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Cardiac afferents attenuate the muscle metaboreflex in the rat.

The influence of cardiac afferents on the muscle metaboreflex was examined in 16 rats instrumented with a Silastic-tipped catheter in the pericardial space and right atrium, Doppler ultrasonic flow probe and a pneumatic vascular occluder around the terminal aorta, and a Teflon catheter in the thoracic aorta. In protocol I (cardiac efferent and afferent blockade), the muscle metaboreflex was examined under three experimental conditions: 1) control, 2) cardiac autonomic efferent blockade [intrapericardial methylscopolamine (10 micrograms/kg) and propranolol (50 micrograms/kg)], and 3) combined cardiac autonomic efferent and afferent blockade (intrapericardial procainamide, 2%). In protocol II (blood volume expansion), the muscle metaboreflex was examined before and after 15% blood volume expansion. Mild treadmill exercise (9 m/min, 10% grade) increased heart rate (71 +/- 9.4 beats/min), mean arterial pressure (12 +/- 2.0 mmHg), and terminal aortic blood flow velocity (6 +/- 1.0 kHz). During exercise, a reduction of terminal aortic blood flow velocity (10.5 +/- 1.1%) reduced mixed venous PO2 18 +/- 6%. The gain of the muscle metaboreflex in the control condition was 14.6 +/- 2.9 mmHg/kHz. Efferent blockade reduced the gain 51 +/- 7%. However, combined cardiac efferent and afferent blockade increased the gain 207 +/- 64% above the efferent blocked condition and restored the gain to levels above those obtained in the control condition (18.3 +/- 4.6 mmHg/kHz). In addition, 15% blood volume expansion reduced the gain of the muscle metaboreflex regulation of mean arterial pressure and heart rate (44 +/- 9.5% and 41 +/- 12.0%, respectively). Thus cardiac afferents tonically inhibit the pressor response to a reduction in terminal aortic blood flow velocity during exercise.

Animals↗

PubMed2005

Comparison of biological effects of non-nucleoside DNA methylation inhibitors versus 5-aza-2'-deoxycytidine.

DNA cytosine methylation plays a considerable role in normal development, gene regulation, and carcinogenesis. Hypermethylation of the promoters of some tumor suppressor genes and the associated silencing of these genes often occur in certain cancer types. The reversal of this process by DNA methylation inhibitors is a promising new strategy for cancer therapy. In addition to the four well-characterized nucleoside analogue methylation inhibitors, 5-azacytidine, 5-aza-2'-deoxycytidine (5-Aza-CdR), 5-fluoro-2'-deoxycytidine, and zebularine, there is a growing list of non-nucleoside inhibitors. However, a systemic study comparing these potential demethylating agents has not been done. In this study, we examined three non-nucleoside demethylating agents, (-)-epigallocatechin-3-gallate, hydralazine, and procainamide, and compared their effects and potencies with 5-Aza-CdR, the most potent DNA methylation inhibitor. We found that 5-Aza-CdR is far more effective in DNA methylation inhibition as well as in reactivating genes, compared with non-nucleoside inhibitors.

Antimetabolites, Antineoplastic↗

PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗

PubMed1981

Effect of cortisone on permeability of the neonatal rat lung to drugs.

The effect of cortisone (5 mg/animal i.p. on day 5 after birth) on the development of adult-type permeability characteristics in the lung was investigated in rats 6-18 days of age. In both treated and control rats, the lipid-soluble drug procainamide was absorbed at similar rates in all age groups. In contrast, in cortisone-treated animals, pulmonary absorption rates for the lipid-insoluble compounds mannitol and p-aminohippuric acid declined to adult levels at the age of 6 days, which was 12 days earlier than in controls. Cortisone treatment thus accelerates development of adult permeability characteristics in the pulmonary epithelium.

Aging↗

PubMed1975

Effect of drugs in the wolff-parkinson-white syndrome.

Electrical stimulation of the heart, using the single test stimulus method, gives the opportunity to study the mechanisms of tachycardias and the effect of drugs on these mechanisms directly in the heart of the patient with the WPW syndrome. Using these methods the effect of digitalis, procainamide, quinidine, ajmaline, lidocaine, propranolol and verapamil has been studied. Understanding of the mechanisms responsible for initiation and maintenance of tachycardias and the way in which they can be influenced by drugs should be of help in the treatment of the symptomatic patient with the WPW syndrome.

Ajmaline↗

PubMed1999

Role of papillary muscle in the generation and maintenance of reentry during ventricular tachycardia and fibrillation in isolated swine right ventricle.

BACKGROUND: The role of papillary muscle (PM) in the generation and maintenance of reentry is unclear. METHODS AND RESULTS: Computerized mapping (477 bipolar electrodes, 1.6-mm resolution) was performed in fibrillating right ventricles (RVs) of swine in vitro. During ventricular fibrillation (VF), reentrant wave fronts often transiently anchored to the PM. Tissue mass reduction was then performed in 10 RVs until VF converted to ventricular tachycardia (VT). In an additional 6 RVs, procainamide infusion converted VF to VT. Maps showed that 77% (34 of 44) of all VT episodes were associated with a single reentrant wave front anchored to the PM. Purkinje fiber potentials preceded the local myocardial activation, and these potentials were recorded mostly around the PM. When PM was trimmed to the level of endocardium (n = 4), sustained VT was no longer inducible. Transmembrane potential recordings (n = 5) at the PM revealed full action potential during pacing, without evidence of ischemia. Computer simulation studies confirmed the role of PM as a spiral wave anchoring site that stabilized wave conduction. CONCLUSIONS: We conclude that PM is important in the generation and maintenance of reentry during VT and VF.

Animals↗

PubMed1999

Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation.

BACKGROUND: Atrial fibrillation (AF) can be initiated by ectopic beats originating from the atrial or great venous tissues. This study investigated the anatomic characteristics and electrophysiological properties of pulmonary veins (PVs), as well as the possible mechanisms and response to drugs of ectopic foci, and assessed the effects of radiofrequency (RF) ablation on AF initiated by ectopic beats originating from PVs. METHODS AND RESULTS: Seventy-nine patients with frequent episodes of paroxysmal AF and 10 control patients were included. Distal PVs showed the shortest effective refractory periods (ERPs), and right superior PVs showed a higher incidence of intra-PV conduction block than left superior PVs. Superior and left PVs had longer myocardial sleeves than inferior and right PVs, respectively. These electrophysiological characteristics were similar between AF and control patients. Propranolol, verapamil, and procainamide suppressed ectopic beats that originated from the PVs. Of 116 ectopic foci that initiated AF, 103 (88.8%) originated from PVs. A mean of 7+/-3 RF applications completely eliminated 110 ectopic foci (94.8%). During the 6+/-2-month follow-up period, 68 patients (86. 1%) were free of AF without any antiarrhythmic drugs. Follow-up transesophageal echocardiogram showed 42.4% of ablated PVs had focal stenosis. One patient had mild exertional dyspnea after ablation, but it resolved 3 months later; 1 patient had onset of mild exertional dyspnea 5 months after ablation. CONCLUSIONS: Electrophysiological characteristics of PVs are different from those in the atria. Ectopic beats from PVs can initiate AF, and beta-adrenergic receptor blocker, calcium channel blockers, and sodium channel blockers can suppress these ectopic beats. Careful mapping and elimination of these ectopic foci can cure paroxysmal AF.

Adult↗

PubMed1978

Long-term tocainide therapy for ventricular arrhythmias.

Long-term tocainide therapy has been evaluated in 17 patients with ventricular arrhythmias. Ventricular tachycardia and/or fibrillation was recurrent and sustained in nine patients, and symptomatic but unsustained in three others. Five patients had frequent but only mildly symptomatic ventricular irritability. In all patients, arrhythmias could not be managed with quinidine, procainamide or propranolol. Tocainide doses ranged from 300 to 700 mg every 8 hours (mean steady-state plasma concentrations ranged from 5.75 to 12.18 microgram/ml). Tocainide therapy was unsuccessful in eight patients; three died during therapy and five had no antiarrhythmic response. The data suggest that evaluation of long-term drug efficacy, using the criterion of reduction of asymptomatic arrhythmias, is best documented by multiple sequential ambulatory electrocardiographic recordings, both on and off the drug. Tocainide controlled arrhythmias in nine patients (53%), with criteria of success being continued reduction of ectopic beats and/or control of symptomatic recurrences. Seven patients remain on therapy. Side effects generally have been minor and well-tolerated.

Adult↗

PubMed1980

Effects of antiarrhythmic drugs on atrioventricular conduction in patients with acute myocardial infarction.

Three hundred fifty-eight of 429 (83%) consecutive patients with acute myocardial infarction (MI) and a normal PR interval received various antiarrhythmic drugs (AD), including lidocaine and/or procainamide, quinidine, digoxin, propranolol or disopyramide. There was no significant difference in the incidence of progression to any degree of atrioventricular (AV) block or to higher degrees of AV block (Mobitz II or third-degree AV block) between those treated and not treated with AD: 38 of 358 (11%) and six of 358 (1.7%) with AD vs 11 of 71 (15%) and two of 71 (2.8%) in the untreated group, respectively. Similarly, there was no significant difference in progression between treated and untreated patients with anterior MI, 14 of 144 (10%) vs five of 32 (16%); inferior MI, 21 of 111 (19%) vs five of 26 (19%), or subendocardial MI, three of 103 (3%) vs one of 12 (8%). Bundle branch block (BBB) (without AV block) was initially present in 89 of 249 (21%). The incidence of AV block (seven of 24, 30%) was higher in treated patients with newly acquired BBB (27 patients) than in the untreated patients (none of three, p less than 0.05). The commonly used ADs did not adversely affect AV conduction in patients with acute MI with narrow QRS and either normal, first-degree, or Mobitz I AV block. Moreover, no subset of patients grouped by infarct location, specific AD used, or BBB (except perhaps for those with newly acquired BBB) appeared to be at risk of development of AV block during AD therapy.

Aged↗

PubMed1981

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

Ninety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 --i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 -- i.v. lidocaine, prereperfusion only (n = 22); protocol 3 -- chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 -- i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 -- i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol 1 -- seven of 15 dogs (47%); protocol 2 -- six of 18 (33%); protocol 3 -- 11 of 16 dogs (69%); protocol 4 -- eight of 17 dogs (47%); and protocol 5 -- 10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs. Using chi-square analysis, protocol 2 was beneficial (p < 0.05). The dogs were then stratified into high- and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. the Mantel-Haenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.

Amiodarone↗

PubMed1983

Direct endocardial recording from an accessory atrioventricular pathway: localization of the site of block, effect of antiarrhythmic drugs, and attempt at nonsurgical ablation.

We recorded a discrete 0.95 mV potential consistent with accessory atrioventricular pathway (AP) activation during serial electrophysiologic studies in a patient with Ebstein's anomaly and Wolff-Parkinson-White syndrome. Bipolar pacing from the catheter electrode in which the AP potential was recorded resulted in a stimulus-ventricle interval identical to the AP-ventricle interval during antegrade conduction, and a stimulus-atrium interval identical to the AP-atrium interval during retrograde conduction. With the patient in the drug-free state, antegrade AP block during atrial pacing and retrograde AP block during ventricular pacing occurred distal to the AP potential (AP-ventricle junction and AP-atrium junction, respectively), supporting the "impedance mismatch" hypothesis. Procainamide and disopyramide each lengthened the antegrade AP effective refractory period by affecting the AP-ventricle junction (possibly by decreasing the current generated by the AP). Both drugs also lengthened the retrograde AP effective refractory period but produced a greater effect on the ventricle-AP junction than on the AP-atrium junction, suggesting marginal geometry of the former. R wave synchronous shocks of 160 and 320 W-sec delivered between the catheter electrode recording the largest unipolar AP potential and a skin electrode produced transient, complete, antegrade block over the AP, suggesting the feasibility of this new nonsurgical technique for AP ablation.

Adult↗

PubMed1987

Conduction over an isthmus of atrial myocardium in vivo: a possible model of Wolff-Parkinson-White syndrome.

Antiarrhythmic drugs appear preferentially to prolong refractoriness of accessory pathways compared with atrial or ventricular muscle in patients with the Wolff-Parkinson-White syndrome. This response may be due to intrinsic properties of accessory pathways or to depressed conduction associated with a narrow strip, or isthmus, of tissue. To test the latter possibility, in 16 anesthetized dogs we surgically isolated a portion of the right atrial myocardium in the form of an ellipse (10 to 25 X 8 to 15 mm). The ellipse was connected to the body of the right atrium by a narrow isthmus (cross-sectional area [CSA] 1 to 13.5 mm2) and was perfused by the sinus node artery or its branch. Diastolic threshold (mean +/- SE 0.16 +/- 0.05 vs 0.13 +/- 0.02 mA) and effective refractory period (ERP; 144 +/- 4 vs 139 +/- 5 msec) were the same proximal and distal to the isthmus. In eight dogs, determination of the ERP of the isthmus was limited by the ERP of the atrial tissue proximal and distal to the isthmus, and the CSA of the isthmus in these dogs was significantly larger than that in the remaining seven dogs in which the ERP of the isthmus could be determined (7.4 +/- 1.4 vs 3.2 +/- 0.6 mm2, p less than .05). The shortest pacing cycle length (PCL) with 1:1 conduction from the proximal to the distal segments did not differ from that in the opposite direction in 16 dogs (154 +/- 9 vs 153 +/- 7 msec). The CSA of the isthmus correlated inversely with the shortest PCL with 1:1 conduction in both directions via the isthmus (r = -.84, p less than .01). Vagal stimulation shortened the shortest PCL with 1:1 conduction from the distal to the proximal segment (153 +/- 14 vs 143 +/- 12 msec, p less than .02), but not in the opposite direction. Procainamide (10 to 20 mg/kg iv, serum concentration 8.6 +/- 0.8 micrograms/ml) prolonged the ERP of the proximal site from 145 +/- 5 to 170 +/- 5 msec (p less than .001), the ERP of the distal site from 143 +/- 6 to 168 +/- 6 msec (p less than .001) in 12 dogs, and the shortest PCL with 1:1 conduction (proximal to distal from 149 +/- 8 to 204 +/- 17 msec, p less than .001; distal to proximal from 149 +/- 7 to 197 +/- 12 msec, p less than .001) in 14 dogs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗