Search PubMed⌕ Search

Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

161 records · Page 9Linked to original sources
PubMed1972

The electrophysiologic effects of low and high digoxin concentrations on isolated mammalian cardiac tissue: reversal by digoxin-specific antibody.

The effects of digoxin on electrophysiologic properties were evaluated in isolated perfused cardiac tissue. In canine Purkinje fiber (PF)-ventricular muscle (VM) preparations, control measurements, using microelectrode technique, were made of: resting potential (RP), action potential (AP) amplitude, rate of rise, overshoot, duration (APD), membrane responsiveness, conduction velocity (CV), and refractory period. The preparation was then exposed to 1 x 10(-7) M digoxin and repeat measurements were carried out every 15 min. At slow (30/min) rates of stimulation APD initially prolonged then markedly shortened. With more rapid stimulation (75 and 120/min) no initial APD prolongation was observed. When stimulated at 75/min, RP and AP rate of rise, amplitude, and CV remained near control values for 60-75 min then rapidly decreased until electrical inexcitability (110+/-15 min). At that time fibers were perfused with serum containing digoxin-specific antibody (DSA) or one of a group of test solutions. In the preparations exposed to DSA, membrane characteristics improved by 15 min, and by 60 min approximated control values. No beneficial effect was seen with the various test solutions. DSA also reversed digoxin-induced enhanced phase 4 depolarization in PF. Effective (ERP) and Functional (FRP) refractory periods of rabbit atrioventricular (AV) node preparations were measured in the control state. The tissue was then exposed to 1 x 10(-7) M digoxin and refractory period measurements repeated. At a time when AV conduction prolonged by 20%, associated with marked prolongation of ERP and FRP, DSA or various test solutions were perfused. The prolongation in ERP, FRP, and AV conduction time rapidly returned to normal only in the DSA perfused tissue. It is concluded that DSA has the ability to reverse pronounced toxic electrophysiological effects of digoxin in in vitro cardiac tissue.

Action Potentials↗
PubMed1970

Effect of lidocaine on the electrophysiological properties of ventricular muscle and purkinje fibers.

Preparations of right ventricular papillary muscle and false tendon (Purkinje fiber) were obtained from dog hearts, placed in a bath perfused with Tyrode solution, and observed both under control conditions and during exposure to lidocaine in concentrations from 1 x 10(-7) to 5 x 10(-4) mole/liter. Transmembrane voltages were recorded from both ventricular muscle (VM) and Purkinje fibers (PF) of spontaneously beating and electrically driven preparations. Low concentrations (1 x 10(-6) and 1 x 10(-5) mole/liter) attenuated or abolished phase 4 (diastolic) depolarization and spontaneous firing in PF without decreasing their diastolic excitability. Concentrations of 1 x 10(-5) mole/liter produced maximal shortening of both action potential duration (APD) and effective refractory period (ERP) and made the ERP long relative to APD; the latter alteration was more prominent in VM. At concentrations </= 1 x 10(-5) mole/liter, lidocaine either caused a slight increase or no change in peak maximum rate of phase 0 depolarization (V(max)) and membrane responsiveness, the relationship between transmembrane activation voltage (MAV) and V(max) of the resultant action potential; these concentrations had no significant effect on resting potential (RP) in VM, maximal diastolic transmembrane voltage (DTMV(max)) in PF, or action potential amplitude in either fiber type. High (toxic) concentrations (>/= 1 x 10(-4) mole/liter) did not cause further shortening of APD or ERP in either VM or PF but did produce a decrease in peak V(max) of phase 0 and membrane responsiveness. In most cases, these concentrations also caused a decrease in RP or DTMV(max) and action potential amplitude, with progression to bizarre action potential depolarization and inexcitability. These properties of lidocaine are strikingly different from those of quinidine or procaine amide. The mechanisms responsible for lidocaine's in vivo antiarrhythmic action are discussed.

Action Potentials↗
PubMed1968

Analysis of T-wave abnormalities associated with myocardial infarction using a theoretic model.

The physiological basis of serial T-wave abnormalities associated with myocardial infarction was studied. After coronary artery ligation in dogs, ventricular functional refractory periods (FRPs) were measured at five to eight epicardial, intramural, and endocardial sites. FRPs measured during acute ischemia shortened an average of 26 msec. FRPs measured 24 to 72 hr after coronary ligation were 24 msec longer at ischemic than at nonischemic sites. Alterations of recovery times were analyzed in terms of a repolarization model which related the form of the action potential downstroke to the form of the T wave of the body surface ECG. Observed FRPs were used to infer action potential duration and T waves were derived. Shortening FRPs in the anterolateral wall of the ventricle increased the amplitude of derived T waves in the X lead and caused T-wave inversion in the Z lead. Prolonging FRPs in the same area caused T-wave inversion in lead X and increased T amplitude in lead Z. The form of derived T waves qualitatively corresponded to serial T-wave abnormalities seen in patients with myocardial infarction.

Action Potentials↗