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S Wolf

Publications and source records attributed to S Wolf.

At least 451 records · Page 25Linked to original sources
PubMedDate not supplied

Sudden cardiac death.

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Death, Sudden, Cardiac↗
PubMedDate not supplied

Heart rate-Qt interval relationship during postural change and exercise. A possible connection to cardiac contractility.

The QT interval of the electrocardiogram, although often coordinated in an inverse relationship to heart rate, appears from the existing evidence to be regulated by mechanisms separate from those that govern heart rate. The purpose of this inquiry was to explore further the relationship of the two and to test other factors that may contribute to the regulation of QT. Heart rate and QT duration were measured in healthy human subjects during postural change and exercise. The data showed that, while coordinated in an inverse relationship under some circumstances, under others heart rate and QT were discordant, leading to the inference that there is no fixed linkage between the two. Previous work by the authors and other published studies have suggested that ventricular contractility may have more predictable association with QT shortening than do increases in heart rate. Observations of force of ventricular contraction (HI and IJ velocity) as reflected in ballisto-cardiographic tracings were made using each of 12 human subjects as the authors' own control. The data revealed a highly significant correlation between the velocity measures and QT duration (p less than 0.01) but not heart rate. These findings led to the conclusion that there is clearly not a fixed relationship between heart rate and QT interval and to the hypothesis that QT may more closely reflect the degree of cardiac contractility.

Adult↗
PubMedDate not supplied

Heart rate--QT relationships during baroreceptor stimulation with diminished autonomic influence on the ventricles. Ventricular autonomic tone and QT interval.

The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Cortical control of sinus arrhythmia in man studied by spectral analysis.

Eighteen healthy male volunteers, 21-26 years old, participated in a study intended to detect cortical control of beat-to-beat heart rate variability independent of the effects on breathing and mean heart rate. They were tested while seated and standing relaxed (baseline), and while performing tasks requiring concentrated attention while sitting. The mental concentration elicited a typical cardiorespiratory response manifested by moderate acceleration and shallowing of respiration with a small increase of mean heart rate (HR), a pattern already widely acknowledged as typically associated with concentration. With the aid of a variable tone delivered to the ear as a guide, the subjects were trained to breathe at the same rate without concentrating in order to test the influence of respiration on the concentration pattern. ECG, thermistor pneumogram and ear-lobe photo-plethysmogram were recorded and data reduction was performed on 3 minute or 1 minute data sequences selected for the best steady-state. Statistical treatment was limited to a subgroup of 10 subjects in whom there was no overlapping of the spectra of respiratory and Traube-Hering-Mayer sinus arrhythmia (RSA and THM-SA, respectively). Mental concentration elicited significant depression of both RSA and THM-SA even if the respiratory parameters were kept constant.

Adult↗
PubMedDate not supplied

Neurocardiac toxicity of racemic D,L-lactate fluids.

Racemic D,L-lactate has long been used in burn therapy as Ringer's lactate and in peritoneal dialysis fluid for treatment of renal failure. The D-lactate component of this racemic mixture is known to cause two forms of neurological toxicity in patients: encephalopathy and, in a subset of the population, panic reaction. Here we demonstrate that coma, similar in degree to that produced by blood levels of 75 mM ethanol was induced in rats by the intraperitoneal infusion of sodium D-lactate sufficient to raise serum D-lactate concentration to 25 mM, whereas infusion of equal quantities of sodium L-lactate produced no observable neurological effect. We further demonstrate that the intravenous infusion of racemic D,L-lactic acid into 48-hour fasted rats produced serious disturbances of cardiac rate and rhythm leading to death. When serum D-lactate concentration had reached 1-2 mM there was bradycardia, at 2-3 mM prolongation of QT interval, at 6-7 mM AV block with ectopic escape rhythms, and at 11 mM death in ventricular standstill or fibrillation. In contrast, intravenous infusion of L-lactic acid to blood levels of 25 mM failed to produce any change in cardiac rhythm. On the other hand, the isolated working heart, free of influence from the central nervous system, displayed no change of cardiac rhythm or physiological function when perfused with 25 mM sodium D,L-lactate.

Adult↗