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)     

Cocaine-induced brainstem seizures and behavior.

A variety of abnormal sensory/motor behaviors associated with electrical discharges recorded from the bilateral brainstem were induced in adult WKY rats by mechanical (electrode implants) and DC electrical current stimulations and by acute and chronic administration of cocaine. The electrode implant implicated one side or the other of the reticular system of the brainstem but subjects were not incapacitated by the stimulations. Cocaine (40 mg/kg) was injected subcutaneously for an acute experiment and subsequent 20 mg/kg doses twice daily for 3 days in a chronic study. Cocaine generated more abnormal behaviors in the brainstem perturbation group, especially the electrically perturbated subjects. The abnormal behaviors were yawning, retrocollis, hyperactivity, hypersensitivity, "beating drum" behavior, squealing, head bobbing, circling, sniffing, abnormal posturing, and facial twitching. Shifts in the power frequency spectra of the discharge patterns were noted between quiet and pacing behavioral states. Hypersensitivity to various auditory, tactile, and visual stimulation was present and shifts in the brainstem ambient power spectral frequency occurred in response to tactile stimulation. These findings suggest that the brainstem generates and propagates pathological discharges that can be elicited by mechanical and DC electrical perturbation. Cocaine was found to activate the discharge system and thus induce abnormal behaviors that are generated at the discharge site and at distant sites to which the discharge propagates. Cognitive functions may also be involved since dopaminergic and serotonergic cellular elements at the brainstem level are also implicated.     

Low-dimensional chaos maps learning in a model neuropil (olfactory bulb).

Quantification of a chaotic system can be made by calculating the correlation dimension (D2) of the data that the system generates (Packard et al., 1980). The D2 algorithm, however, requires stationarity of the generator, a feature that biological data rarely reflect (Mayer-Kress et al., 1988). So we developed the "point correlation dimension" (PD2), an algorithm that accurately tracks D2 in linked data of different dimensions (Carpeggiani et al., 1991). We now present a mathematical argument that, for stationary data, individual PD2s converge to D2 and we demonstrate that the algorithm rejects contributions made by bursts of noise. Data were obtained from the surface of the olfactory bulb of the conscious rabbit (64 electrodes, 640 Hz each, 1.3 sec epochs) before and after presentation of a novel or habituated odor. D2 could be calculated in only 1 of 10 novel-odor trials, whereas PD2 could be calculated in all. Both algorithms indicated that a novel odor evokes a spatially uniform dimensional increase. The PD2 uniquely exhibited the dimensional decreases that occur during inspiration and the gradients of mean dimension present during the nonstimulated control state. These control gradients remained unchanged without odor experience, but showed spatially specific PD2 increases following odor habituation. It is interpreted that, 1) the PD2 is sensitive, accurate, and appropriate for dimensional assessment of biological data, 2) that during analysis of unfamiliar information a single global process is transiently evoked in the neuropil, and 3) after experience multiple spatially specific processes tonically map the sites of learning.     

Extinction instead of incubation following classical aversive conditioning in dogs.

Two dogs received a single paired classical conditioning trial, with tone CS and 12 mA shock US. Both dogs then showed a conditioned blood pressure increase in response to the nonreinforced CS, which extinguished with additional nonreinforced presentations. The CR showed spontaneous recovery four days later, but reextinguished with additional nonreinforced presentations. The results were interpreted as not supporting Eysenck's theory of "incubation" following one-trial aversive conditioning.     

Severe psychosis and the adrenal androgens.

Past literature suggests a link between certain psychotic states and adrenal androgen production, including Dehydroepiandrosterone (DHEA). A group of severely psychotic androgenized females, refractory to substantial amounts of neuroleptics, has been identified for whom endocrine testing revealed abnormally high levels of DHEA. A similar group has been identified among the severely psychotic male population. Improvement in psychosis appears to occur as DHEA returns to its normal range using standard low dose Dexamethasone suppression.     

Predictors of myocardial infarction over a span of 30 years in Roseto, Pennsylvania.

Predictors of myocardial infarction with or without survival were sought in a 30-year study of Roseto, Pennsylvania, a nearly exclusively Italian community of approximately 1,600, compared to the immediately adjacent town of Bangor with a population of approximately 5,000. At the start of the study the death rate from myocardial infarction among men in Roseto was less than half that in Bangor despite an equal prevalence of the usual risk factors, mainly smoking and diet. The communities were followed prospectively for 30 years during a striking social change in Roseto toward less family and community cohesion and more commitment to individual goals and adherence to materialistic values. During this period the prevalence of and mortality from myocardial infarction increased sharply to equal the situation in Bangor. The predictive values of measurements made of Rosetans during individual examinations in 1962-63 were tested against the outcome in 1990. Those who experienced fatal myocardial infarction and those who had a well documented infarction and survived were matched with and compared to controls. Although subjects with cholesterol concentration above 200 were twice as likely to experience myocardial infarction as those with concentrations below 200, less than 20% of those whose cholesterol concentration was above 200 experienced any evidence of myocardial infarction over the nearly 30-year period. Moreover, there were no significant differences between the coronary patients, with or without survival, and their sex, age, and cholesterol matched controls; nor were smoking, evidence of hypertension, diabetes, or obesity predictive of significant differences between the two groups. These data lead to the inference that while those with the conventional risk factors are more likely to develop myocardial infarction than are those without the risk factors, an even larger proportion of the population may have the risk factors and not succumb to myocardial infarction over a period of nearly three decades.