Effects of permanent residence with foster mothers and new siblings upon numbers of mast cells within the thalamus of preweaned rats.

In a split-litter, cross-fostered design, the numbers of mast cells per 10 micrometer sections within the thalamic boundaries in rats that had been reared by 8 natural or 8 foster mothers were counted 5 days and 10 days after the transfer had occurred on postnatal Day 10. The rats from 4 litters with the highest numbers of thalamic mast cells exhibited marked reductions in these numbers when fostered by mothers of the 4 litters with the fewest numbers of thalamic mast cells. The reverse influence was not observed. These results suggest that adaptation to changing maternal environments for rats with congenitally elevated numbers of mast cells may increase the risk of degranulation and transient anomalies within cerebral vasculature or the blood-brain barrier.

Mast cell numbers in the young rat thalamus: a search for control factors.

Numbers of mast cells within brain space can be influenced by exposures to weak, complex magnetic fields. The present studies were designed to help isolate the factors that control numbers of mast cell within the thalamus (n=96) of 15 and 20 day old rat pups. In Experiment I, rat pups were injected daily with either 1 microliter/g or 10 microliter/g of either distilled water, isotonic saline or 0.5 M saline; another group served as controls. The numbers of thalamic mast cells did not differ significantly between the four groups. In Experiment II, that employed a cross-fostering, split litter design, the rats whose mothers had consumed 0.9% taurine during pregnancy contained about twice as many mast cells within the thalamus compared to controls. Fifteen day old pups that had been reared by other mothers showed more mast cells than those reared by their own mothers. There were negative correlations (-.60) between the numbers of mast cells within the leptomeninges of the pups and the mothers' ovarian weights but no significant associations between the numbers of mast cells within the brains of the pups and the mothers.

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans.

PURPOSE: To describe the relative effects of graded central nervous system (CNS) depression, using increasing propofol infusion rates, on neurovegetative brainstem-mediated circulatory control mechanisms and higher cortical activity in healthy humans. METHODS: Propofol was administered using an infusion scheme designed to achieve three target blood concentrations in ten healthy volunteers. Blood propofol concentrations and sedation scores were determined at baseline, during the three propofol infusion levels, and 30 min into the recovery period. Electroencephalographic (EEG) power was measured in three frequency bands to quantify cortical activity, and autonomic heart rate control was quantified using spontaneous baroreflex assessment and power spectral analysis of pulse interval. RESULTS: Sedation scores closely paralleled propofol blood concentrations (0, 0.53 +/- 0.34, 1.24 +/- 0.21, 3.11 +/- 0.80, and 0.96 +/- 0.42 microg x mL(-1) at baseline, three infusion levels and recovery respectively), and all subjects were unconscious at the deepest level. Indices of autonomic heart rate control were decreased only at the deepest levels of CNS depression, while EEG effects were apparent at all propofol infusion rates. These EEG effects were frequency specific, with power in the beta band being affected at light levels of sedation, and alpha and delta power altered at deeper levels. CONCLUSIONS: The results of this study support a relative preservation of neurovegetative circulatory control mechanisms during the early stages of CNS depression using gradually increasing rates of infusion of propofol. Indices of circulatory control did not reliably reflect depth of sedation.

Change in atrial volume following restoration of sinus rhythm in patients with atrial fibrillation: a prospective echocardiographic study.

OBJECTIVES: To determine if restoration of sinus rhythm in patients with atrial fibrillation decreases atrial size, 16 patients undergoing elective cardioversion were prospectively studied. The frequent coexistence of atrial fibrillation and atrial dilation is well recognized. Recent data have demonstrated that atrial enlargement may be the result, rather than the cause, of atrial fibrillation. DESIGN: Echocardiographic examinations were performed before cardioversion, and at 24 h, three and six months of follow-up. Atrial dimensions were assessed in multiple orthogonal imaging planes and atrial volume was calculated using an ellipsoid formula. SETTING: A tertiary care university teaching hospital. PATIENTS: All patients admitted to hospital between June 1989 and June 1990 for elective cardioversion were considered for enrollment. Informed consent was obtained in all cases. Patients were excluded if echocardiographic images were technically inadequate or reversion to normal sinus rhythm was not achieved. Twenty-five patients were considered for inclusion. The final study population consisted of 16 patients. Complete follow-up data were obtained in 10 cases. MAIN RESULTS: Conversion to sinus rhythm resulted in a decrease in mean left atrial volume from 38.5 cm3 to 34.2 cm3 (P < 0.01) at 24 h, 21.7 cm3 (P < 0.02) at three months and 19.6 cm3 (P < 0.02) at six months. Mean right atrial volume decreased from 33.4 cm3 to 29.4 cm3 (P < 0.01) at 24 h, 19.1 cm3 (P < 0.02) at three months and 16.3 cm3 (P < 0.02) at six months of follow-up. CONCLUSIONS: Conversion from atrial fibrillation to sinus rhythm results in a significant decrease in both left and right atrial volumes.

Progressive accumulation of large aggregates of calcium-containing polysaccharides and basophilic debris within specific thalamic nuclei after lithium/pilocarpine-induced seizures.

Between 30 and 50 days after the induction of seizures by a single injection of lithium and pilocarpine, large aggregates of Nissl-staining material appeared; they occupied up to 35% of the thalamic volume. Both histochemical and atomic absorption analyses indicated elevated concentrations of Ca++ (and possibly Mg++) within this substance that was also composed of polysaccharides and nucleic acids. Significant interactions between time since seizure induction and form of the material indicated a progressive accretion of this material from diffusely scattered micrometer granules to large crystalline forms. We suggest this material is composed of endoplasmic reticular debris that is bound by bivalent cations; because the severity of damage exceeds local phagocytic capacity, the material aggregates and then crystallizes. Possible relation to thalamic calcification in neonatal ischemic brains is considered.

Thyroid morphology and activity does not respond to ELF electromagnetic field exposures.

The hypothesis that the thyroid is the sensitive organ for extremely low freqency electromagnetic field effects was tested. Rats that had been exposed either preinatally or as adults to several intensities of 0.5 Hz magnetic fields displayed no significant alterations in thyroid morphology or circulating hormone measures.

Oral taurine effects on inhibitory behavior: response transients to step-like schedule changes.

Rats habituated to DRL 6-s schedules that required response inhibition in order to obtain reward did not alter their total responses or efficiency ratios (response/reinforcement) when placed ad libitum (orally) on 0.9% taurine (1.1 +/- 0.4 g/kg/24-h) relative to controls. In three separate experiments, taurine-administerd rats did show significantly poorer adjustment profiles (higher response/reinforcement ratios) during the 15 min immediately following step-like increases in inhibition time demand to DRL 12 s. The effect was transient and was not signficant in subsequent sessions. Taurine rats had been habituated to a DRL schedule intended to induce "frustration" before and step-change did not differ from the taurine group maintained on the normal DRL schedule. No significant differences were noted between taurine and control groups, either before or after taurine administration or before or after the step-change in inhibition demand, with respect to defecation in the test chamber, daily fluid consumption, body weight or total responses. We concluded that oral taurine may inhibit learning during labile periods of adjustment following sudden changes of input demand but does not influence a well learned or established response pattern. These results imply taurine's role in the brain as a "stabilizer" against short-term input fluctuations.