Objective
The aim of this work was to evaluate the hypothesis that the distribution of circulating immune cell subsets, or their activation state, is significantly different between peripartum cardiomyopathy (PPCM) and healthy postpartum (HP) women.
Background
PPCM is a major cause of maternal morbidity and mortality, and an immune-mediated etiology has been hypothesized. Cellular immunity, altered in pregnancy and the peripartum period, has been proposed to play a role in PPCM pathogenesis.
Methods
The Investigation of Pregnancy-Associated Cardiomyopathy (IPAC) study enrolled 100 women presenting with a left ventricular ejection fraction of <0.45 within 2 months of delivery. Peripheral T-cell subsets, natural killer (NK) cells, and cellular activation markers were assessed by flow cytometry in PPCM women early (<6 wk), 2 months, and 6 months postpartum and compared with those of HP women and women with non–pregnancy-associated recent-onset cardiomyopathy (ROCM).
Results
Entry NK cell levels (CD3−CD56+CD16+; reported as % of CD3− cells) were significantly (P < .0003) reduced in PPCM (6.6 ± 4.9% of CD3− cells) compared to HP (11.9 ± 5%). Of T-cell subtypes, CD3+CD4−CD8−CD38+ cells differed significantly (P < .004) between PPCM (24.5 ± 12.5% of CD3+CD4−CD8− cells) and HP (12.5 ± 6.4%). PPCM patients demonstrated a rapid recovery of NK and CD3+CD4−CD8−CD38+ cell levels. However, black women had a delayed recovery of NK cells. A similar reduction of NK cells was observed in women with ROCM.
Conclusions
Compared with HP control women, early postpartum PPCM women show significantly reduced NK cells, and higher CD3+CD4−CD8−CD38+ cells, which both normalize over time postpartum. The mechanistic role of NK cells and “double negative” (CD4−CD8−) T regulatory cells in PPCM requires further investigation.
Using a push-pull cannula method the amygdala of rats was perfused to examine the release of labeled norepinephrine (NE) and labeled serotonin (5-HT) during electrical stimulation of the brain (ESB) determined by prior behavioral testing to be rewarding or non-rewarding. Simple sensory stimulation was used during perfusion to examine further the degree of specificity of release of these amines. Highly rewarding ESB, but not the sensory stimulation, was accompanied by release of both NE and 5-HT. Varying current intensity had significant effects on the amount of these amines released. Furthermore, non-rewarding ESB was accompanied by inhibition of release of NE and 5-HT and a control substance, urea, was not significantly released during rewarding ESB. The results were discussed as implicating both noradrenergic and serotonergic mechanisms in the mediation of reinforcement.
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