[Volume regulation in cardiac insufficiency : possibilities of telephone coaching and peritoneal dialysis]. / Volumenregulation bei Herzinsuffizienz : Möglichkeiten des Telefon-Coachings sowie der Peritonealdialyse.

Volume retention is the hallmark of progressive heart failure, both systolic and diastolic (heart failure with preserved ejection fraction). It represents the cause of the main symptoms (dyspnea, edema, liver synthesis) and also the main target of drug therapy. Antagonizing excessive volume retention is also the most important therapy element. Many patients can be stabilized with sequential nephron blockade (thiazide + loop diuretics) combined with afterload reduction [blockade of the RAAS (renin-angiotensin-aldosterone) system]. Personal patient coaching combined with telemetric components (weight, blood pressure) has evolved as another cornerstone of treatment in heart failure patients. If these measures are insufficient to control volume retention, renal replacement therapy is effective and can improve quality of life. More specifically, aquaresis via peritoneal dialysis has been shown to be effective and adequate to control volume overload. Many patients may qualify for this evolving therapy as it effectively prevents repeat hospitalization for heart failure decompensation, can be performed in an out-patient setting and has a low complication rate, thus significantly improving quality of life.

Parvalbumin-containing interneurons of the human cerebral cortex express nicotinic acetylcholine receptor proteins.

Cholinergic fibers from the basal forebrain are known to contact cholinoceptive cortical pyramidal neurons. Recent electrophysiological studies have revealed that nicotinic acetylcholine receptors are also present in human cerebrocortical interneurons. A direct visualization of nicotinic receptor subunits in cortical interneurons has, however, not yet been performed. We have applied double-immunofluorescence using antibodies against parvalbumin --a marker for the Chandelier and basket cell subpopulation of interneurons--and to the alpha4 and alpha7 subunit proteins of the nicotinic acetylcholine receptor. The vast majority of the parvalbuminergic interneurons was immunoreactive for the alpha4 and the alpha7 nicotinic acetylcholine receptor. Provided these receptors would be functional--as suggested by recent electrophysiological findings--the connectivity pattern of cholinergic afferents appears much more complex than thought before. Not only direct cholinergic impact on cortical projection neurons but also the indirect modulation of these by cholinergic corticopetal fibers contacting intrinsic cortical cells would be possible.

Postpartum thrombosis of the great vein of Galen.

Severe fits occurred in a patient 52 hours after placental abruption. Early use of computerised tomography scanning enabled a definitive diagnosis of thrombosis of the great vein of Galen to be made. The case illustrates the point that not all fits in the early postpartum period should be attributed to eclamptic toxaemia.

Mechanism of recovery from acute virus infection. IV. Questionable role of mononuclear phagocytes in the clearance of lymphocytic choriomeningitis virus from spleens of mice.

After intravenous infection of mice with 10(3) infectious units (IU) the WE strain lymphocytic choriomeningitis (LCM) virus multiplied in the spleens (as in all other major organs), reaching more than 10(8) IU/g of tissue on days 4 to 5. Subsequently, the virus was quickly eliminated, being below detectability usually by day 10. During the time of virus clearance, the mononuclear phagocytes (MNP) of the spleen were activated as revealed by suppression of growth of Listeria monocytogenes and increase of cell-associated hydrolytic enzymes. In athymic nude mice, in whom the MNP system is assumed to be permanently activated, the virus replicated slightly but reproducibly less than in their euthymic counterparts. However, when the MNP were activated by Corynebacterium parvum, virus in spleens attained higher concentrations than in mice not so treated, and the rate of elimination was not altered. In mice whose MNP had been damaged by injection of dextran sulfate 500, the spleen virus titers were also increased, but the subsequent immune elimination was slightly delayed. Activation of spleen MNP was not evident at the time virus was rapidly cleared as a result of transfusion of LCM-immune T lymphocytes. Adoptive immunization was as successful in mice that had been pretreated with gamma-rays or cyclophosphamide, suggesting that replicating cells or their descendants, in particular monocytes, did not participate measurably in the process of elimination. Pretreatments of recipients with dextran sulfate 500 reduced the efficacy of transfused LCM-immune T lymphocytes, but this compound probably directly affected the cells. We interpret these findings to mean that the LCM virus in the mouse's spleen is controlled by a mechanism in which MNP do not play an essential role.