A microcomputer-based stimulator for clinical and experimental investigations in cardiac electrophysiology.

A cardiac stimulator is described which combines the ease of operation required in clinical investigations, particularly endocavitary studies of cardiac arrhythmias, and the versatility needed in a research context. This instrument uses a microcomputer to control two independent optically-isolated stimulation ports which can be addressed either independently or jointly to stimulate at two different sites. The main software module operates as a cascade of ten real time pulse generators with individually presettable parameters: amplitude, duration, period, initial delay, periodic and cyclic modifiers, triggering mode, etc. A simple interactive procedure allows the operator to define a stimulation protocol either by accessing the generator structure directly, or by calling any of five pre-programmed stimulation protocols. With this combination, the instrument can provide a large variety of pulse patterns. The operator can intervene at any time during stimulation to change parameter values or modify the pulse pattern. Concurrently with stimulation, the instrument generates time-codes to help relate cardiac responses recorded on paper chart and magnetic tape, and reference them to specific events. The instrument can be readily expanded by the addition of parallel microprocessor modules; other real time tasks such as acquisition and processing of cardiac responses can thus be incorporated.     

Self-inhibiting action of nortriptyline's anti-immobility effect at high plasma and brain levels in mice

Animals were treated acutely with 0, 2.5, 5, 10, 20 and 40 mg/kg nortriptyline (NT) 30 min before the tail suspension test (TST). They were sacrificed after test for evaluation of plasma and brain levels of NT. The anti-immobility effect increased with increasing doses and concentrations of the drug, reaching statistical significance (P<0.01, Dunnett test) at a dose of 20 mg/kg, 865 ng/ml in plasma and 11 µg/g in brain tissue. The anti-immobility effect was, however, blocked with the highest, non-toxic, concentrations. Results seem to indicate a biphasic curvilinear relationship between plasma and brain levels of NT and behaviour in mice.     

Le système nerveux sympathique est un médiateur des contraintes mécaniques dans le tissu osseuxSympathetic nervous system as transmitter of mechanical loading in bone

Sympathetic innervation has been demonstrated in bone. Adrenergic stimulation is one of the transmitters of bone loss by uncoupling between decreased bone formation and increased bone resorption.Objective. – By using a non specific antagonist of β-adrenergic pathway (propranolol per os), we hypothesized that we could rescue the uncoupling induced mechanical unloading bone loss in the rat model of tail-suspension.Materials and methods. – Twenty-two female rats Wistar, 12 week-old, have been divided into three groups: eight tail-suspended rats (SR), six tail-suspended rats treated by propranolol (SRP) and eight non suspended rats (NSR) during 30 days. Bone mineral density (BMD, g/cm²) has been measured by DXA (Hologic QDR-4500A) at D0 and D30 of the study, in the distal femoral metaphysis (DFM), the femoral diaphysis (FD), the whole body (WB, g) and body composition.Results. – Between D0 and D30, in DFM a significant variation in BMD is observed between NSR and SR (% BMD change: NSR +15.6 ± 3.1% vs. SR –1.0 ± 1.4%, P < 0.0001) and BMD rescue in SRP group (% BMD change SRP +5.3 ± 1.5% vs. SR –1.0 ± 1.4%, P = 0.03). In FD, gain of BMD is significant in NSR compared to SR (+17.5 ± 1.5% vs. +8.2 ± 2.8%, P = 0.007), and to SRP (+17.5 ± 1.5% vs + 10.1 ± 2.4%, P = 0.046). Gain in SRP group is not significant compared to SR group (P = 0.6). In WB SRP gain more BMD than NSR (+14.0 ± 1.8% vs. +5.4 ± 0.7%, P = 0.0002) and than SR (+14.0 ± 1.8% vs. +7.8 ± 1.4%, P = 0.0043). There is no difference between NSR and SR groups (P = 0.19).Conclusion. – We demonstrate that β-adrenergic pathway of sympathetic nervous system is a major transmitter pathway of mechanical loading in rat bone. A specific study is necessary to analyse a possible systemic effect of propranolol in rat bone. Propranolol could be used to prevent induced mechanical unloading bone loss as weightlessness.