Effects of the phosphodiestrase-4 inhibitor rolipram on lung resistance and inflammatory reaction in experimental asthma.

The aim of this study was to evaluate the influence of pretreatment with the phosphodiesterase-4 inhibitor rolipram on pulmonary resistance, influx of inflammatory cells, and histamine concentration in bronchoalveolar lavage fluid (BALF) during an experimental asthmatic reaction induced in ovalbumin (OA)-sensitized guinea pigs, challenged with OA inhalation. The experiment was performed in three groups of guinea pigs: two experimental groups, pretreated with rolipram or dexamethasone, and a control group without any pretreatment. Lung resistance (LR) was continuously recorded under suppression of spontaneous breathing during early asthmatic reaction. BALF was obtained before and at three time points up to 24 hr after the challenge. In the untreated, control animals a transient, significant increase in neutrophils, total and CD4+ lymphocytes, macrophages, eosinophils, and in histamine concentration in BALF was noted. Pretreatment with rolipram significantly reduced LR, eosinophils infiltration, and histamine release into the bronchoalveolar space during the early asthmatic reaction. These effects were generally comparable with those of dexamethasone, except that dexamethasone also reduced the influx of neutrophils into BALF.

A hybrid (numerical-physical) model of the left ventricle.

Hydraulic models of the circulation are used to test mechanical devices and for training and research purposes; when compared to numerical models, however, they are not flexible enough and rather expensive. The solution proposed here is to merge the characteristics and the flexibility of numerical models with the functions of physical models. The result is a hybrid model with numerical and physical sections connected by an electro-hydraulic interface - which is to some extent the main problem since the numerical model can be easily changed or modified. The concept of hybrid model is applied to the representation of ventricular function by a variable elastance numerical model. This prototype is an open loop circuit and the physical section is built out of a reservoir (atrium) and a modified windkessel (arterial tree). The corresponding equations are solved numerically using the variables (atrial and arterial pressures) coming from the physical circuit. Ventricular output flow is the computed variable and is sent to a servo amplifier connected to a DC motor-gear pump system. The gear pump, behaving roughly as a flow source, is the interface to the physical circuit. Results obtained under different hemodynamic conditions demonstrate the behaviour of the ventricular model on the pressure-volume plane and the time course of output flow and arterial pressure.