Vagal pulmonary afferents and central respiratory effects of 5-HT in newborn rats.

In decerebrate newborn rats, serotonin (5-HT) is a respiratory depressant via activation of 5-HT2 receptors, whereas it evokes respiratory stimulant effects when applied to the isolated brainstem obtained from the newborn rat. This discrepancy could be due to deafferentation in the in vitro preparation. The aim of our study was to analyse the role of vagal afferents in the modulation of central respiratory effects of 5-HT. In decerebrate cervically or abdominally bivagotomized newborn rats aged between 0 and 3 days, we recorded electrical activity from the diaphragm and from a hypoglossally innervated tongue muscle, as well as cardiac frequency (Fc), before and after application of 5-HT to the floor of the IVth ventricle. The effects of related agents (a 5-HT1A agonist, 8-OH DPAT, and a 5-HT2 agonist, DOI) were studied in cervically bivagotomized animals. For comparison, and to assess the spontaneous variability in inspiratory frequency (Fi) and Fc, sham groups were studied. Each group comprised ten newborn rats. In cervically bivagotomized newborn rats, 5-HT induces a significant increase in Fi, which is the opposite to that observed in decerebrate newborn rats with intact vagi. This respiratory effect is mediated in particular, via activation of 5-HT1A. By contrast, in abdominally bivagotomized newborn rats, a decrease in Fi was observed in response to 5-HT (as previously described in decerebrate animals with intact vagi). We conclude that pulmonary vagal afferents modulate the central respiratory action of 5-HT in decerebrate newborn rats, explaining the conflicting results between in vivo and in vitro experiments.

Oxygen consumption and PEEPe in ventilated COPD patients.

The intrinsic positive-end-expiratory pressure (PEEPi) increases the inspiratory load, the cost of breathing and thus oxygen consumption (V(O2)). It has been shown that applying an extrinsic positive-end-expiratory pressure (PEEPe) reduces the inspiratory threshold load but the optimal PEEPe level is still in debate. We hypothesize that the best level of PEEPe could induce a decrease in V(O2) by reducing the V(O2) demands from PEEPi. Nine mechanically ventilated COPD patients were included. The level of PEEPe was determined in accordance with the static PEEPi. V(O2) was measured using an automatic gas analyser during synchronized intermittent mandatory ventilation (SIMV): without PEEPe, with a PEEPe equal to 50% of static PEEPi and with a PEEPe equal to 100% of static PEEPi. Static PEEPi appeared to be significantly correlated with the degree of airflow obstruction (FEV1) (P<0.05). Applying a PEEPe equal to static PEEPi resulted in a significant decrease in V(O2) (P<0.05) whereas the change in V(O2) proved to be unpredictable for a PEEPe level of 50% of static PEEPi. In conclusion, V(O2) decreases progressively when increasing PEEPe up to a level equal to 100% of static PEEPi. Thus, in mechanically ventilated COPD patients with a FEV1 < or = 1000 ml, applying a PEEPe of 5 cmH2O should be recommended.

[Transudative pleural effusions and the ovarian hyperstimulation syndrome]. / Epanchements pleuraux transsudatifs et syndrome d'hyperstimulation ovarienne.

INTRODUCTION: Pleural effusions occurring in the ovarian hyperstimulation syndrome (OHS) are frequently associated with haemoconcentration. OBSERVATIONS: We report three cases of symptomatic pleurisy with ascites, requiring therapeutic pleural aspiration. Biochemical analysis of these effusions may give rise to confusion as consideration of the pleural fluid protein levels in isolation may lead to the incorrect diagnosis of an exudate. On account of the electrolyte disorders and haemoconcentration seen in OHS a pleural fluid protein level of over 30 g per litre (the traditional definition of an exudative pleurisy) should be interpreted in relation of a serum concentration. CONCLUSIONS: Measurement of the pleural and serum protein and LDH levels, complemented by a serum-effusion albumin gradient, should permit confirmation of the transudative nature of the pleural effusions. It seemed important to us to confirm this concept in three personal cases, as the data reported in the literature are more often reported as evidence for an exudates. Furthermore, a favourable response to symptomatic treatment tends to confirm the transudative nature of the effusions in OHS.