[Premature rupture of membranes at term on unfavourable cervix: immediate or delayed induction?]. / Rupture prématurée des membranes à terme sur col défavorable: quel délai pour déclencher ?

OBJECTIVES: To define the optimal delay before inducing labor in the management of premature rupture of the membranes (PRM) at term with unfavourable cervix in order to reduce the risk of caesarean section as well as the risk of maternal and foetal infection. MATERIALS AND METHODS: Retrospective study of three homogeneous groups carried out over on a period of 4years in two centres. All the patients were included after premature rupture of membranes at term with unfavourable cervix (Bishop score<6). We defined three expected delays after PRM at term: less than 7h (group 1), between 7 and 12h (group 2) and more than 12h (group 3). We have assessed the obstetrical, maternal and foetal consequences for each group. RESULTS: Sixty patients were allocated in group 1, 49 in group 2 and 46 in group 3. There was no significant difference in the rate of caesarean between the three groups but it was lower in group 2: 6.1% versus 18.3% in group 1 and 21.7% in group 3. No statistical difference was observed concerning maternal or foetal infections. CONCLUSION: In PRM at term, neither our study nor literature data allow us to conclude about the optimal delay before inducing labor.

Effects of tachykinins on identified dorsal vagal neurons: an electrophysiological study in vitro.

Intracellular current-clamp recordings were performed using in vitro brainstem slice preparations to compare the actions of substance P, neurokinin A, neurokinin B and their agonists on rat dorsal vagal nucleus neurons with or without antagonists of neurokinin 1 and 2 receptors. The agonists used were either [Sar9,Met(O2)11]substance P or septide for neurokinin 1 and [Nle10]neurokinin A(4-10) for neurokinin 2 receptors. The antagonists were spantide, SR 140333 or RP 67580 for neurokinin 1 receptors and SR 48968 for neurokinin 2 receptors. Identification of vagal neurons was achieved electrophysiologically by testing antidromic responses and confirmed morphologically by an intracellular injection of biocytin. Of the 70 neurons tested, substance P led to depolarization in 36, hyperpolarization in six and no effect in 28. Depolarization was concentration dependent and generally associated with an increase of the membrane input resistance. Addition of tetrodotoxin (1 microM) to the medium had no effect on depolarization. RP 67580 (1 microM) blocked depolarization, but spantide and SR 140333 (microM to 50 microM) did not. Hyperpolarization was never observed using agonists. Neurokinin A and neurokinin 2 agonist induced concentration-dependent depolarization associated with an increase in membrane input resistance in eight of 14 neurons and in four of nine neurons, respectively. Depolarization was only partially abolished by the neurokinin 2 antagonist SR 48968. Neurokinin B had no effect in any of the eight neurons tested. These data prove that vagal neurons have neurokinin 1 and 2 receptors and that tachykinin could produce either depolarization or hyperpolarization. Since membrane potential variations were associated with an increase (during depolarization) or decrease (during hyperpolarization) in the membrane input resistance and since the reversal potential was close to the potassium equilibrium potential, we speculate that these effects are mediated by modulation of potassium conductance.

A new interface chamber for the study of mammalian nervous tissue slices.

We describe a new interface-type chamber for electrophysiological studies in mammalian brain slices. Thermoregulation of the inner recording chamber is achieved using the Peltier effect and a feedback control unit. Between 15 and 40 degrees C, and for perfusion rates from 1 to 5 ml/min, the temperature can be maintained within +/- 0.1 degrees C of the command value; it can also be rapidly and reliably changed. An external bath, heated by a coiled resistor, generates a humidified, oxygenated atmosphere diffusing above the slices. Survival of neuronal tissue is excellent and stable intracellular recordings can be obtained using either sharp or patch-clamp micropipettes. Perfusion solutions can be readily exchanged, rendering this chamber suitable for the study of bath-applied neuroactive compounds.

Effects of substance P on cardiovascular regulation in the rabbit.

The effect of substance P on blood pressure and aortic reflex was investigated in rabbits. Microinjections of substance P and Sar9, Met(O2)11-SP (a selective NK1-receptor agonist) into the floor of the fourth ventricle led to a dose-dependent increase of blood pressure and a sharp enhancement of the baroreflex. These effects were abolished by pretreatment with SR 140333 (a selective NK1-receptor antagonist). Intraventricular injection of the antagonist alone significantly decreased the amplitude of the aortic reflex. After bivagotomy, the amplitude of the parasympathetic component of the baroreflex decreased dramatically and substance P injections were no longer effective. Our results demonstrate that substance P activation of NK1 receptors plays a major role in the modulation of the parasympathetic component of the baroceptor reflex.

Spike conduction properties of T-shaped C neurons in the rabbit nodose ganglion.

The electrical activity of C-type neurons was recorded intracellularly in the rabbit nodose ganglion maintained in vitro. The initial segment of their axon is spirally wound close to the cell body and a primary branching point divides it into a central process (CP) projecting to the nucleus of solitary tract in the medulla oblongata and a peripheral process (PP) which conveys sensory inputs from the viscera. Stimulation of the CP induced either somatic ("S") spikes or low-amplitude axonal ("A") spikes ("A1" or "A2"). In some cases abrupt changes in the latency of "S" or "A" spikes (jumps) were observed by gradually increasing the stimulus intensity. They are discussed in relation to a secondary branching on the central axon located inside or near the ganglion. Collision experiments showed that antidromic "A" spikes are blocked at the primary bifurcation of the axon (T-shaped neuron). Stimulation of the PP induced either "S" spikes or high amplitude "A" spikes ("A3" or "A4"). Orthodromic spikes could be blocked either before or after the primary bifurcation. When blocking occurs after the bifurcation on the stem axon, the spike can invade the central axon without invading the soma. The study of the refractory periods of the two processes and the application of high frequency stimulation showed that the PP allows higher frequencies than the soma and the CP, and thus that branching and the CP act as low-pass filters. These data support the view that the primary branching point and the CP of these T-shaped cells represent a strategic area to modulate visceral afferent messages.