Humidity control tool for neonatal incubator.

In the first days of life, the daily evaporative loss from premature neonates can reach up to 20% of body mass. Such loss can be reduced by increasing the air humidity inside the incubator. Neither passive humidification nor open loop systems allow high humidity rates to be maintained or easily controlled: at 34 degrees C, the maximum levels vary with the system from 40% to 77% of relative humidity. The skin evaporative exchanges between the neonate and the environment are directly proportional to the water vapour partial pressure difference between the neonate's skin and the air. An active closed loop system has been designed, which permits reliable and accurate control of humidity according to the water vapour partial pressure set, between 1 and 6 kPa, in an air temperature range of 28-39 degrees C. It is characterised by variations of about 0.05 kPa around the set value and a maximum humidification speed of 0.25 kPa min-1. The algorithm is based on optimal control and the dynamic programming principles. Test results place this active system above usual systems for its power, precision and adaptability. It is an exploitable tool in fundamental and clinical research, to precisely study the humidity effects on neonatal comfort and thermo-regulation evolution.

Dynamic programming approach for newborn's incubator humidity control.

The anatomy, physiology, and biochemistry of the human skin have been studied for a long time. A special interest has been shown in the water permeability of the premature infant's skin, which is known to be an important factor in the maintenance of a controlled water and heat balance. The rate of evaporative heat exchange between the skin surface of a very premature infant and the surrounding incubator air may be so high that evaporative heat loss alone may exceed the infant's total metabolic heat production. However, it has been demonstrated in several investigations published in recent years that basal evaporative water loss can be consistently reduced by increasing the ambient humidity. Nevertheless, the passive humidification system (water reservoir) used in most incubators cannot achieve high and steady humidity levels. In this paper, we propose an active humidification system. The algorithm is based on a combination of optimal control theory and dynamic programming approach. The relative-humidity (R.H.) regulation is performed in range of 35-90% at 33 degrees C with small oscillations (+/- 0.5% R.H.) around the reference value (i.e., prescribed R.H.).

Neutral temperature range in incubators: performance of equipment in current use and new developments.

Low-birth-weight neonates should be nursed at thermoneutrality inside incubators. Thermoneutrality control is essential to enhance body growth and to reduce neonatal illnesses and mortality. Guidelines have been published to provide the thermoneutral range, but the recommendations did not always take into account all ambient and physiological parameters influencing thermoneutrality. In most marketed incubators, the heat supply is controlled through convective air flow (closed incubators) or through radiant power density (radiant warmer beds). The heating unit (on/off cycling or adjustable proportional control) is activated by an error signal calculated from the difference between a controlled temperature and a reference value preset by the clinician. The controlled variable can be either the incubator air or the skin temperature of the anterior abdominal region of the neonate. The neonate's size, thermal properties of the mattress and of incubator walls, air temperature and humidity, air velocity, incubator wall temperatures all influence the heat exchanges between the neonate and the surroundings, and, consequently, modify the obtention of thermoneutrality. Moreover, studies of the physiological mechanisms by which the neonate regulates body heat storage suggest that metabolic rate, behavior, vigilance level, nursing care, and heater control processes should also be taken into account. Little attention has been paid to these factors, and incubator performances are often disappointing. This article reviews the different factors that modify thermoneutral condition. An attempt is made to suggest new ways to design equipment incorporating these factors in algorithms controlling heater processes in order to reach the optimal thermal environment in which the neonate should be nursed.

[Role of home monitoring in the context of sudden infant death prevention. Current methods indications, monitoring]. / La place du monitorage à domicile dans le contexte de la prévention de la mort subite du nourrisson. Moyens actuels, indications, surveillance.

Some infants are cared with a home monitoring system during their first year of life. An international clinical consensus has been obtained and has proposed this technique mainly for infants who have presented an apparent life threatening event or for ex-premature with bradycardia or apnea, rather than for siblings of sudden infant death syndrome or other infants. In any case, this monitoring must be held after a complete clinical evaluation of the infant and after a real education of the parents about the use of the device. Many types of devices are used. The most efficient is the cardio-respiratory monitoring. Some of them include a processor and record the alarms. The need to see or to call the medical team to decode them allows close collaboration between the family and the clinical team. Knowledge of the alarms and the circumstances in which they have occurred help the medical team to propose the withdrawal of the home monitoring. Thus, sometimes preventive, sometimes prophylactic, this device will provide us for an optimal help.

In vivo determination of the profile of benzodiazepine ligands by comparing the inhibition of 3H-Ro 15-1788 binding to the modulation of cGMP levels in mouse cerebellum.

The in vivo effects of various benzodiazepine (BZD) ligands belonging to different chemical families were studied comparatively in mouse cerebellum using displacement of 3H-Ro 15-1788 binding and cGMP content as biochemical tools. It was possible to differentiate four classes of compounds with regard to these biochemical parameters. The first class of compounds such as diazepam and suriclone induced a net effect on in vivo 3H-Ro 15-1788 binding and a dose-dependent decrease of cGMP levels. A second class of drugs such as ZK 91296 and CGS 9896 showed in vivo activities in displacement studies but relatively small or moderate activities on cGMP levels. A third class was represented by Ro 15-1788 itself which prevented dose-dependently the in vivo 3H-Ro 15-1788 binding but was devoid of effect on cGMP levels. Finally, a fourth class of compounds (CGS 8216, FG 7142, beta-CCM and DMCM) showed in vivo displacement of 3H-Ro 15-1788 with concomitant increase of cGMP levels. The first class of compounds represents full agonists, the second class, partial agonists, the third class, the antagonist Ro-15-1788 itself, and the fourth class corresponds to inverse agonists. Thus it is proposed to use 3H-Ro 15-1788 binding and cGMP levels to differentiate in vivo BZD ligands acting on the BZD receptor/GABA receptor/chloride ionophore complex.

Enhancing effect of dopamine blockers on evoked acetylcholine release in rat striatal slices: a classical D-2 antagonist response?

The effects of chlorpromazine, pipotiazine, haloperidol, domperidone, sulpiride and SCH 23390 on the potassium-evoked release of [3H]acetylcholine [( 3H]ACh) were studied in rat striatal slices. All 5 dopamine (DA) antagonists with D-2 blockade efficacy induced an increase of [3H]ACh release whereas the specific D-1 antagonist SCH 23390 was devoid of significant effects. The maximal effect (about 100% increase) was obtained with haloperidol, pipotiazine and sulpiride but not with domperidone and chlorpromazine. Interestingly, sulpiride was found to exert an unexpected marked potency. The comparison of the activities of the 6 compounds on evoked ACh release to their affinities for D-2 receptors [( 3H]N-propylnorapomorphine binding sites) indicates that the pharmacological profile of the dopamine receptor implicated in the regulation of ACh release cannot be superimposed on that of the classical D-2 receptor. Participation of DA presynaptic receptors could however explain the differences in efficacy observed with the compounds studied.