Apart from in cystic fibrosis, where sweat analysis provides valuable diagnostic information, sweat yields remain an overlooked biological fluid. Technical problems (dilution, condensation, contamination, evaporation, etc.) linked to currently available collection procedures are of concern and thwart their use. To overcome some of these technical difficulties, an original sweat-collection technique is described. A collection capsule is created inside a flexible, adhesive and disposable anchoring membrane pasted onto the skin. A fluid-tight window is positioned in the upper part of the pocket and gives access to its content. Through the collection window, complete emptying of the sweat collector can be achieved repeatedly by suction using a vacutainer tube inserted in a tube holder equipped with a long dull needle. With prior addition of a suitable marker, fractional samplings can also be performed using a precision micropipette. This collecting method allows for kinetic studies on sweat rate and sweat content. The limited bias-inducing manipulations linked to the described technique, coupled with the ease of performing kinetic studies on sweat volume and content, make this original tool a reliable and accurate sweat-collection technique.

To determine the effects of maternal hyperglycemia on fetal hemodynamic and cardiac function, a study was carried out on nine chronically catheterized fetal sheep. In six fetuses, glucose was infused intravenously with an initial dose of 5 mg/kg per min. Data were compared with controls. This dose was gradually increased to 16 mg/kg per min by the fifth day. The initial blood glucose was 14.7±3.0 mg/dl and increased to 54.6±16.4 mg/dl by the last day of the infusion period (P < 0.001). The P02 decreased from a baseline of 20.25±3.40 to 15.88±5.24 mmHg (P < 0.01). Similarly significant decreases were also observed for the blood 02 content and 02 hemoglobin saturation: 8.5±1.7 to 6.4±2.2 ml/dl and 62.3±13.6 to 46.1±17.6%, respectively, during hyperglycemia (P < 0.01). The duration of the preejection period (PEP) before the start of the experiment was 45±4 ms; a final value of 57±10 ms was obtained (P < 0.01). However, the electromechanical delay and ejection time (ET) showed no significant variation. The ratio of the PEP/ET increased from 0.31±0.04 to 0.38±0.07 (P < 0.01) during hyperglycemia. The reticulocytes increased from 1.4±1.8 to 3.1±2.9% (P < 0.05) and the 2,3-diphosphoglycerate decreased from 4.4±1.1 to 2.8±1.2 ,mol/g hemoglobin (P < 0.005). This study demonstrated that fetal hyperglycemia depresses myocardial function in the fetal lamb. The changes in cardiac function could not be explained by the small drop in 02 saturation.

No abstract

To determine the effects of maternal ketamine anesthesia on fetal hemodynamic and cardiac function, a study was carried out on 8 chronically catheterized fetal lambs. Ketamine was administered intravenously to the mother every 15 min during 1 h. The fetal PO₂ and pH remained within physiological limits whereas the PCO₂ decreased from 44.35 ± 1.36 to 37.32 ± 4.75 Torr (p < 0.05). The following changes of the fetal heart systolic time intervals were observed: a progressive lenghtening of the preejection period (PEP) (from 52 ± 10 to 63 ± 11 ms, p < 0.01), a shortening of the ejection time (ET) and a significant increase of the PEP/ET ratio (from 0.32 ± 0.04 to 0.47 ± 0.01, p < 0.01). The two components of PEP, electromechanical delay and the isovolumetric contraction time were both prolonged. A progressive rise of fetal systolic and diastolic pressures was also noted (p < 0.01). Fetal heart rate increased (145 ± 33 to 190 ± 28 beats/min, p < 0.01) and cardiac beat-to-beat variability decreased (from 0.028 to 0.009, p < 0.01) during the ketamine anesthesia. This study demonstrates that maternal anesthesia with ketamine can alter indices of fetal myocardial function and other cardiac parameters used in fetal and neonatal monitoring, without affecting tissular oxygenation.

the resting potential of hypoxic substrate-deprived myocardium. Can. I. Physiol. Pharmacol. 66: 202-206. Insulin stimulates ionic transport by the sodium pump and induces hyperpolarization in skeletal and cardiac muscle among other cells. The insulin-induced hyperpolarization in most cases cats be inhibited by exposure to cardiac glycosides or metabolic inhibition. However, extracellular accumulation of K ions leaking from hypoxic cells in superfused preparations may distort the effects of insulin on the resting potential. We used standard microelectrode techniques and p d u s e d rabbit hearts submitted to hypxia and substrate deprivation $0 reinvestigate the effects of insulin (6.4 nM) on the membrane potential. The membrane deplaized by about 6 mV and the action potential was reduced to a sharp spike without overshoot. Insulin restored the resting potential to control values but did not change the action potential configuration substantially. The insulin-induced repolarization was not due to reuptake of potassium as revealed by spectrophotometric determinations of myocardial K content. In addition, the diffusion component of the resting potential measured after inhibition of the sodium pump with 10-% ouabain was not modified by insulin. Our results suggest that an increase in the contribution of electrogenic Na extmslon to the resting potential underlies the repolarizing effect (BE insulin of hypoxic substrate-deprived myocardium.RUIZ-CERETTI, E., DELORENZI, F., LAFOND, J. S., et CHARTIER, D. 1988. Insulin and the resting potential sf hypxic substrate-deprived myocardium. Can. I . Physiol . Phxmacol. 66 : 202-206. L9insuline stimule la p o m p Na-K et hyperpolarise la membrane de plusieurs types de cellules dont les muscles squelettique et cardiaque. Dans la plupart des cas, cette hyperpolarisation peut-&re inhibde par une exposition prialable B I'ouabaine ou par inhibition mitabolique. Cependant, I'accumulation extracellulaire d'ions K chez des priparations supedusies peut masquer les effets de l'insuline sur le potentiel de repos. Nsus avons appliquk Ea technique de rnicroilectrodes h des coeurs de lapin pPfusCs, soumis 2 I'hypoxie et au manque de substrat, afin de reinvestiguer les effets de E'insuline (6,4 nM). L'inhibition mttabslique prduisait une dCpolaisation membranaire d'environ 6 mV et rkduisait le potentiel d'action B un court pic sans << overshoot a. L'insuline rttablissait B e potentiel de repos & des valeurs contr6Bes mais ne modifiait pas significativernent B a morphologie du potentiel d9action. La repolarisation n'Ctait pas due B une captation accrue du potassium tel que montrd par la ddtermination spectrophotom6trique du contenu potassique du myocarde. De plus, la composante diffusionnelle du potentiel de repos mesbarke aprks I'application Be l'ouabaine B lo-%, n'itait pas modifide p a lqI'insuline. Nos rksultats suggkreent qu'une augmentation de la contribution de la p m p e Na-K rau potentiel de repos est sous-jacente B l'effet repolarisant de I'insuline chez le myscade hypoxique en absence...