Journal of developmental physiology最新文献

The energy cost of growth includes two components: the energy stored in new tissues and the energy expended in all energy requiring steps associated with nutrient intake and net tissue accretion. Most of the energy expended in growth is accounted for by the energy cost of tissue anabolism: peptide bonds, lipogenesis, substrate transport, etc. However, to the extent that additional work is required of the heart and lungs for growth-related increases in O2 and CO2 transport, increased energy is also expended in cardiorespiratory work. Indirect estimates of these costs can be gained by examining the effects of diet and weight gain on heart rate and respiratory frequency. We studied 66 healthy low birth weight infants, mean study weight = 2010 g, fed constant intakes of protein (2.25-3.9 g/kg per day) and energy (100-150 kcal/kg per day). These diets led to rates of weight gain ranging from 13.9 to 21.7 g/kg per day, among the diet groups. Bi-weekly 6-h assessments of energy expenditure, heart rate, respiratory frequency and state of sleep were made after full enteral intake was achieved. After adjustment of heart rate for the effect of postnatal age, heart rate during active sleep was related to weight gain (y = 0.97 x + 144, r2 = 0.15), nitrogen-energy ratio of the diet (y = 5.9 x + 139,2 r2 = 0.22), and energy expenditure (y = 0.53 x + 129, r2 = 0.13). Multiple regression analysis revealed that age-adjusted heart rate during active and quiet sleep was significantly related to a combination of the same three variables (r2 = 0.31).(ABSTRACT TRUNCATED AT 250 WORDS)

Allylestrenol or benzpyrene, given either between the 15th and 19th days of fetal life or from birth to the postnatal 7th day, caused dramatic decrease in the sexual activity of adult female rats. Allylestrenol, given in fetal life, resulted in a profound increase in the sexual activity of male rats. Given in newborn conditions, a decrease of sexual activity was caused by the same chemical. Considering, that one of the molecules has importance in medical practice and the other is an environmental pollutant, the experiments forecast the probability of modification in the sexual behaviour of human adults.

Experiments were done on seven lambs between the ages of 18 and 24 days to investigate the effects of sleep on systemic and coronary hemodynamics. Each lamb was anesthetized and instrumented for recordings of electrocorticogram, electro-oculogram and nuchal electromyograms, and for measurements of cardiac output and coronary blood flow as well as systemic arterial blood pressure and arterial-, mixed-venous- and coronary-sinus- hemoglobin oxygen saturations. No sooner than three days after surgery, measurements were made during periods of quiet wakefulness (QW), quiet sleep (QS) and active sleep (AS) at an ambient temperature of 25 degrees C. Cardiac output and heart rate were decreased during AS compared to QW and QS. A significant increase in systemic vascular resistance during AS prevented more than a slight decrease in systemic arterial blood pressure. Coronary blood flow decreased during AS compared to QW and QS. Furthermore, myocardial work as estimated from the product of systolic blood pressure and heart rate decreased during AS compared to QW and QS as did myocardial oxygen consumption and myocardial oxygen transport. Transient hypertensive phases--defined as transient increases in mean blood pressure of greater than 15 mmHg above the mean blood pressure for a period of AS--occurred during eight of 13 periods of AS in four of the seven animals. These transient hypertensive phases were caused primarily by an increase in systemic vascular resistance; surprisingly, coronary vascular resistance also increased at this time when estimated myocardial work was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of protein kinase C activation on phospholipase A2 and phospholipase C activity in permeabilised cultured myometrial cells from guinea pig uterus have been studied. Phospholipase A2 activity was followed by measurement of [3H]arachidonic acid release from [3H]arachidonic acid-prelabelled membrane lipids. [3H]Arachidonic acid release was stimulated by Ca2+ at 1-10 microM and by GTP gamma S at 1 microM to 1 mM in the presence of 10 microM Ca2+. The activation by calcium was enhanced 89.5 +/- 12.7% (P < 0.01) in the presence of 1 microM phorbol 12-myristate 13-acetate (PMA) and that by 1 microM GTP gamma S by 65.4 +/- 4.4% (P < 0.001). The PMA enhancement of arachidonic acid release was completely blocked by 3 microM staurosporine. Phospholipase C activation was followed by measurement of [3H]inositol polyphosphate production from [3H]inositol-prelabelled membrane lipids. This was stimulated by Ca2+ at 0.1 and 10 microM and by 1 and 50 microM GTP gamma S. PMA at 1 microM caused a consistent reduction in the extent of Ca2+ and GTP gamma S-stimulated inositol polyphosphate production and 3 microM reversed the inhibitory action of PMA. The data are consistent with arachidonic acid release in permeabilised myometrial cells from guinea pigs reflecting in large part phospholipase A2 activation and with that pathway being stimulated by protein kinase C activation. They are also consistent with protein kinase C activation causing reduction in phospholipase C pathways in uterine myocytes, at least as measured by inositol polyphosphate release.

A comparative chronological study (from 1 to 33 days post partum) was performed to establish the capacity for nonshivering thermogenesis (NST) in rats born and reared at 28 degrees C and at 16 degrees C. The resting metabolism measured at 33 degrees C was higher in the 16 degrees C rats than in the 28 degrees C rats from the 3rd day. When expressed per weight or per surface area units it was higher in 16 degrees C pups than in 28 degrees C pups until the end of the 3rd week. In fact the resting metabolism was significantly proportional to different powers of weight (W0.67 at 16 degrees C and W0.75 at 28 degrees C) during the suckling period. At birth, respiratory quotient (RQ) was the same in both groups (0.70); it increased slowly to the end of the 3rd week (about 0.80). During the 3rd week RQ was lower in 16 degrees C rats than in 28 degrees C animals. This indicates that 16 degrees C rats are more dependent on the milk supplied by their mother. After weaning there were no differences in RQ values (0.90). Rectal temperature was low in both groups on day 1 (about 32 degrees C). It increased until weaning when it stabilized at 37 degrees C. From day 1 to day 18, it was significantly lower in cold reared rats. The capacity for NST was measured by investigating the effect of an injection of norepinephrine (NE) on the metabolic rate at 33 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Fluid secretion by the fetal pulmonary epithelium is thought to be important for normal lung development yet little is known about factors regulating its production. As prostaglandins are synthesized in human fetal lung and stimulate secretion in a variety of epithelia, we investigated the effect of prostaglandins E2 and F2a (PGE2 and PGF2 alpha) on ion transport and fluid secretion in cultured first trimester human fetal lung tissue explants. We used conventional microelectrodes to continuously record the transepithelial potential difference (psi t). The addition of either PGE2 or PGF2 alpha to the bathing solution significantly hyperpolarized the lumen negative psi t and the subsequent addition of bumetanide, an inhibitor of chloride secretion in other systems, depolarized psi t by approximately 60% suggesting chloride transport contributed to the voltage. To assess whether this acute change in psi t represented stimulation of fluid secretion, we measured the change in luminal area of the explants after a 24-h exposure to prostaglandins. Both PGE2 and PGF2 alpha caused significant increases in the mean % luminal area of the explants compared with control tissues consistent with a stimulation of lung fluid secretion. Cultured lung tissue explants produced prostaglandins E2 and F2 alpha as assessed by radioimmunoassay of cell culture media samples and both prostaglandins stimulated cAMP accumulation in the explants. These findings show that lung fluid secretion in the human fetal pulmonary epithelium can be stimulated by prostaglandins. This effect may be mediated through cAMP dependent pathways. Prostaglandins may play a physiologic role in regulation of fetal lung fluid transport in vivo.

Present study tried to evaluate the influence of different diets (low- and high-salt, bicarbonate) administered during prenatal period on body and organ weights of newborn Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Blood pressure of DR dams was not influenced by dietary loading but it was significantly increased by high-salt diet in DS rats. Blood pressure of all DS dams was higher when compared to the respective DR rats. There were significant negative correlations between mean arterial pressure of DS (but not DR) dams and body weight of newborns in all dietary groups. Litter sizes were comparable in all groups studied. High-salt diet increased body weight and relative heart weight of newborns of both genotypes. On the other hand, the influence of bicarbonate diet on body weight was more pronounced in DS pups whereas the effect on relative heart weight was seen only in DR newborns. The relative heart and kidney weights were significantly higher and relative liver weight significantly lower in newborns of DR dams when compared to those of DS dams irrespective of mother's diet. There was a tendency in all organs of DS newborns to contain less water in comparison with respective DR pups. It should be noted that in newborns of both genotypes bicarbonate diet lowered relative DNA content more than relative protein content. In conclusion, high-salt and bicarbonate diets exert dissimilar effects on prenatal body and organ development in Dahl rats.

To make the chick embryo accessible to electrophysiological measurements in its mesonephric kidney during the period between embryonic days (e.d.) 5 and 10, a special "chick-embryo-incubation bath" was constructed. It consists of an aerated chamber covering the egg and maintaining the gas exchange across the shell, and of a warmed reservoir of the incubation medium, into which the embryo is pulled out of the egg through a window in the shell. The two compartments are separated with a rubber membrane tightly fitting to the edges of the shell-window. The incubation medium contains a modified Krebs-Henseleit-Ringer solution and anesthetic Tricaine (Sigma). Access to the mesonephric nephrons is achieved by surgical excision of the body wall on the right side performed at e.d. 5. On average only about 35 percent of the operated embryos survive till the third day after surgery but during the next two days a mortality rate recedes to zero. The tolerance of short-term survival of embryos placed in the incubation bath was tested for up to 4 1/2 h. It was very good in embryos of age 5 to 7 e.d. as assessed by a steady heart rate and the presence of arterio-venous differences. A modified differential amplifier containing circuits for frequency compensation of the two channels was used for high-fidelity registration of voltage changes in the embryonic nephron with a single double-barrel microelectrode.

This study examines the effects of altering the prenatal maternal metabolic and hormonal environment via chronic cold exposure of under-fed ewes on developmental changes in breathing control of developing lambs. Breathing frequency and timing were measured during non rapid-eye-movement (non-REM) sleep in lambs born from either shorn or unshorn ewes after being maintained for at least one hour at warm (28-19 degrees C) and cool (14-5 degrees C) ambient temperatures at 1, 4, 14 and 30 days of age. Breathing frequency and oxygen consumption were significantly higher in 1 day old lambs born from shorn ewes compared with those lambs born from unshorn ewes, at both warm and cool ambient temperatures. In the shorn group breathing frequency decreased between 1 and 4 days of age and continued decreasing upto 30 days of age, during which period inspiratory and to a greater extent expiratory time, lengthened. Laryngeal "braking" of expiratory airflow was observed in more than 50% of lambs born from shorn ewes during non-REM sleep in the warm at 4, 14 and 30 days of age, and in the cold at 14 and 30 days of age. In contrast, lambs born from unshorn ewes showed no change in breathing frequency between 1 and 4 days of age, but a decrease was observed between 4 and 14 days of age, whilst laryngeal "braking" of expiratory airflow was rarely observed at any age.(ABSTRACT TRUNCATED AT 250 WORDS)

Umbilical cord occlusion in the presence of adequate oxygenation induces continuous breathing and arousal in the chronic unanesthetized fetal sheep preparation. The mechanism responsible for this is unknown. We hypothesized that if a placental factor is responsible for the inhibition of breathing in the fetus, the administration of a placental extract while the fetus is breathing continuously after cord occlusion should reverse these changes. Thus, at about 10 min after the induction of continuous breathing by cord occlusion, we administered a placental extract and three subfractions separated by ultrafiltration to 14 chronically instrumented fetal sheep at 133 +/- 1 day gestation. The Krebs solution in which the placental extract was prepared was used as control. Within two minutes of the infusion of the whole placental extract in the carotid artery of the fetus, breathing output (integral of EMGdi x f) diminished in all experiments and was completely abolished in 15/17 (88%). Krebs solution had no effect on breathing. The infusion of subfractions of different molecular weight showed that the inhibition was primarily related to the subfraction between 3.5 and 10 kD. There were no significant changes in blood gas tensions, pH, blood pressure, and heart rate associated with the infusions of the extracts. The ECoG switched from low to high voltage in the majority of the experiments using whole extract and the subfraction 3.5 to 10 kD. These findings suggest that a placental factor, probably a peptide with a molecular weight between 3.5 and 10 kD, inhibits breathing in fetal life.