Journal of developmental physiology最新文献

To investigate the role of thyroid hormone in the expression of the gene encoding the growth hormone receptor (GHR) and growth hormone binding protein (GHBP), fetal rats were made hypothyroid through the administration of the goitrogen methimazole to the mother. Euthyroidism was maintained in the mother by concurrent administration of L-thyroxine, which crosses the placenta poorly. Methimazole and L-thyroxine were continued in the mothers until weaning. After birth, groups of methimazole-treated or control pups were sacrificed immediately and at one, two, three, four, five, or six weeks after birth. In each group, weight was recorded, blood was obtained for measurement of T4, thyroid stimulating hormone (TSH), and growth hormone (GH), and liver tissue was obtained for quantitation of GHR and GHBP mRNA. The methimazole-treated pups were demonstrated to be hypothyroid, with markedly higher TSH and lower T4 concentrations, until weaning occurred between weeks three and four, after which they transiently became hyperthyroid at week five (T4 = 17 +/- 5 micrograms/dL vs. 6 +/- 0.5 micrograms/dL for controls) but returned to an euthyroid state at week six. In control pups the relative abundance of GHR and GHBP mRNA increased abruptly in week one, and increased three to four fold over the ensuing six weeks. Immediately after birth, the hypothyroid pups expressed significantly more GHR and GHBP mRNA than did the controls (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Many pregnant women are exposed to low frequency sounds and vibrations while at work or play. How the fetus is affected by these physical stimuli is not clearly documented. We recorded behavioral state and intrauterine sound pressure levels in eight fetal sheep previously instrumented with electrocortical, electroocular and neck electromyographic leads, and with a miniature hydrophone. Data were collected before, during and after 30 min of abdominal vibration using a belt vibrator commonly used by humans in weight reduction programs. A sudden shift in behavioral state occurred at the onset of vibration. There was a decrease in non-rapid eye movement sleep (P < 0.02) and an increase in time during which the sleep state could not be determined (P < 0.03). A 63% increase in number of epochs spent in this indeterminate period was evident during vibration. During the post-stimulus period, percentage of time spent in rapid eye movement sleep decreased as compared to the pre-stimulus period (P < 0.04), and non-rapid eye movement sleep increased as compared to the stimulus period (P < 0.01). Vibration-induced intrauterine sound pressures ranged from 131-142 dB at the fundamental frequency of 19 Hz and were 20-40 dB lower at the overtones which appeared in the spectrum between 35-200 Hz. Results indicated that environmental vibration can disrupt fetal behavioral state, induce abnormal state changes, and alter distribution of sleep states.

Summary measures of heart rate variation describe those aspects of heart rate change that can be averaged over relatively long periods of time. We examined the postnatal maturation of a dynamic feature of cardiac rate--the dependency of each beat-to-beat change in cardiac interbeat interval on the previous beat-to-beat change. In each sleep-waking state, the number of delta RR (the difference between two successive R-R intervals) 4msec was determined as a percent of the total number of intervals (delta RR > 4ms/total delta RR), and each pair of successive interval differences was categorized based on the directions of the two changes (whether they reflected increases or decreases in cardiac intervals). Analysis of variance was used to identify alterations in the proportion of interval differences exceeding the minimum over ages and sleep-waking states, and to describe developments in the temporal patterns of cardiac interval changes. At all ages, infants showed fewer beat-to-beat interval changes during waking than during either sleep state. In all states, older infants showed significantly more beat-to-beat cardiac interval changes and a higher proportion of sustained changes (intervals increasing or decreasing consistently over several beats) than did young infants. Furthermore, infants 2 months and younger showed significantly more sustained increases than decreases in interbeat intervals, indicating gradual declines in heart rate and rapid increases, while older infants showed the opposite pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Norepinephrine (NE) content and turnover rate, and the activity of dopamine-beta-hydroxylase (DBH) were measured in the brown adipose tissue (BAT) of developing Zucker rats of the three genotypes: Fa/Fa and Fa/fa (with a lean phenotype) and fa/fa (phenotypically obese). As early as 15 days of age, namely at a pre-obese stage, BAT NE content and turnover rate are already reduced in fa/fa rats, just like they are at 50 days. The development of DBH activity is completely impaired in fa/fa rats. These results demonstrate that the reduction in sympathetic tone in BAT of fa/fa rats is already present before the onset of phenotypic obesity.

Effects of extracellular Ca2+ and inotropic agents on contractile force were examined in myocardial preparations from embryonic and hatched chicks. Measurement of contractile force was performed in an organ bath with whole hearts for the young embryo (5 to 6 days old) and with isolated strips from the right ventricles for the old embryos (16 to 18 days old), hatched chicks (within 24 hours after hatching) and 1 week old chicks. The extracellular Ca2+ concentration-contractile force curve was in a lower concentration range in young embryonic hearts when compared with older ones. 2 mM Ca2+ and 8 mM Ca2+ produced about 60% maximum contraction in preparations from young embryos and the older ages, respectively. The sensitivity to nicardipine and diltiazem was similar among all ages examined under 2 mM Ca2+. When the two drugs were applied to preparations from the older ages under 8 mM Ca2+, the sensitivity was lower than that of the young embryo under 2 mM Ca2+. Ryanodine produced a negative inotropic response at all ages but the effect was smaller in the young embryo when compared with those of older ages. Mn2+ produced a negative inotropic effect at all ages. In the older three ages, Mn2+ produced a late augmentation of the contractile force in addition to the initial negative inotropic response, while such augmentation was not observed in the young embryo. In conclusion, the chick myocardium was shown to undergo developmental changes in excitation-contraction mechanisms including increase in sarcoplasmic reticulum function during the embryonic period, and thus provides an interesting model for studies on excitation-contraction mechanisms.

This study was designed to determine the effects of hypothyroidism during late fetal life in pigs on (1) the perinatal pattern of plasma levels of thyroxine (TT4), total 3,5,3'-triiodothyronine (TT3) and free T3 (FT3), and liver 5'-deiodinase activity, and (2) the early postnatal development of thermoregulation. Fetal hypothyroidism (test animals) was induced by feeding the sow a high glucosinolate rapeseed diet. Plasma levels of thyroid hormones, thyroid gland weights and liver 5'-deiodinase activity of control animals increased during late gestation (P < 0.01). The early postnatal period was characterized by a surge in thyroid hormone levels during the first 6 h (P < 0.05), followed by a transient decrease at 12 h and a second rise by 24 h after birth. This surge was much higher (P < 0.01) for TT3 than for TT4, but liver 5'-deiodinase activity did not change during the first 24 h of life. Fetal hypothyroidism was characterized by lower plasma levels of thyroid hormones (P < 0.05), and lower hepatic 5'-deiodinase activities (P < 0.01) than in control fetuses at 110 d of gestation. During the first 6 h of life, test pigs had lower levels of TT4 (P < 0.05) but exhibited a greater postnatal surge in TT3 and FT3 (P < 0.05) than did the controls. The minimal and summit metabolism of the control pigs increased markedly (P < 0.01) during the first 2 d of life, without any significant change in thermal body conductance, suggesting that this age-related improvement in thermoregulation was due to the development of the ability to produce heat.(ABSTRACT TRUNCATED AT 250 WORDS)

During the critical period of receptor maturation within the first 5 days after birth female rats were treated with benzpyrene three times and their uterus estrogen receptor characteristic were examined in adulthood. Estrogen receptor density decreased significantly. There was no alteration in receptor affinity. Present experiment draws attention to the disadvantageous effect of aromatic hydrocarbons coming from the polluted air on steroid receptor development.

Lungs from near-term fetal guinea pigs were supported in vitro for 3 h; lung liquid production rates were measured by a dye dilution technique. Seventy preparations were used to study the effects of arginine vasopressin (AVP) placed in the outer saline for the middle hour, at concentrations reported at birth [fetuses 61 +/- 2 days of gestation; 94.7 +/- 16.2 g (SD) body weight]. At 1200 microU/ml, AVP arrested fluid production (rates, successive hours, 3.03 +/- 0.60, 0.50 +/- 0.14 and 0.02 +/- 0.08 ml/kg body weight per h; falls significant, P < 0.01-0.0005). At 600, 300 and 100 microU/ml there were significant but smaller reductions. Reabsorptions were seen in 8 preparations given 600-1200 microU/ml, AVP. Preparations given 10 microU/ml AVP, AVP carrier or control saline showed no significant change. The responses (% reductions during treatment), were linearly related to the log concentration of AVP (r = 0.99); theoretical threshold, 8 microU/ml). Increasing treatment to 2h did not increase final responses. Preparations from 5 fetuses > 120 g body weight showed significantly greater responses (P < 0.025) [fetuses 64 +/- 2 days of gestation; 135.1 +/- 18.6 g (SD) body weight]. 10(-6) M amiloride abolished responses to AVP [fetuses 62 +/- 1 days of gestation; 93.4 +/- 18.5 g (SD) body weight, n = 30; rates, succeeding hours; AVP alone, 1.78 +/- 0.22, 0.48 +/- 0.09, 0.16 +/- 0.99 (P < 0.01-0.0005); AVP with amiloride, 1.15 +/- 0.07, 0.93 +/- 0.10, 0.86 +/- 0.08 (no significant fall) ml/kg body weight per h]. Thirty-six preparations treated with arginine vasotocin (AVT, 10-600 microU/ml) showed closely similar responses to those from AVP. These studies extend results to fetal guinea pigs, and show that AVP, at concentrations reported at delivery, can slow lung liquid production or cause reabsorption by a direct action on the lung. The effect increases close to term, and is due to activation of amiloride-sensitive Na+ channels.

The present studies were designed to characterize the developmental aspects of Na(+)-dependent phosphate transport, across the hepatocyte basolateral membranes of the suckling and weanling rats. A well validated technique of plasma membrane vesicles (BLMV) was utilized. Phosphate uptake was driven into an osmotically active intravesicular space as evident by a linear relationship between uptake and 1/osm with no binding component y = 0.04 x-0.03, r2 = 0.99 and y = 0.035x + 0.01, r2 = 0.95 in suckling and weanling BLMV's respectively. The presence of inwardly directed Na+ and pH gradient stimulated phosphate uptake in suckling and weanling BLMV's, however, uptake values under Na+ and pH gradients were greater in weanling rats compared to suckling rats. Kinetics of Na(+)-dependent phosphate uptake were 0.14 +/- 0.01 and 0.28 +/- 0.035 at pH 6.1 (P < 0.05) and 0.1 +/- 0.007 and 0.15 +/- 0.03 nmoles/mg protein/10s (P < 0.05) at pH 7.4 in suckling and weanling rats respectively. Km values were not significantly different. Na+ arsenate and phosphonoformonic acid inhibited Na(+)-dependent phosphate uptake, whereas ATP and P-MB (para-chlomercuribenzoic acid) did not effect Na(+)-dependent phosphate uptake. These studies demonstrate for the first time the presence of a specialized transport system for phosphate across the basolateral membranes of the rat liver during development. This transport system exhibit ontogenic characteristics in regard to its transport capacity.

The administration of 17-beta estradiol to human, and all the animals species tested, results in blood volume expansion. This effect has been postulated to be mediated through an increase in the circulating levels of aldosterone. We infused 17-beta estradiol (30 micrograms/kg/day) into 5 chronically-castrated ewes over a 3-week period, and determined the plasma concentrations of 17-beta estradiol, PRA, and aldosterone at weekly intervals. By the end of the third week, 17-beta estradiol plasma concentration had increased 150-fold, while PRA increased 2-fold; aldosterone decreased 40% from baseline values. Thus, during a period in which we have previously observed blood volume expansion, there was a dissociation between the levels of 17-beta estradiol and aldosterone. These findings question the theory that the estradiol-mediated blood volume increase observed during pregnancy is secondary to an increase in the circulating aldosterone levels.