Amniotic membranes from fetal guinea pigs at 0.46 of term were maintained in vitro by means of salines which reproduced the electrolytes of the natural fluids, and. which maintained small osmotic and hydrostatic gradients from the fetal to the maternal solutions. Water passed slowly from the fetal to the maternal side (average rate = 3.93 mg/cm 2 per minute). Synthetic arginine vasotocin (AVT) at 8–100 vasopressor mU/ml of amniotic saline slowed the fetal–maternal flow, or reversed it to give a net uptake of water into the amniotic saline (maximum reversed flow = 10.4 mg/cm 2 per minute). Despite individual variability between membranes, there was a linear relationship between the change in the rate of flow, and the log of the dose of AVT (AVT threshold indicated = 6.4 mU/ml). Synthetic arginine vasopressin (AVP) and fetal pituitary extracts produced similar responses (AVP threshold = about 1.0 mU/ml). Synthetic oxytocin was without effect in doses up to 100 oxytocic mU/ml. Although the doses tested appeared to be pharmacological, evidence is reviewed for a possible physiological significance. It is suggested that amounts of AVT, or more probably AVP, are liberated from the fetal pituitary by osmotic or other stimuli, and pass in the fetal urine into the amniotic cavity; there they act on the amnion to stimulate it to conserve or augment amniotic fluid by transporting water inwards from the maternal environment.
Abstract. The pre-ovulatory fall in plasma kininogens in rats with 4 day oestrous cycles started between 12.00 and 15.00 h pro-oestrus, reached a maximum decline of 51% by 18.00 h pro-oestrus, and started to recover before ovulation. Because these changes appeared to correspond with the LH-surge, and to follow the peak in plasma oestradiol-17β levels, both of these hormones were tested for possible effects on plasma kininogens. Intracardiac injections of 110 IU of equine LH into dioestrous rats were followed by a decline of 30.8 ± 6.7% in plasma kininogens, 6 h after injection (significant, P < 0.01). Values were still depressed, but recovering, 12 h after treatment; the reduction was 21.3 ± 5.8% (significant, P < 0.01). Controls showed no decline. Injections of oestradiol-17β (1.0 μg/100 g body weight) produced no significant effects. It is suggested that the LH surge may be responsible, at least in part, for the decline in plasma kininogens seen before ovulation.
Lungs from near-term fetal guinea pigs (61 ± 2 days of gestation) were supported in vitro for 3 h; lung liquid production was monitored by a dye dilution method. Untreated control preparations produced fluid at 1.38 ± 0.30 mL·kg-1 body weight·h-1, with no significant change (ANOVA; regression analysis); those given 1.24 × 10-9 or 1.24 × 10-8 M norepinephrine during the middle hour showed no significant change, but those given concentrations between 5.24 × 10-8 and 1.24 × 10-5 M all showed significant reductions or fluid reabsorption (based on 42 fetuses). The responses showed a linear relationship with the log concentration (r = 0.97). They appeared to involve alpha-adrenoreceptors, since responses to 10-7 M norepinephrine were unaffected by 10-6 M propranolol, but those to 10-7 and 1.24 × 10-6 M norepinephrine were abolished by 10-6 and 1.78 × 10-5 M phentolamine, respectively (based on 48 fetuses). Activation was through alpha2-adrenoreceptors, since responses to 10-7 and 10-5 M norepinephrine were abolished by 10-4 M yohimbine, but not by 10-5 M prazosin (based on 60 fetuses). The results show that norepinephrine is able to reduce lung liquid production when at plasma levels present at birth, and that it can produce reabsorption; unlike epinephrine, there was no reduction in responses at high concentrations. This work reintroduces a neglected factor, norepinephrine, into possible controls of lung liquid reabsorption, and opens up the potential for neural controls.Key words: fetus, norepinephrine, adrenoreceptors, lung liquid.
Lungs from fetal guinea pigs of 61 ± 3 days of gestation were supported in vitro for 3 h, and lung liquid secretion rates were measured by a dye dilution technique based on Blue Dextran 2000. Ten preparations that had received no treatment showed an average secretion rate of 1.12 ± 0.28 mL∙kg −1 body weight∙h −1 during the first hour, and there were no significant changes over the following 2 h. In studies of 54 fetal lungs, furosemide, bumetanide, control ethanol carrier, or saline alone were placed in the supporting medium during the middle hour of the 3-h incubations (ABA design). Furosemide at 10 −3 M reduced secretion 83.4 ± 16.8%; at 10 −4 and 10 −5 M it produced smaller reductions. Bumetanide at 10 −3 M usually produced reabsorption (129.9 ± 23.0% reduction), at 10 −4 M it reduced secretion 30.9 ± 11.8%, but at 10 −5 M it was ineffective. Control carrier and saline were without effect. The ability of the loop diuretics to produce reabsorption of fluid in some preparations suggests the unmasking of an active reabsorptive process. The results also suggest that lung liquid secretion in the fetal guinea pig, as in the sheep, is dependent on a Na + and Cl − cotransport system.Key words: fetus, lung fluid, bumetanide, furosemide.
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