Biomedical subjects
Publications and source records attributed to F G Smith.
Dietary administration of the growth promoter, clenbuterol, ameliorated denervation-induced atrophy in rat soleus muscles. In acutely denervated muscles the drug inhibited the appearance of atrophy, and in chronically denervated muscles the atrophy was almost fully reversed. Responses in slow twitch oxidative fibres were particularly marked.
To see if the variability in fetal urine flow and sodium excretion was related to fetal drinking activity, renal function was investigated in two groups of oesophageally-ligated fetuses and one group of non-ligated fetuses. There was no significant difference in urine flow, sodium excretion or glomerular filtration rate in the ligated fetuses compared with the non-ligated fetuses. Furthermore, oesophageal ligation had no effect on the variability in urine flow and sodium excretion rate. The response of fetal kidney to ingestion of fluid was investigaeed in 2 groups of oesophageally-ligated fetuses. In one group it was shown that ingestion of 20 ml/kg of amniotic fluid by the fetus had no consistent effect on fetal renal function. In the other group it was shown that the ingestion of 200 ml water also had no consistent effect on fetal renal function. The water load caused a rise in fetal blood pressure and a fall in plasma osmolality. Since there was no significant increase in free water clearance and fetal plasma osmolality decreased then rose towards control levels, it is concluded that the oral water load was absorbed from the fetal gastrointestinal tract and diffused out of the fetal compartment across the placenta. These experiments show that fetal drinking is probably not responsible for the variability often seen in fetal urine flow and sodium excretion rate.
If fetal drinking activity is prevented and it is assumed that in the latter third of gestation the fetus is capable of maintaining itself in fluid balance, then the net amount of fluid gained across the placenta by the fetus is equal to the amount of fluid lost from the fetus, by routes other than the placenta, plus fluid deposited in growing tissues minus the amount of water produced as a result of oxidative metabolism. Net transplacental transfer of fluid to the fetus over a 3 h period was measured in eight chronically catheterized fetal sheep in which drinking activity was prevented by ligating the oesophagus. Urine and lung liquid flow rates were measured. In the latter third of gestation, these are the only significant sources of fluid loss from these fetuses during the 3 h experimental period. Water produced as a result of oxidative metabolism was calculated, as was the amount of fluid deposited in growing tissues during the course of the experiment. The weight of the fetus at the beginning of the experiment and the change in weight that occurred during the experiment was calculated by measuring the weight of the fetus at death (within 30 h) and applying an equation which describes the body weight-gestation age relationship for merino sheep. Net transplacental fluid transfer was 0.40 +/- 0.09 ml min-1 kg-1 (range 0.30-0.54 ml min-1 kg-1). Fetal urine flow rate averaged 0.30 +/- 0.11 ml min-1 kg-1. It was 72.8 +/- 10.0% of the volumes used to calculate net transplacental fluid transfer to the fetus. Lung liquid flow rate was 0.079 +/- 0.039 ml min-1 kg-1. It was 20.2 +/- 9.2% of the volumes used to calculate net fluid intake. The amount of fluid deposited as a result of tissue growth was 0.023 +/- 0.001 ml min-1 kg-1; it was 5.94 +/- 1.1% of the volumes used in the equation, while the production of water as a result of metabolism was 3.9 X 10(-3) ml min-1 kg-1 (Conrad & Faber, 1977) and constituted 1.01 +/- 0.22% of the volumes used in the equation. This method of measuring net transplacental fluid transfer to the fetus can be used to measure fetal fluid intake over relatively short periods of time. It also means that the effects of disturbances in maternal fluid and electrolyte balance on fluid transfer to the fetus can be studied and quantitated.
Factors modulating the fetal aldosterone response to hypoxemia were studied in three groups of chronically catheterized fetal lambs between 131 and 143 days of gestation (term, 145 days). One group (control group) received an infusion of 5% dextrose in water; the second group (captopril-treated group) was given captopril, an inhibitor of angiotensin-converting enzyme; the third group (captopril plus dexamethasone-treated group) received dexamethasone in addition to captopril. In all groups of fetuses, hypoxemia was associated with a significant increase in plasma K+ concentration (+0.7 +/- 0.1 meq/liter). In control fetuses, changes in plasma aldosterone concentration during hypoxemia correlated closely with changes in plasma K+ concentration r = 0.79; P less than 0.001) and with changes in plasma angiotensin II concentration (r = 0.77; P less than 0.001). In the captopril-treated fetuses, the rise in plasma aldosterone concentration during hypoxemia correlated closely with plasma K+ (r = 0.79; P less than 0.001) but not with plasma angiotensin II values (r = 0.17). No significant correlation was found between percent changes in maternal aldosterone and percent changes in fetal aldosterone during hypoxemia and following recovery (r = 0.36; P greater than 0.1) in captopril-treated fetuses. Administration of dexamethasone to fetuses receiving captopril completely inhibited the rise in plasma aldosterone associated with hypoxemia. Taken together, the present results suggest that the rise in plasma aldosterone during hypoxemia is not related to the level of activity of the renin-angiotensin system but depends probably on the increased secretion of adrenocorticotrophin by the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)
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The adrenal and renal responses to similar increases in plasma angiotensin II (AII) were studied in chronically catheterized fetal lambs (112-131 days gestation: term 145 days) and adult nonpregnant sheep. The rate of AII infusion was adjusted to compare the effect of similar rises in plasma AII concentration between fetuses and adult ewes. Increases in plasma AII were associated with a decrease in plasma renin activity (PRA) in both fetuses (5.55 +/- 1.53 to 2.11 +/- 0.59 ng/ml per hr, P less than 0.05) and adult ewes (1.28 +/- 0.34 to 0.62 +/- 0.16 ng/ml per hr, P less than 0.05), but the percent changes in PRA for similar increases in plasma AII were not different when fetuses were compared to adult ewes. Contrary to the effect of AII on PRA, the increase in plasma AII did not produce parallel changes in plasma aldosterone concentration when fetuses were compared to adult ewes. The percent changes in plasma aldosterone concentration for similar increases in AII concentration were significantly higher in adult ewes (+165 +/- 37%) than in fetuses (+58 +/- 15%)(P less than 0.01). Finally, there were no significant changes in fetal urinary excretion of PGE and PGF2alpha when a significant rise (P less than 0.05) was observed in adult ewes at the highest level of plasma AII concentration. In summary, the present results tend to suggest that there are differences between fetuses and adult ewes in the response to AII, the response being smaller in fetuses.
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The effects of fetal hypoxemia on renal hemodynamics and renal function were studied in two groups of chronically catheterized young (< 120 days of gestation) and near-term lamb fetuses (> 130 days). Fetal hypoxemia produced, in both groups, a significantly decrease in renal blood flow (RBF) and a significant increase in the filtration fraction. However, the glomerular filtration rate (GFR) did not change significantly suggesting that the renal vasoconstriction associated with fetal hypoxemia was more important at the efferent than at the afferent arteriolar level. In the group of near-term fetuses, the decrease in RBF correlated closely with changes in plasma renin activity (PRA) (r = 0.77). No changes in PRA were observed during hypoxemia in the group of young fetuses. After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF2 alpha) was observed in near-term fetuses but not in young fetuses. It also was demonstrated that fetal hypoxemia produced a significant increase in fetal plasma concentrations of vasopressin associated with an antidiuresis in all but one near-term fetus and in 50% of the young fetuses, suggesting that the ability of the fetal kidney to reabsorb free water is more developed in near-term fetuses. Finally, fetal hypoxemia had no effect on mean arterial pressure and heart rate in young fetuses; however, in near-term fetuses, a significant increase in blood pressure and a decrease in heart rate were observed. In summary, it appears that the response of the fetal kidney to hypoxemia depends on the degree of fetal maturation.
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The renal response to endogenous aldosterone production at different times during gestation and immediately after birth, as well as factors controlling aldosterone secretion during fetal life have been studied in 34 lamb fetuses (106-142 days of gestation, term 145 days) and in 6 newborn lambs (3-8 days postnatal age). It was demonstrated that the increase in fetal plasma aldosterone concentrations correlated with the increase in fetal plasma renin activity (PRA) (r = 0.67, p < 0.001). Moreover, it was fond that the slope of the regression line between plasma aldosterone and PRA during fetal life was significantly steeper (p < 0.05) than after birth. Significant correlation coefficients were found between the fetal urinary to plasma ratios (U/P) of sodium over potassium [(U/P)Na+/(U/P)K+] and either fetal plasma aldosterone (r = -0.53, p < 0.005) or fetal age (r = -0.52, p < 0.005). Moreover, in 7 out of 9 fetuses over 125 days, frank secretion of potassium by the fetal tubular cells was demonstrated; such a secretion was present in only 1 of the 15 fetuses between 101 and 125 days of gestation. Finally, it was demonstrated that the increase in mean arterial blood pressure during fetal life and after birth is not a major factor in the increase in fetal glomerular filtration rate during gestation or in the adaptation of glomerular filtration rate to extrauterine life.
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In order to investigate the metabolic effects of a constant hypertonic glucose infusion in well-oxygenated fetuses, ten experiments were carried out in nine long-term experiments in fetal lambs. It appeared that a constant hypertonic glucose infusion did not significantly affect the fetal blood gases, pH, and plasma lactate levels when fetal glucose was kept below 150 mg. per 100 ml. It was also demonstrated that glucose infusions significantly increased the fetal lactate levels and decreased the blood pH when fetal plasma glucose was over 150 mg. per 100 ml. However, there was no decrease in fetal PO2 and pco2 until fetal glucose reached values over 300 mg. per 100 ml. These studies suggest that constant hypertonic glucose infusion does not improve fetal blood gases or pH and that fetal hyperglycemia over 300 mg. per 100 ml. produces severe metabolic acidosis.
The capacity of the fetal renal carbonic enzyme to facilitate the renal reabsorption of bicarbonate was studied in 8 long-term fetal lamb preparations (103-124 days of gestation). After acetazolamide administration the fetal arterial blood pH and PCO2 values decreased significantly (p less than 0.05). Significant increases in fetal urinary pH (p less than 0.001), and urinary excretion of bicarbonate (p less than 0.001), potassium (p less than 0.05) and total cation (Na+ + K+) were observed after carbonic anhydrase inhibition. It is suggested from these in vivo studies that renal carbonic anhydrase is present and active during fetal life and does not limit the capacity of the fetal kidney to reabsorb bicarbonate.
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The maturation of the glomerular filtration rate (GFR) and the interrelationship between the GFR and the renal transport of sodium and chloride have been evaluated during the last trimester of gestation with the use of long-term experiments in fetal lambs. An increase in GFR (milliliters per minute) parallel to the increase in fetal body weight was demonstrated; however, no significant change was shown when the GFR (milliliters per minute per kilogram of fetal body weight) (1.141 +/- 0.079) was related to fetal body weight or gestational age. There was a constant increase in sodium and chloride reabsorption (microequivalents per minute) during the last third of gestation. This increase in sodium and chloride reabsorption was less than the increase in GFR (milliliters per minute) before 129 days but became higher than the rise of GFR (milliliters per minute) after 129 days of gestation.