Biomedical subjects

E E Faridy

Publications and source records attributed to E E Faridy.

At least 19 recordsLinked to original sources

PubMed1989

Fetal lung growth: influence of maternal exposure to cold and exercise in rats.

The consequences of maternal exposure to low ambient temperature and exercise on maternal and fetal lung growth and in particular on the relationship between the three gas exchange organs (lungs and placenta) were studied in albino rats. Pregnant rats were subjected to 10 degrees C ambient temperature or to daily 10 min swimming exercise beginning at day 3 or day 11 of pregnancy till day 21 when they were sacrificed. Maternal lung growth was assessed by measuring the lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. Comparisons were made in rats with litter sizes of 9-14. The major findings were as follows. Cold increased: (1) the maternal lung, liver, kidney and heart size, and fetal body weight, in both groups, but to a greater degree in rats exposed to cold at day 3; and (2) fetal lung DNA content in rats subjected to cold at late gestation. It abolished the relationship between maternal and fetal lung DNA content which exists in large litter size pregnancies. Exercise did not enlarge the maternal lungs; it decreased the placental weight and fetal lung DNA content and abolished the relationship between maternal and fetal lung DNA content in rats subjected to exercise at early gestation. Neither cold nor exercise had an effect on fetal lung maturation. It is postulated that reduction in fetal lung DNA content with maternal exercise may result from the effects of hypoxemia which may be the consequence of reduced uterine blood flow; and that abolition of normally existing direct relationship between maternal and fetal lung DNA content may be the outcome of the effects of alterations in metabolic and endocrine functions, in both the mother and the fetus, in response to cold temperature and exercise, offsetting the influence the growing maternal lung may have on fetal lung growth.

Animals↗

PubMed1989

Role of hyperventilation in hypoxia on lung growth in rats.

This study was conducted in an attempt to differentiate the contribution of hyperventilation, if any, from that of low PO2 on adaptive lung growth in response to hypoxia. Male albino rats were exposed to one of the following: (1) Room air for 7 days, as control; (2) 10% O2 in N2 for 7 days; (3) 10% O2 for 6 h, 1 day or 2 days and air for the remaining of 7 days; (4) 10% O2 for 2 days and 7% CO2 in air for 5 days; (5) air for 2 days and 7% CO2 for 5 days; or (6) 7% CO2 in air for 7 days. Lung growth was assessed by measuring the lung weight, lung air volume, lung DNA content and rate of DNA synthesis in lung explants. Hypoxia stimulated lung DNA synthesis even when administered for only 6 h, and the effects persisted for a few days after discontinuation of hypoxia. Hypercapnia did not stimulate DNA synthesis in lung. In 2 day hypoxic 5 day air rats the lung weight and lung DNA content increased, in 2 day air 5 day hypercapnic rats only the lung volume increased, and in 2 day hypoxic 5 day hypercapnic rats all parameters of lung growth, i.e., lung weight, DNA content and air volume increased as in 7 day hypoxic rats. The results suggest that adaptive or compensatory lung growth in hypoxia is brought about on one hand by the direct effect of low PO2 on lung cells, resulting in lung hyperplasia, and on the other hand by the mechanical stimulation of lung tissue by hyperventilation, causing lung distension.

Animals↗

PubMed1989

Role of cyclic AMP in proliferation of lung tissue in organ culture.

The role of cyclic AMP in cell proliferation and division has been the subject of study by a number of investigators in the past 30 years, but the argument of whether cyclic AMP is a negative or a positive regulator has not been settled. We studied the effect of cyclic AMP on proliferation of normal and postpneumonectomized lung tissues in young adult rats by measuring the incorporation of tritiated thymidine into lung DNA in organ culture. In normal lung tissues the incorporation of [3H]thymidine was increased by exogenous dibutyryl cyclic AMP, or by isoproterenol or forskolin to stimulate adenylate cyclase, or by caffeine, which inhibits cAMP phosphodiesterase. The effect of isoproterenol, but not forskolin, was abolished by the beta-adrenergic blocking agent propranolol. The effect of caffeine on [3H]thymidine incorporation was further enhanced in normal lung tissues in the presence of dibutyryl cyclic AMP and in postpneumonectomized lung tissues. Imidazole, a cAMP phosphodiesterase stimulator, also increased [3H]thymidine incorporation in culture, but the effect was not magnified in the presence of exogenous dibutyryl cyclic AMP, nor in postpneumonectomized lung tissues. The data suggest that cyclic AMP acts as a positive regulator in proliferation of lung tissues.

Animals↗

PubMed1988

Relationship between maternal and fetal lung growth.

This study analyzes the relationship between the maternal and fetal lungs, in rats in relation to litter size, to determine whether the enlargement of maternal lung during pregnancy is concurrent with that of the fetal lung. Pregnant albino rats were sacrificed on gestation day 21 (term 22 days). Maternal lung growth was assessed by measuring the lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. The findings were as follows: (1) no differences were noted between the lungs of non-pregnant rats and pregnant rats with small litter size (1-4); (2) pregnant rats with large litter size (10-18) had larger lungs than rats with small litter size; (3) there was a direct relationship between cellularity (DNA content) of the fetal lung and maternal lung when the latter underwent a growth change during pregnancy; (4) no relationship in cellularity was found between the maternal lung and placenta nor between the fetal lung and placenta. The results suggest that factors or processes which regulate the growth and dictate the size of the maternal lung during pregnancy similarly influence the fetal lung.

Animals↗

PubMed1988

Maternal lung growth in surgically reduced litter size pregnancy.

In our previous study (Faridy et al., this issue) we observed that pregnant rats with large litter size have larger lungs than rats with small litter size. The present study was conducted to test the hypothesis that in large litter size pregnancy, the maternal lung may not enlarge if, during pregnancy, the large litter size of 11-18 is surgically reduced to a small litter size of 3. A laparotomy was performed in pregnant albino rats at gestation day 7 (R7) or 14 (R14), all fetuses except 3 were removed and the rats were sacrificed at gestation day 21 (term 22 days). Maternal lung growth was assessed by measuring lung weight, lung DNA content and lung air volume, and the fetal lung growth by lung DNA content. The results were then compared with control pregnant rats of large (11-18) and small (1-3) litter size. The findings were: (1) reduction of litter size hindered maternal lung enlargement; (2) the earlier in pregnancy the surgical reduction was performed the smaller was the maternal lung, such that control (11-18) greater than R14 greater than R7 = control (1-3); (3) fetuses of R14 rats had larger lungs per body weight than R7 rats; (4) oxygen consumption of sham-operated rats with large litter size was higher (by 8-12%) than R7 rats. The results suggest that enlargement of maternal lung during pregnancy is related to litter size and perhaps to VO2. The fact that R14 fetal lung is larger than that of R7, supports our previous notion (Faridy et al., this tissue) that factors regulating the maternal lung growth similarly influence the fetal lung.

Animals↗

PubMed1988

Influence of maternal pneumonectomy on fetal lung growth.

This study was conducted to test the hypothesis that the compensatory growth of the maternal lung during pregnancy influences fetal lung growth, specifically the fetal lung DNA content. A left pneumonectomy (PN) was performed in pregnant albino rats at different gestation days (GD 3, 7, 9, 10, 12, 14, 16 and 18) and the rats sacrificed at GD 21. Only mothers with litter size of 9-14 fetuses were used for this study. Maternal lung growth was assessed by measuring lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. The findings were: (1) pregnancy did not influence the rate of compensatory growth of the remaining lung following PN; (2) neither thoracotomy nor PN had any effect on placental weight or DNA content; (3) lung DNA content for body weight was larger in fetuses of PN rats when PN was performed in the first half of gestation; (4) there was a direct relationship between DNA content of the fetal lung and maternal lung in PN rats; and (5) neither thoracotomy nor PN in pregnant rats influenced the maturation of the fetal lung. The results suggest that a growth factor(s), specific for lungs, is released into maternal circulation following PN, crosses the placenta and enhances the fetal lung growth without affecting its maturation.

Animals↗

PubMed1988

Fetal lung growth: influence of maternal hypoxia and hyperoxia in rats.

The consequences of maternal hypoxia and hyperoxia on maternal and fetal lung growth and in particular on the relationship between the three gas exchange organs (lungs and placenta) were studied in albino rats. Pregnant rats were exposed to one of the following: (1) 10% O2 in N2 or 100% O2 for 2 days beginning at day 7, 11, 14, or 18 of pregnancy; (2) 10% O2 in N2 or 100% O2 for 10 h/day beginning at day 7; or (3) 14-11% O2 in N2 continuously beginning at day 14 till day 21 when they were sacrificed. Maternal lung growth was assessed by measuring the lung weight, lung air volume and lung DNA content, and the fetal lung growth by lung DNA content. Hypoxia and hyperoxia of short duration (2 days) had no significant effect on maternal and fetal lungs and placenta. The major findings with intermittent hypoxia and hyperoxia, and with 1 week continuous hypoxia were as follows: (1) hypoxia initiated enlargement in maternal lung, liver, kidney and heart, and growth retardation in the fetus; (2) the direct relationships which exist in normal pregnancy between placental weight or DNA content and fetal body weight were abolished by maternal hypoxia, and that which exists between maternal and fetal lung DNA content, by hypoxia and hyperoxia; (3) both hypoxia and hyperoxia, applied at early pregnancy, caused small for body weight placenta and lung; and (4) neither maternal hypoxia nor hyperoxia influenced fetal lung maturation. It is speculated that reduction in fetal lung DNA content with maternal hypoxia may result from the direct and indirect effects of hypoxia on fetal lung, namely inhibition of cell multiplication and reduced pulmonary blood flow; and that a small fetal lung with maternal exposure to 100% O2, may result from redistribution of blood flow and nutrient supplies to fetal organs with lungs receiving a smaller proportion of it.

Animals↗

PubMed1987

Rate of secretion of lung surfactant before and after birth.

Using electron microscopic techniques, we defined the percentage of intracellular lamellar bodies (LB) in the process of extrusion from type II cells, designated that as an index of secretion of surfactant, and studied the rate of release of surfactant in the lungs of fetal and newborn rats. The index of secretion increased twice in perinatal period. The most dramatic increase occurred during labor which consequently declined to fetal level within 15 min of birth. The second rise began at 30 min after birth and reached maximum in 2 h. Thereafter, it gradually declined reaching its lowest at 24 h. The number of LB/type II cell decreased with an increase in the rate of release and began to rise at about 1-2 h after increase in the rate of release. It is speculated that the rise in secretion rate during labor is in response to the change in circulating hormone levels, and that for after birth in response to lung distension and air ventilation. We also used this method of analysis in lavaged fetal lungs to test our unconfirmed belief that lung lavage promotes release of intracellular LB. The results, consisting of a 5-fold increase in the index of secretion and a 20% reduction in the number of LB/cell in lavaged lungs, were in favour of the notion. This should be taken into consideration when lung lavage is used to obtain 'extracellular surfactant'.

Animals↗

PubMed1987

Air opening pressure in fluid-filled lungs.

The present study was conducted to gain understanding of the role of pulmonary fluid and of concentration of surfactant in the pulmonary fluid on the air pressure-volume characteristics and in particular on the opening pressure (OP). The excised rat lungs were degassed, inflated with isotonic saline and subsequently deflated to a predetermined volume. These lungs were then inflated with air and OP recorded. As the lung saline volume decreased from about 90% to about 20% of maximal lung saline volume, the OP decreased from 22 to 14 cm H2O, respectively, in parallel to the elastic recoil (saline deflation P-V curve) of the lung. This suggests that the terminal airways are patent, and fully dilated at a transpulmonary pressure of 14 cm H2O. With further reduction in lung saline volume, however, the OP increased and approached the OP of fluid-free degassed lungs at 22 cm H2O, indicating closure of terminal airways at low lung volumes. The OP was reduced by increasing the concentration of surface active material in isotonic saline prior to instillation in the lung. These studies suggest that pulmonary fluid and excess surfactant reduce the OP and facilitate uniform distribution of inspired air.

Air Pressure↗

PubMed1987

Air opening pressure in fetal lungs.

The volume of pulmonary fluid (PF) in fetus decreases at late gestation and with initiation of labor. In addition there is a massive release of surfactant in PF during labor. In postmaturity the reduction in PF continues till the lungs become virtually fluid-free. Furthermore there is a loss of surface activity with prolongation of gestation. The present study was conducted to determine the role of the volume and surface activity of pulmonary fluid on the opening pressure (OP) in fetal lungs. Fetal (term and post term) and degassed newborn lungs were inflated with air and OP recorded. The lowest OP was noted in lungs of term fetuses delivered after labor. As the lung became dryer, either after birth or during postmaturity, the OP increased. The OP was greater in postmature compared to degassed postnatal lungs. Instillation of minute volumes of isotonic saline in post term to restore the volume of pulmonary fluid to that of term lungs decreased the OP. Thereafter as the volume of intrapulmonary fluid was increased beyond that of term, either in term or post term lungs, the OP was also increased. The angle of deflection from fluid-removed to fluid-instilled segments of the OP-volume curve was more acute in the fetal lung that in the adult. These studies suggest that a reduction in the volume of pulmonary fluid at birth beyond that of term fetus (FRC) may not be beneficial for newborn and that massive release of surfactant in PF during labor serves to enhance opening of air saccules.

Aging↗

PubMed1983

Instinctive resuscitation of the newborn rat.

Pregnant albino rats were observed during labour and delivery to determine whether they assist the newborn rat to breathe, and if so, in what way. The maternal rat actively resuscitates and assists the newborn. This appears to involve four distinct stages. (1) Cleaning of airways. Immediately after birth, the maternal rat holds the head of the newborn with both paws, cleans and sucks the nares and the mouth of the newborn. She then cuts the umbilical cord and eats the placenta. (2) Assistance. When necessary, she presses the pup's chest with one paw for a few seconds, licks the spine from caudal to cervical region, which causes extension of the body and expansion of the chest, or bites the tail, which makes the newborn squeak. (3) Rest. The newborn is then left alone for as long as 20 min while the mother is delivering the rest of the litter. (4) Stimulation. This involves periodic pushing, rolling, licking, and biting of the newborn. Stillbirths are left alone and not attended. If pups are removed from their mother immediately after birth and prevented from being cleaned, they develop respiratory distress, with mouth breathing, gasping, chest retraction, and cyanosis. This model in nature emphasizes the importance of cleaning the upper airways of the newborn.

Animals↗

PubMed1983

Morphological observations of the fetal rat spleen during prolonged gestation.

The ultrastructure of splenic cells and frequency of cell types were examined in fetal rats during progesterone-induced (P23, 24, 25) and surgically-induced (S23, 24, 25) prolonged gestation, and compared to term (T) fetuses and newborn animals (N1, N2, N3). Statistical analysis revealed an increase in numbers of erythroblasts and a decrease in numbers of neutrophils in post-term fetuses distinct from that seen in term and newborn animals. However, there were also significant differences between the post-term groups: the frequency of erythrocytes and total number of cells were higher in the drug-treated group, despite similar splenic weights in the two. The results are interpreted as a response by the spleen (increased erythropoiesis) to fetal hypoxia, which is known to exist during prolonged gestation.

Animals↗

PubMed1983

Ultrastructural observations of the fetal rat heart during prolonged gestation.

The ultrastructure of myocardial cells was examined from fetal rat hearts during experimentally induced prolonged gestation (GD 23, 24 and 25), and compared to those from term fetuses (GD 22) and newborn animals (N1, N2, N3). Gestation was prolonged by daily subcutaneous injections of 5 mg progesterone to gravid females on days 20 through 24. The 4 chambers of the heart were assessed individually for structural differences by morphometric analysis. Comparison between the 2 atria at each stage revealed no differences as was the case between the 2 ventricles. At term and throughout the newborn period, atrial and ventricular cells were characterised by numerous mitochondria, moderate amounts of glycogen, few lipid droplets and membrane-bounded granules, which, moreover, were peculiar to atrial tissue. During prolonged gestation (GD 24 and 25), there was a statistically significant increase in the size of mitochondria in both atria and ventricles and a reduction of membrane-bounded atrial granules. Whole heart glycogen content was also assessed, biochemically, and found reduced on GD 24 and 25. In addition to the morphological and biochemical findings, fetal rat heart weights were obtained from each designated day of prolonged gestation and compared to newborn rat hearts of comparable age. A statistically significant increase in heart weight was noted on GD 24. Meconium staining, which is indicative of fetal distress was also observed on GD 24 and 25. The morphological and biochemical changes observed suggest a response by the fetal heart to stressful conditions, namely hypoxia and hypoglycemia, which are known to exist during prolonged gestation.

Animals↗

PubMed1981

Relationship between lung intra and extracellular DSPC in fetal and neonatal rats.

Using lamellar bodies (LB) as an index of intracellular disaturated phosphatidyl choline (DSPCin) and biochemical measurements of the total lung DSPC, we studied the relationship between the intra and extracellular DSPC (DSPCex) in the lungs of fetal and neonatal rats. A linear correlation was found between the number of LB and the amount of DSPC in fetal lungs. A similar correlation was found in fetal lungs after lung lavage. The difference between the two corresponded to the DSPCex, which was greater than anticipated. Prior to birth there was a massive release of DSPC, into the extracellular space, which was lost from the lungs during labor and upon initiation of respiration at birth. The DSPCin, however, continued to increase during labor and the first 5 min after birth. Thereafter release of DSPCin and accumulation in extracellular space occurred. After age 12 hours, there was a gradual reduction in DSPCex till 24 hours. Thereafter, a linear correlation between number of LB and total DSPC resumed. The results suggest that lung lavage promotes release of DSPCin and that excess DSPCex, from birth to 24 hours, is removed by two different mechanisms: initially through the airways and subsequently by alveolar macrophages.

Animals↗

PubMed1981

Fetal lung development in surgically induced prolonged gestation.

In our previous study we prolonged gestation in rats with daily subcutaneous injections of progesterone starting on gestation day 20 (P20). To determine whether exogenous progesterone affects the growth of post-term fetal lungs, we utilized surgical techniques to prolong gestation by retaining 4 living fetuses 1, 2, or 3 days beyond the date of spontaneous delivery of the rest of the litter. The retained fetuses were harvested by caesarean section on gestation days 21 through 25. In spite of an improved general appearance in the retained fetuses, there were many similarities between the retained and the post-term P20 fetuses such as: increase in fetal body, kidney and spleen weights; reduction in lung and liver weights; progressive lung atelectasis; loss of lung and liver glycogen; hypoglycemia; and reduction in placenta DNA content. The significant differences between the two were in the amount of lung disaturated phosphatidyl choline (DSPC) and lung DNA (cell number), expressed per lung or per body weight. In contrast to the P20 post-term fetuses, which exhibited a biphasic phenomenon in DSPC and DNA contents, the retained fetuses showed no change in lung DSPC and DNA contents after term. The P20 fetuses had larger adrenals, which increased with prolongation of gestation. The results suggest that exogenous progesterone does not affect the fetal lung growth post-term. It is speculated that the cellularity and the DSPC content of the post-term fetal lung is adversely affected by the degree of fetal distress.

Animals↗

PubMed1981

Pressure-volume characteristics of lungs of rats during pregnancy and postpartum.

Measurements of lung volumes in pregnant women show that the functional residual capacity and residual volume are reduced by 17-25% at late pregnancy. The present study was conducted to test the hypothesis that a decrease in FRC at pregnancy may result from an increase in retractive forces of the lung. The air and saline pressure-volume characteristics of excised lungs were studied in rats daily during pregnancy and the postpartum period. In comparison to non-pregnancy rats, the air PV measurements indicated that: (1) the retractive forces of the lungs were increased late in pregnancy resulting in reduction in both MLV (lung air volume at 40 cm H2O Ptp) and in V%10 (volume at 10/volume at 40 cm H2O Ptp X 100); (2) MLV was greater in lactating than in non-lactating and in non-pregnant rats. Lung saline volume was also greater in lactating than in non-lactating rats at early postpartum period. Lung phospholipids content was increased at late pregnancy and in lactating rats; (3) there was an increase in MLV and in V% immediately after delivery and 2-3 days after an abrupt cessation of lactation ("dried" rats). The minimal surface tension of lung lavages also decreased in these rats. A shift to that left of the air PV curve in "dried" rats suggest that under normal circumstances lung surface forces are not at their lowest.

Animals↗

PubMed1980

Development of fetal rat lung during prolonged gestation.

Pregnancies were prolonged by daily subcutaneous injection of progesterone to the maternal rats from day 20 through 24 of gestation (Term is 22 days). The fetuses were harvested by cesarean section on gestation days (GD) 21 through 25. In spite of reduction in placental weight the fetal body weight increased during prolonged gestation. Both lung wet and dry weights decreased resulting in smaller lung per body weight. Compared to term fetuses, post term fetuses (GD 25) exhibited a 10% reduction in lung cell numbers, and a 90% reduction in lung glycogen. Lung disaturated phosphatidyl choline expressed per lung increased up to GD 23 and subsequently decreased by GD 25. Surface tension of lung extracts and pulmonary lavage fluids increased with prolongation of gestation. Histological studies revealed a decrease in the number of lamellar bodies in the Type II cells and a gradual reduction in the size of terminal sacs leading to areas of complete atelectasis at GD 25. It is suggested that lung hypocellularity, depletion of lung glycogen, reduction in intracellular reserve of phospholipids, loss of pulmonary fluid leading to atelectasis, and loss of surface activity of pulmonary fluid may be predisposing factors for the development of respiratory distress in postmaturity.

Animals↗

PubMed1976

Effect of distension on release of surfactant in excised dogs' lungs.

The freshly excised lower lobes of lungs of dogs were washed by filling and emptying the lobe with isotonic saline. The wash fluid was then discarded and the procedure was repeated 9 times. The 9th wash was collected and used for measurements of surface tension and lecithin content. The lobe was then constantly inflated for 3 hr; washed again with isotonic saline (10th wash) and surgace tension and lecithin content of wash fluid measured. When the lobe was inflated with air, at room temperature, the surface activity and the lecithin content of the 10th wash were increased in comparison to the 9th wash. This increase waoom temperature, or with air at 6 degrees C. Increase in the surface activity of the 10th wash was directly related to the inflating pressures used. This study suggests that distension of the lung enhances the release of surfactant and that this release is a metabolically active process. It appears also that 100% O2 has an inhibitory effect on this process.

Animals↗