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M L Bauer

Publications and source records attributed to M L Bauer.

At least 19 recordsLinked to original sources
PubMed2003

The effect of pregnancy on visceral growth and energy use in beef heifers.

Beef heifers (24 mo; 378 +/- 32 kg of BW; 22 pregnant, PR; 17 nonpregnant, NP) were grouped in common pens and fed corn silage- and hay-based diets formulated to provide an ADG of 0.45 kg in NP heifers. Both PR and NP heifers were slaughtered on d 40, 120, 200, and 270 of the study. Intestinal and hepatic tissues were analyzed for protein, DNA, RNA (mg/g of fresh tissue), and in vitro oxygen use. Jejunal samples were analyzed for cellular proliferation via immunohistochemical analysis. For ileum, DNA, which provides an estimate of cell number per unit of tissue, revealed an interaction (P = 0.06) between pregnancy and slaughter day; both PR and NP decreased with time, but NP increased on d 270 (P = 0.09). Cell number in the ileum was reduced at d 200 and 270 in the PR heifers (P < 0.09). Liver protein concentration was less (P = 0.07) in PR than in NP heifers (NP = 291.1 vs. PR = 210.5 +/- 33.9 mg/g). Hepatic protein:DNA ratio was not affected (P > 0.10) by pregnancy or day. Energy use (kcal/d) of duodenum and jejunum, calculated from in vitro oxygen consumption, increased linearly (P < 0.02) with time for both PR and NP. Pregnant and NP ileal energy use increased linearly (P < 0.01), but ileal energy use by PR was less throughout gestation (P = 0.07) than ileal energy use by NP. Cellular proliferation in the crypt region of the jejunum was decreased on d 120 and 200 (P < 0.02). These data indicate that the small intestine and liver of PR heifers may conserve energy expenditure compared with NP heifers. Energy conservation can partially be explained by differences in growth and cell proliferation and by energy use of the liver and small intestine.

Animals↗
PubMed2002

Effects of supplementation on intake and growth of nursing calves grazing native range in southeastern North Dakota.

A 2-yr study was conducted to determine the first limiting nutrient for gain in nursing calves grazing native range in southeastern North Dakota. Thirty-two calves (20 steers, 12 heifers) in Trial 1 (169 +/- 5 kg initial BW) and 31 (16 steers, 15 heifers) in Trial 2 (214 +/- 5 kg initial BW) grazed common pastures. Calves were blocked by sex and stratified by weight. Calves were stratified by age of dam in Trial 1 and by pretrial milk intake (MI) in Trial 2. Treatments were nonsupplemented control (CON); energy supplement (ENERGY; 100% soyhulls); degradable intake protein supplement (DIP; 68% soyhulls, 32% SBM); and degradable with undegradable intake protein supplement (DIP+UIP; 80% sulfite-liquor treated SBM, 16% feather meal, 4% blood meal). In Trial 2, 5% molasses was added to all supplements with the ratios of other ingredients held constant. Supplements were formulated to be similar in NE. The DIP and DIP+UIP supplements supplied equal amounts of degradable protein. Supplemented calves were fed individually, with similar supplement DMI. Weight and MI were measured in July, August, and September. Forage intake (FI) was measured in July, August, and September of Trial 1 and July and August of Trial 2. Gain data were analyzed as a randomized complete block and MI and FI as a split-plot in time. Orthogonal contrasts were used to separate means and included CON vs supplemented, ENERGY vs protein, and DIP vs DIP+UIP. No trial effect or trial x treatment interactions (minimum P-value = 0.30) were detected for ADG. Supplemented calves gained faster than CON (P = 0.06). No other contrast differences were observed (minimum P-value = 0.50). Treatment did not affect FI (P > or = 0.55). Forage intake was lower (P < 0.001) in Trial 1 than in Trial 2. A linear increase (P = 0.0001) in FI (kg OM/d and percentage BW) occurred over time. Calves in Trial 2 consumed more (P = 0.004) fluid milk than calves in Trial 1, though no difference (P = 0.28) was observed relative to BW. No treatment or period differences were detected for fluid MI (minimum P-value = 0.23). Relative to BW, MI declined linearly (P = 0.0001) with successive periods. Energy may be limiting weight gain of nursing calves grazing native range in southeastern North Dakota.

Animal Feed↗
PubMed2001

Influence of alpha-linked glucose on jejunal sodium-glucose co-transport activity in ruminants.

Eight steers and 12 lambs were used in a completely randomized experimental design to determine the effect of partial alpha-amylase starch hydrolysate (SH) on small intestinal sodium-dependent glucose transport activity. Starch hydrolysate was delivered ruminally or abomasally to steers (960 g/day) and sheep (144 g/day) for 7 days. On day 7, the steers were rendered unconscious, exsanguinated and eviscerated. A 1-m section of jejunum was collected starting at the duodenojejunal flexure. Sheep were anaesthetized with pentobarbital and the second meter of small intestine (jejunum) was collected. Brush-border membrane vesicles were prepared and sodium-dependent glucose uptake activity was measured using the rapid uptake/filtration technique. Alkaline phosphatase and maltase activity was enriched by 8.2+/-0.5- and 8.4+/-1.2-fold in the vesicle preparation, respectively, and was not different between treatments. Abomasal SH increased (P=0.03) the Na/glucose co-transport approximately two-fold in both cattle (47.2-114.0+/-31.5 pmol/mgxsec) and sheep (77.4-152.0+/-25.7 pmol mg(-1) s(-1)). We conclude that Na/glucose co-transport activity by enterocytes responds to luminal alpha-linked glucose (from abomasal infusion) in ruminants, compared with controls. Intestinal maltase-specific activity does not respond to alpha-linked glucose in cattle, and decreases slightly in sheep.

Alkaline Phosphatase↗
PubMed2001

Influence of alpha-linked glucose on sodium-glucose cotransport activity along the small intestine in cattle.

Thirteen steers (378+/-23 kg) were used in a split-plot experimental design to evaluate the effect of small intestinal carbohydrate on sodium-glucose cotransport in brush border membrane vesicles prepared from five equidistant sites along the small intestine. The steers consumed 7.2+/-0.4 kg/d ground fescue hay and soybean meal-based supplement and were infused ruminally or postruminally with a partial alpha-amylase starch hydrolysate (914.5+/-8.3 g/d) for 7 d. On d 7, five equidistant 1-m small intestinal sections were harvested and frozen in liquid N for later preparation of brush-border membrane vesicles. Maltase activity of the homogenate and vesicle preparations changed (P < 0.001; lowest in the duodenum, highest in the jejunum) and alkaline phosphatase decreased (P < 0.001) along the small intestine. With respect to the original homogenates, the vesicle preparations were enriched 9.80+/-0.83- and 7.64+/-0.67-fold for alkaline phosphatase and maltase, respectively; enrichments were not different between treatments (P = 0.76 and 0.39, respectively). However, alkaline phosphatase and maltase enrichment changed (P < 0.001) along the small intestine. Recoveries of alkaline phosphatase and maltase activities (25.0+/-0.2% and 19.5+/-0.2%, respectively) in the vesicle preparation were not affected (P = 0.29 and 0.21, respectively) by treatment but changed (P < 0.001) along the intestine. Recovery of protein in the vesicle preparation was 2.60+/-0.01% and was not affected by treatment or intestinal site. Sodium-glucose cotransport activity (220+/-44 pmol x mg(-1) x s(-1)) was not affected (P = 0.34) by treatment but did change (P < 0.001; lowest in the ileum, highest in the proximal and mid-jejunum) along the small intestine. Apparent Km of the sodium-glucose cotransporter for glucose was 62.8+/-5.8 microM. The specific activity of maltase was highest in the jejunum, and sodium-glucose cotransport was highest in the first two jejunal sites. However, duodenal maltase activity was lowest and ileal sodium-glucose cotransport activity was lowest. Sodium-glucose cotransport activity may limit small intestinal starch assimilation in the distal small intestine. It does not seem that glucose arising from carbohydrate hydrolysis regulates activity of sodium-dependent glucose transport in cattle.

Alkaline Phosphatase↗
PubMed2001

Influence of pregnancy on body weight, ruminal characteristics, and visceral organ mass in beef heifers.

Crossbred heifers (initially 24 mo, approximate age and 378 +/- 32.1 kg BW) were used to evaluate the influence of pregnancy and advancing gestation on DMI, BW, carcass weight, ruminal characteristics, and visceral organ mass. Heifers (naturally serviced (n = 22; nonpregnant controls, n = 17), were grouped in common pens. Heifers were provided corn silage and hay-based diets formulated to provide 0.45 kg of ADG. Treatments were pregnancy and nonpregnancy; pregnant and nonpregnant heifers were slaughtered on d 40, 120, 200, and 270. Live weight at slaughter and BW change throughout the trial were not influenced by pregnancy (P > 0.1). Carcass weight per unit of BW was decreased due to pregnancy (P < 0.05) and an interaction was found in eviscerated BW (EvBW; P < 0.1), with the pregnant heifers having greater live weights, carcass weights, and EvBW at the d-200 slaughter period. Ruminal fluid fill and total fill (g/kg BW) declined as slaughter period advanced, resulting in the pregnant heifers having less fill at d 270 (P< 0.07). However, ME intake was not different between pregnant and nonpregnant heifers (P > 0.1) at any of the slaughter periods. Heart mass responded differently when nonpregnant and pregnant were analyzed over time and an interaction was detected as slaughter period advanced (P < 0.1). Liver, duodenum, jejunum, and large intestinal mass were not responsive to pregnancy (P > 0.1). Data indicate that ruminal fill is altered by pregnancy but visceral organ mass is not greatly changed by treatment.

Animals↗
PubMed1999

Chronic aspiration in children: evaluation of the lipid-laden macrophage index.

Chronic pulmonary aspiration (CPA) causes significant morbidity, but is underdiagnosed because of difficulties in establishing a diagnosis. The lipid-laden macrophage index (LLMI) is said to differentiate between those with and without CPA. Records of 113 patients were reviewed to determine specificity and sensitivity of the LLMI for CPA. Diagnostic accuracy was inferred from treatment outcome. Mean LLMI for aspirators was 104 +/- 62 (range, 20-233), and for nonaspirators, 44 +/- 39 (range, 0-170) (P < 0.05). Sensitivity and specificity were 0.69 and 0.79, respectively. While the LLMI provides clinically helpful information, it does not stand alone as the gold standard for the diagnosis of CPA. Failure to thrive and neurological impairment correlated with CPA, using Fisher's exact test. CPA was not diagnosed in any patient with normal growth, normal neurological development, and an LLMI <86. No other clinical observation (cough, wheeze, vomiting, difficulty feeding, choking with feeding, recurrent pneumonia, bronchopulmonary dysplasia, chronic chest X-ray changes, endotracheal tube, tracheostomy tube, nasogastric feeding tube, or transpyloric feeding tube) or diagnostic study (upper gastrointestinal series, gastroesophageal scintigraphy, modified barium swallow, or pH probe) correlated with the diagnosis of CPA.

Adolescent↗
PubMed1999

Flutter flap.

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Cost-Benefit Analysis↗
PubMed1999

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: small intestinal amino acid flow and disappearance in steers.

Six Angus steers (260+/-4 kg initial BW) fitted with ruminal, duodenal, and ileal cannulas were used in a 6 x 6 Latin square design to evaluate the effect of feeding poultry by-product meal (PBM) on small intestinal flow and disappearance of amino acids. The diets were provided at 2% of BW on a DM basis, formulated to contain 11.5% CP, and consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement on a DM basis. Supplements were formulated to contain 37% CP with sources of supplemental N being soybean meal (100% SBM) and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. Duodenal flow of all amino acids increased linearly (P < .07) as PBM increased in the diet and, except for His, increased (P < .09) for 100% PBM compared with 100% SBM. Similar results were observed for duodenal flow of nonbacterial amino acids, which linearly increased (P < .05) with PBM and were greater (P < .05) for 100% PBM than for 100% SBM. Soybean meal increased (P < .09) the duodenal flow of nonbacterial Lys compared with 0% PBM, and 0% PBM increased (P < .04) flow of Val, Ala, and Pro compared with 100% SBM. Duodenal bacterial essential, nonessential, and total amino acid flows were not affected (P > .80) by PBM; however, they were greater (P < .02) for 100% SBM than for 100% PBM. In addition, nonessential and total bacterial amino acid flows were increased (P < .06) for 100% SBM compared with 0% PBM. Small intestinal disappearance of Lys and Pro increased linearly (P < .09) as PBM increased, and 100% PBM increased (P < .07) disappearance of Arg and Ala compared with 100% SBM. Supplemental N source had no effect (P > .31) on apparent small intestinal disappearance of essential, nonessential, and total amino acids. These data suggest that when PBM, SBM, and urea were used as sources of supplemental N, the daily disappearance of amino acids from the small intestine of steer calves consuming a corn silage- and cottonseed hull-based diet was similar.

Amino Acids↗
PubMed1999

Estimating true digestibility of nonstructural carbohydrates in the small intestine of steers.

Four Angus steers (318 +/- 16 kg) fitted with ruminal, duodenal, and ileal cannulas were used in a 4 x 4 Latin square design to determine carbohydrate disappearance from the small intestine (SI). Steers were fed fescue hay at 1.8% of BW and abomasally infused with starch hydrolysate (SH) at 10, 20, or 40 g/h or glucose (G) at 30 g/h. Starch hydrolysate was raw cornstarch digested by a heat-stable alpha-amylase. Experimental periods were 10 d with 6 d of adaptation, 3 d of digesta and feces collection, and 1 d of rest. Glucose (% of infused) had greater (P < .001) apparent small intestinal and postruminal disappearance (% of infused) compared with 20 and 40 g/h SH. Starch hydrolysate infusion linearly increased (P < .001) apparent SI, large intestinal (LI), and total intestinal starch disappearance (g/d) and quadratically increased (P < .003) apparent SI and total intestinal starch disappearance (% of infused). Ileal starch flow from infusion increased quadratically (P < .03) as SH infusion increased. True SI and total intestinal starch disappearance increased linearly (P < .001; g/d) with SH infusion. However, SH infusion quadratically decreased (P < .02) efficiency of true SI starch disappearance (% of infused). True LI starch disappearance (g/d and % of infused) quadratically increased (P < .03) as SH infusion increased. These data demonstrate that, even in animals fed all-forage diets, there is a significant flow of alpha-glucosides, and these need to be considered when evaluating intestinal carbohydrate digestion.

Animals↗
PubMed1998

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: effects on performance and nutrient flow and disappearance in steers.

We conducted three studies with steers to evaluate poultry by-product meal (PBM) as a supplemental N source for ruminants. An in situ study compared the solubility, degradation rate, and ruminal escape of PBM N with blood meal (BM), corn gluten meal (CGM), and soybean meal (SBM) N. Additionally, an 84-d growth study (n = 95, 228+/-5 kg BW) and a digestion trial (6 x 6 Latin square) were conducted. The basal diet for the growth and digestion studies consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement (DM basis). Sources of supplemental N (% of total supplemental N) were 100% SBM and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. In situ ruminal escape N (25.2, 55.3, 86.7, and 98.9% for SBM, PBM, CGM, and BM, respectively) was greater (P < .05) for PBM than for SBM; however, a greater (P < .05) proportion of BM and CGM N escaped ruminal degradation compared with PBM. Dry matter intake, ADG and gain/ feed increased linearly (P < .003) as PBM increased; however, no differences (P > .48) were observed in these variables for 100% PBM compared with 100% SBM. Duodenal N flow and small intestinal N disappearance increased linearly (P < .05) as PBM increased in the diet. Bacterial N flow to the small intestine was not affected (P > .19) by treatment; however, 100% SBM decreased (P < .04) bacterial CP synthesis (g bacterial N/kg OM disappearance from the stomach) compared with 0 and 100% PBM. In vivo ruminal escape N of PBM and SBM was 40.6 and 13.7%, respectively. Ruminal NH3 N decreased linearly (P < .001) as PBM increased. These data suggest that PBM can replace SBM as a source of supplemental N for steer calves that consume a diet based on corn silage and cottonseed hulls.

Ammonia↗
PubMed1997

Effects of exogenous somatostatin and cysteamine on net nutrient flux across the portal-drained viscera and liver of sheep during intraduodenal infusion of starch hydrolysate and casein.

We used eight Polypay wethers (36 +/- .6 kg BW) fitted with hepatic portal, hepatic venous, mesenteric arterial and venous, and duodenal catheters in a crossover design experiment to determine the influence of somatostatin (SRIF) on splanchnic metabolism. Each crossover period consisted of 14 d, with net flux of nutrients and hormones (venoarterial differences x blood flow) measured on d 14. Before flux measurements, wethers received an i.v. dose (0 h) of either 0 (vehicle) or 50 mg x kg BW(-1) x 10 min(-1) cysteamine (CSH, SRIF-depleting agent) followed by a continuous duodenal infusion (h 10 to 22) of a starch hydrolysate-casein solution. Six sets of arterial, portal, and hepatic blood samples were obtained (h 12 to 16), after which a primed (10 microg), continuous jugular infusion of SRIF-14 (5.0 microg x kg BW(-1) x h(-1)) was initiated and sampling protocol repeated (h 18 to 22). Cysteamine administration increased (P < .01, vs control) portal and hepatic blood flow in the absence of exogenous SRIF (CSH x SRIF, P < .01). Net portal-drained viscera (PDV) release of glucose, alpha-amino N, ammonia N, beta-hydroxybutyrate, and oxygen consumption were decreased (P < or = .10) and lactate release increased (P = .005) during SRIF infusion. The CSH increased (P < .05) PDV release of beta-hydroxybutyrate and insulin and increased (P = .09, CSH alone vs control) net release of glucose in the absence of exogenous SRIF. Exogenous SRIF increased (P = .10) and CSH decreased (P = .09) net hepatic glucose output, whereas liver oxygen consumption was decreased (P = .04) with exogenous SRIF and increased (P = .01) with CSH. Net total splanchnic alpha-amino N release and oxygen consumption were decreased (P < .10) with exogenous SRIF, but CSH increased (P < .05) insulin release and oxygen consumption. These data provide initial evidence for a regulatory involvement of SRIF in visceral metabolism in ruminants.

3-Hydroxybutyric Acid↗
PubMed1995

Efficacy of laidlomycin propionate to reduce ruminal acidosis in cattle.

Three trials were conducted to evaluate the efficacy of laidlomycin propionate (LP) to reduce the incidence and severity of ruminal acidosis in cattle fed high-grain finishing diets. In each trial, LP was fed at 0, 6, or 12 mg/kg of diet DM. In two acidosis-challenge trials, ruminally fistulated steers were fed (DM basis) a 50% concentrate diet and then fed a 95% concentrate diet at a specific intake (2.75% BW) or steers were dosed intraruminally with a 100% concentrate diet. Laidlomycin propionate did not alter ruminal pH or total acid concentrations, but in Trial 1 the 6 mg/kg level altered (P < .10) the molar proportions of the acids, increasing total ruminal VFA and decreasing ruminal lactate. In Trial 3, a finishing trial, LP reduced (P < .10) intake day-to-day variation of individually fed steers during a 13-d adaptation period from a 65 to a 100% concentrate diet, suggesting reduced incidence of subacute acidosis. Feed intake was lower (P < .05) during the first 13 d of the trial due to LP but was not affected over the entire trial. Laidlomycin propionate improved feed efficiency (gain/feed) when calculated on a live weight basis (linear, P = .05) or carcass weight basis (linear, P = .20). Laidlomycin propionate does not prevent ruminal acidosis, but it may reduce the severity of ruminal acidosis during adaptation to a 100% concentrate diet.

Acidosis↗
PubMed1995

Adaptation to small intestinal starch assimilation and glucose transport in ruminants.

Four crossbred steers (380 +/- 6 kg) and seven Polypay wethers (40.3 +/- 6 kg) fitted with hepatic venous, hepatic portal, mesenteric venous and arterial, ruminal, and abomasal (steers) or duodenal (wethers) catheters were used in two crossover design experiments to evaluate adaptation to small intestinal starch and glucose transport. Steers were fed 8.6 kg/d and sheep were fed .9 kg/d of alfalfa hay in 12 equal portions and infused with an alpha-amylase partial starch hydrolysate (SH) either postruminally (adapted) or ruminally (unadapted) for 4 (steers; 40 g/h) or 5 (sheep; 6 g/h) days before measuring splanchnic flux of metabolites. On the day of flux measurements, ruminal SH infusion was switched to the postruminal site in unadapted animals. Flux measurements were made 3 to 6 h after switching infusion site for steers and 2 to 5 h for sheep. Phlorizin, a competitive inhibitor of Na/glucose cotransport, was then postruminally infused (550 and 500 mumol/h for steers and sheep, respectively) and flux measurements repeated from h 9 to 12 (steers) and h 7 to 10 (sheep). In the steers, adaptation increased (P < or = .09) portal-drained visceral (PDV) glucose release 26 mmol/h and decreased hepatic uptake of lactate 20 mmol/h. Abomasal infusion of phlorizin decreased (P = .01) net PDV glucose flux 40 mmol/h and concomitantly increased (P = .05) hepatic release of glucose by 47 mmol/h. In sheep, duodenal infusion of phlorizin increased (P < or = .005) portal and hepatic blood flow and decreased (P < or = .02) PDV release of glucose and lactate by 9 and .4 mmol/h, respectively. The liver released 4.2 mmol/h more (P = .09) glucose and removed 3.2 mmol/h more lactate (P = .09) glucose and removed 3.2 mmol/h more lactate (P = .001); arterial glucose decreased (P = .003) .75 mM in response to phlorizin. Phlorizin also caused loss of glucose in the urine of sheep (.09 mmol/h). Adaptation did not alter net splanchnic flux of glucose, lactate, oxygen, or alpha-amino N. These studies indicate that ruminants maintain the Na/glucose cotransporter when consuming little preformed alpha-glucosidic polymers and that the liver increases glucose release to compensate for reduced PDV delivery of glucose to maintain glucose homeostasis. In addition, the steers maintain at least 960 mmol/d and the sheep maintain at least 216 mmol/d of glucose transport capability regardless of adaptation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1994

Comparison of manual and mechanical chest percussion in hospitalized patients with cystic fibrosis.

We compared the efficacy of manual and mechanical chest percussion during hospitalization for acute exacerbations of cystic fibrosis by evaluating changes in spirometry values. Fifty-one participants were randomly assigned to receive manual or mechanical chest percussion three times a day. Twenty-two participated during one subsequent admission and were assigned to the opposite form of chest percussion. The two groups were equal in severity of illness (mean National Institutes of Health score (+/- SEM): manual = 66.7 +/- 2.2; mechanical = 35.8 +/- 2.2; p = not significant). Mean improvement in forced expiratory volume at 1 second, forced vital capacity, and forced expiratory flow between 25% and 75% of forced vital capacity (+/- SEM) for manual percussion was 32.6% +/- 7%, 27.2% +/- 5%, and 38.1% +/- 10%, and for mechanical percussion was 28.5% +/- 4%, 28.7% +/- 4%, and 25.1% +/- 8%, respectively; p = not significant. Our participants did not prefer mechanical chest percussion. Although equal efficacy of outpatient therapy remains to be proved, this study suggests that patients can be encouraged to use the form of chest percussion that they prefer.

Adolescent↗
PubMed1993

Chronic pulmonary aspiration in children.

According to established diagnostic and therapeutic guidelines for chronic pulmonary aspiration, clinical suspicion is raised by coughing and choking with feeding, coughing during sleep, recurrent pneumonia, failure to thrive, and radiologic signs of chronic lung injury. The upper gastrointestinal series accurately defines anatomy and function, can differentiate between direct and reflux aspiration, and identifies conditions that predispose to aspiration. Gastroesophageal scintigraphy lacks anatomic detail but increases observation time, may differentiate between direct and reflux aspiration, and identifies delayed gastric emptying and gastroesophageal reflux. The lipid-laden macrophage index improves identification of aspiration, but cannot differentiate between direct and reflux aspiration. The esophageal pH probe identifies gastroesophageal reflux. Treatment options include medical therapy (thickened feedings, prone positioning, and metoclopramide) and surgical intervention (gastrostomy, fundoplication, and definitive correction of predisposing conditions). Therapy is determined by severity of illness and results of diagnostic evaluation.

Bethanechol↗
PubMed1993

Fetal lung epithelial cells contain two populations of amiloride-sensitive Na+ channels.

Active Na+ transport by the alveolar epithelium plays a major role in reabsorption of the fetal lung fluid after birth. We characterized the biochemical and physiological characteristics of Na+ conductive pathways in distal fetal lung epithelial (FLE) cells isolated from 20-day-old rat fetuses. We demonstrated that a polyclonal antibody to Na+ channel protein (NaAb) binds to the plasma membranes of FLE cells. In Western blot studies, this NaAb and an anti-idiotypic monoclonal antibody to the amiloride-binding subunit of the Na+ channel protein recognized 150- and 90-kDa polypeptides in plasma membrane vesicles of FLE. 22Na+ flux measurements across plasma membrane vesicles of FLE revealed the existence of electrogenic Na+ transport, which was twice as high as the corresponding adult value. One hundred micromolars of amiloride, benzamil, and 5-(N-ethyl-N-isopropyl)-2'-4'-amiloride inhibited 30, 40, and 70% of the electrogenic Na+ transport across plasma membrane vesicles of FLE cells, respectively. The half-maximum inhibition of electrogenic Na+ transport by these substances occurred between 0.3 and 1 microM. [3H]benzamil equilibrium binding studies in membrane vesicles of FLE cells revealed the existence of two binding sites that had dissociation constant values of 19 and 1,525 nM, respectively. These data indicate the presence of both high- and low-amiloride affinity Na+ conductive pathways (channels) in FLE cells.

Amiloride↗