Regional alveolar hypoxia does not affect air embolism-induced pulmonary edema

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema resulting from venous air embolization. Anesthetized dogs had the left upper lobe removed and a double-lumen tube placed so that right lung and left lower lobe (LLL) could be ventilated independently. Air was infused into the femoral vein for 1 h during bilateral ventilation at an inspiratory O2 fraction (FIO2) of 1.0. After cessation of air infusion the LLL was then ventilated with a hypoxic gas mixture (FIO2 = 0.05) in six animals and an FIO2 of 1.0 in six other animals. Lung hydroxyproline content was measured as an index of lung dry weight. LLL bloodless lobar wet weight-to-hydroxyproline ratio was 0.33 +/- 0.06 mg/micrograms in the animals exposed to LLL hypoxia and 0.37 +/- 0.03 mg/micrograms (NS) in the animals that had a LLL FIO2 of 1. Both values were significantly higher than our laboratory normal values of 0.19 +/- 0.01 mg/micrograms. We subsequently found in four more dogs exposed to global alveolar hypoxia before and after air embolism that the air injury itself significantly depressed the hypoxic vasoconstrictor response. We conclude that regional alveolar hypoxia has no effect on pulmonary edema formation due to air embolism. The most likely reason for these findings is that the air embolism injury itself interfered with hypoxic pulmonary vasoconstriction.     

Autolytic enzyme system of Streptococcus faecalis. V. Nature of the autolysin-cell wall complex and its relationship to properties of the autolytic enzyme of Streptococcus faecalis

Cell walls from exponential-phase cultures of Streptococcus faecalis ATCC 9790 contain an autolysin (a beta-N-acetylmuramide glycanhydrolase, E.C. 3.2.1.17) which has been isolated from trypsin-speeded wall autolysates. The autolysin, which was excluded from Bio-Gel P-60, was further fractionated by diethylaminoethyl (DEAE)-cellulose chromatography or filtration on Bio-Gel P-200. After DEAE-cellulose chromatography, which removed most of the wall polysaccharide, autolysin activity was extremely labile and was rapidly lost at -20 C, even in the presence of albumin. The P-60-excluded enzyme was rapidly bound by walls at both 37 C (50% bound in about 1 min) and 0 C (50% bound in less than 4 min). Wall-bound autolysin could not be removed by 1.0 m ammonium acetate (pH 6.9). Autolysin was also bound by walls that had been extracted with 10% trichloroacetic acid or treated with 0.01 n periodate, suggesting that the nonpeptidoglycan wall polymers are not important for binding. Wall-bound autolysin was more stable than the soluble enzyme to proteinase digestion, acetone (40%), 8 m urea (at 0 C), or to inactivation at 56 C. Two bacterial neutral proteinases (which do not hydrolyze ester bonds) activated latent wall-bound autolysin, suggesting that activation results from the cleavage of one or more peptide bonds. The group A streptococcal proteinase activated latent autolysin but differed from the other proteinases in that it did not inactivate soluble autolysin. The results suggest that the autolysin is not covalently linked to the wall. The high affinity of the walls for the autolysin appears to be responsible for the firm, not easily reversed binding.     

Extracellular fluid volume during pneumothorax and hypoxemia in rabbits

This study was designed to test the hypothesis that persistent pneumothorax of greater than or equal to 6 days duration causes a decrease of extracellular fluid volume (ECF). Such changes are of interest as they may be causally related to persistent hypotension that has occurred in humans following pneumothorax evacuation. Experiments were done in rabbits to determine the effect on ECF of persistent pneumothorax with or without systemic hypoxemia. Animals were divided into four treatment groups: 1) pneumothorax with hypoxemia [fractional concentration of O2 in inspired gas (FIO2) = 0.21, n = 30], 2) pneumothorax without hypoxemia (FIO2 = 0.40, n = 25), 3) hypoxemia alone (FIO2 = 0.14, n = 11), and 4) normal controls (FIO2 = 0.21, n = 15). Measurements of ECF were made in the base-line control state and after 6 days of treatment using the dilution volume of thiocyanate sodium as an estimate of ECF volume. We found a reduction of ECF in 53% of animals with pneumothorax plus hypoxemia (range -47% to +13%) and in 54% of animals with hypoxemia alone (range -26% to +25%). ECF declined in only 7% of normal controls and 20% of animals with pneumothorax without hypoxemia. Arterial O2 tensions after 6 days of treatment were 58 +/- 12.6, 141 +/- 28, 60 +/- 5.1, and 97 +/- 9.3 Torr (mean +/- SD) in groups 1-4, respectively. The results suggest that pneumothorax with hypoxemia or hypoxemia alone may contribute to depletion of ECF, but this response is variable and unpredictable in individual animals.     

Location of a protein of the fodrin-spectrin-TW260/240 family in the mouse intestinal brush border

We have determined that a protein of the fodrin-spectrin-TW260/240 (FST) family is a component of the thin fibrils (～5 nm wide, 100–200 nm long) that cross-link bundles of actin filaments to adjacent actin bundles and to the plasma membrane in the terminal web of the brush border of the intestinal epithelium. When isolated brush borders were incubated with anti-fodrin antibodies and prepared for electron microscopy by the quick-freeze, deepetch technique, these ～5 nm fibrils were specifically decorated with the antibody. In addition, these cross-linking fibrils disappeared when the anti-fodrin-reactive proteins were extracted from the brush border. We conclude that FST is a component of a cross-linking system composed of ～5 nm fibrils that are morphologically distinct from the ～8 nm myosin-containing fibrils which were identified by antimyosin decoration. In addition to linking actin bundles to adjacent actin bundles and to the plasma membrane, these FST fibrils may mediate actinvesicle, actin-intermediate filament and vesicle-plasma membrane linkages.     

Oxalate uptake by everted sacs of rat colon. Regional differences and the effects of pH and ricinoleic acid

Hyperoxaluria is a complication of disorders associated with steatorrhea. The colon is the presumed site of enhanced oxalate absorption in patients with steatorrhea. We performed studies of colonic mucosal oxalate uptake in everted sacs of rat colon to determine the kinetics of colonic oxalate transport and to evaluate the effect of both pH and ricinoleic acid, a hydroxy fatty acid, on colonic oxalate uptake. Our study demonstrated that oxalate is transported throughout the colon by passive diffusion. Tissue uptake increased linearly with increasing oxalate concentrations and was unaffected by metabolic inhibitors, oxygen deprivation, or temperature changes. There were pH-dependent regional differences of oxalate uptake both in the presence and absence of ricinoleic acid. In the absence of ricinoleic acid, the highest oxalate uptake occurred at the lower pH values (5.4 and 6.4). In the presence of ricinoleic acid oxalate uptake was enhanced at the higher pH values (7.4 and 8.4); a finding most likely related to decreased solubility of ricinoleic acid at pH 5.4 and 6.4. Intraluminal pH is an important determinant of colonic oxalate uptake in the presence and absence of ricinoleic acid.     

On the role of fibronectin during the compaction stage of somitogenesis in the chick embryo

During the early stages of somitogenesis in the chick embryo the presomitic cells in the segmental plate undergo compaction. The aggregation of segmental plate cells is stimulated by fibronectin. The stimulation of segmental plate cells to aggregate and undergo compaction can be effected in isolated segmental plate cells, in isolated segmental plates, and in intact embryos removed from the yolk. The fact that the segmental plate cells react with greater vigor to cellular fibronectin than to plasma fibronectin suggests a specific molecular mechanism in the initiation of somitogenesis.     

Effect of regional alveolar hypoxia on permeability pulmonary edema formation in dogs

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.     

Hypoxic pulmonary vasoconstriction does not affect hydrostatic pulmonary edema formation

We studied the effects of regional hypoxic pulmonary vasoconstriction (HPV) on lobar flow diversion in the presence of hydrostatic pulmonary edema. Ten anesthetized dogs with the left lower lobe (LLL) suspended in a net for continuous weighing were ventilated with a bronchial divider so the LLL could be ventilated with either 100% O2 or a hypoxic gas mixture (90% N2-5% CO2-5% O2). A balloon was inflated in the left atrium until hydrostatic pulmonary edema occurred, as evidenced by a continuous increase in LLL weight. Left lower lobe flow (QLLL) was measured by electromagnetic flow meter and cardiac output (QT) by thermal dilution. At a left atrial pressure of 30 +/- 5 mmHg, ventilation of the LLL with the hypoxic gas mixture caused QLLL/QT to decrease from 17 +/- 4 to 11 +/- 3% (P less than 0.05), pulmonary arterial pressure to increase from 35 +/- 5 to 37 +/- 6 mmHg (P less than 0.05), and no significant change in rate of LLL weight gain. Gravimetric confirmation of our results was provided by experiments in four animals where the LLL was ventilated with an hypoxic gas mixture for 2 h while the right lung was ventilated with 100% O2. In these animals there was no difference in bloodless lung water between the LLL and right lower lobe. We conclude that in the presence of left atrial pressures high enough to cause hydrostatic pulmonary edema, HPV causes significant flow diversion from an hypoxic lobe but the decrease in flow does not affect edema formation.