Changes in left ventricular geometry during spontaneous breathing

The purpose of these experiments was to determine the effects of a spontaneously generated inspiration on the size and shape of the left ventricle (LV) in anesthetized supine dogs. We implanted markers in the LV to establish three perpendicular axes and recorded the motion of these markers using biplane cinefluoroscopy at 60 Hz. The primary changes in LV size that accompanied inspiration occurred at end diastole (ED). The largest change in LVED dimension was a 2.46-mm narrowing of the septal-lateral wall dimension, but the apex-base dimension decreased also, by 0.74 mm. The anteroposterior dimension actually widened by 1.07 mm. The septal-lateral narrowing was caused by both a 1.0-mm narrowing of the distance between the septal marker and the apex-base axis, as well as by a 1.4-mm narrowing between the apex-base axis and the lateral wall marker. Narrowing of the septal portion seemed expected because of presumed enhanced right ventricular filling during inspiration. Narrowing of the lateral portion of the LV, while the anteroposterior dimension widened, was surprising because a change in LVEDV shape is implied. Assuming ventricular homogeneity, this change in LVED shape implies that the forces applied to the epicardial surface were not uniform. There must have been a retraction on the anterior and posterior surface that was not experienced by the lateral LV wall. The net effect of these dimensional changes of the LV at end diastole (estimated from the product of the three ED axes) was a 3.5-cm3 reduction in LVED volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Altered lipid synthesis in type II pneumonocytes exposed to lung surfactant.

When type II pneumonocytes were exposed to purified lung surfactant that contained 1-palmitoyl-2-[3H]palmitoyl-glycero-3-phosphocholine, radiolabelled surfactant was apparently taken up by the cells since it could not be removed by either repeated washing or exchange with non-radiolabelled surfactant, but was released when the cells were lysed. After 4 h of exposure to [3H]surfactant, more than half of the 3H within cells remained in disaturated phosphatidylcholine. Incorporation of [3H]choline, [14C]palmitate and [14C]acetate into glycerophospholipids was decreased in type II cells exposed to surfactant and this inhibition, like surfactant uptake, was half-maximal when the extracellular concentration of surfactant was approx. 0.1 mumol of lipid P/ml. Inhibition of incorporation of radiolabelled precursors by surfactant occurred rapidly and reversibly and was not due solely to dilution of the specific radioactivity of intracellular precursors. Activity of dihydroxyacetone-phosphate acyltransferase, but not glycerol-3-phosphate acyltransferase, was decreased in type II cells exposed to surfactant and this was reflected by a decrease in the 14C/3H ratio of total lipids synthesized when cells incubated with [U-14C]glycerol and [2-3H]glycerol were exposed to surfactant. Phosphatidylcholine, phosphatidylglycerol and cholesterol, either individually or mixed in the molar ratio found in surfactant, did not mimic purified surfactant in the inhibition of glycerophospholipid synthesis. In contrast, an apoprotein fraction isolated from surfactant inhibited greatly the incorporation of [3H]choline into lipids and this inhibitory activity was labile to heat and to trypsin. It is concluded that the apparent uptake of surfactant by type II cells in vitro is accompanied by an inhibition of glycerophospholipid synthesis via a mechanism that involves a surfactant apoprotein.     

The influence of myo-inositol on phosphatidylglycerol synthesis by rat type II pneumonocytes.

Type II pneumonocytes isolated from adult rat lung were incubated in a serum-free medium containing [14C]glycerol and the incorporation of 14C into glycerophospholipids was measured. After 24 h, more than 80% of the 14C incorporated into total lipids or into phosphatidylcholine and approx. 90% of the 14C incorporated into phosphatidylglycerol after 24 h was recovered in the glycerophosphoester moieties of these molecules. Supplementation of the incubation medium with foetal-bovine serum (10%, v/v) did not alter the incorporation of [14C]glycerol by type II pneumonocytes after 24 h into either a total lipid extract or phosphatidylcholine. In the presence of foetal-bovine serum, however, the incorporation of 14C into phosphatidylglycerol was decreased and the incorporation of 14C into phosphatidylinositol was increased. In the absence of foetal-bovine serum, the incorporation of 14C into phosphatidylglycerol was decreased progressively as the concentration of myo-inositol in the incubation medium was increased. The range of concentration (0.04-0.50 mM) over which myo-inositol had the greatest influence on [14C]glycerol incorporation into phosphatidylglycerol by type II pneumonocytes in vitro encompassed the concentration range measured in foetal-rat serum late in gestation. At 4 days before birth, the concentration of myo-inositol in foetal-rat serum was 0.36 mM and decreased to 0.23 mM 1 day before birth. The concentration of myo-inositol in adult rat serum increased from 0.03 mM to 0.06 mM during pregnancy. Isolated rat type II pneumonocytes were found to take up myo-inositol by a saturable process. A half-maximal rate of myo-inositol uptake occurred at a concentration of myo-inositol of 0.29 mM. The results of this investigation are consistent with the hypothesis that late in gestation there is a decreasing availability of myo-inositol to the foetal lungs and that this favours the biosynthesis of phosphatidylglycerol for surfactant at the expense of phosphatidylinositol biosynthesis.     

Radioimmunoassay of human plasma corticosterone: method, measurement of episodic secretion and adrenal suppression and stimulation

A radioimmunoassay for human plasma corticosterone has been developed. Antisera were obtained by immunizing rabbits with corticosterone-21-hemisuccinate-BSA. An antiserum titer of 1:4000 was used for standard curves ranging from 0–1000 pg. Interfering steroids were removed from plasma extracts by paper chromatography. Plasma blanks obtained from adrenalectomized or Addisonian patients ranged from 29 to 42 ng/dl. Recovery of radioactive corticosterone through the entire method was 67.6 ± 5.2%. The coefficient of variation within assays was 19% and between assays 13%. The average 8 a.m. value in males was 396 ± 228 ng/dl and in females it was 655 ± 271 ng/dl. Corticosterone was found to be secreted episodically, in parallel with cortisol. Secretion of this steroid was suppressed by dexamethasone and stimulated by ACTH infusion.     

The snapping strength of the egg shells of various orders of birds

A study of the snapping strength (S) of egg shells and its relationship to the square of the thickness (T²) has been made on seven orders of birds and also in respect of a few shells of ratite birds, domestic fowl and guinea fowl.
There are considerable differences in strength between the egg shells of different orders of birds and when shells are snapped outwards the egg shells of Sphenisciformes are almost twice as strong as those of Podicipitiformes for a given thickness. The shells of the guinea fowl are very strong and those of the domestic fowl weak compared with the seven orders when they are snapped inwards.
Comparisons of the strength of shells with and without the outside chalky cover, which occurs on the egg shells of Sphenisciformes, Pelecaniformes and Podicipitiformes, show very variable relationships, while comparisons of inward and outward snapping strength indicate that in some orders the difference is great but that in others it is negligible.
The presence or absence of a cover on the shell could not explain any difference in snapping strength, nevertheless, a few tests on Pelecanus shells using impact strength showed that then the cover adds considerably to the strength. No other shell characteristics could explain the differences in snapping strength.     

Plasma 11-Hydroxycorticoid Levels after Carbenoxolone Sodium

A definite rise in plasma 11-hydroxycorticoid levels has been shown in eight patients with duodenal ulcer following the oral administration of carbenoxolone sodium. A similar rise was seen in one patient with sarcoidosis whose pituitary A.C.T.H. secretion had been acutely suppressed with dexamethasone. No such rise, however, was seen in three patients suffering from adrenal insufficiency. It is suggested that carbenoxolone acts directly on the adrenal cortex, causing an increased production of corticosteroids.