Peer interviewing: sharing the selection process.
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Child↗
Biomedical subjects
L Eckstein
Publications and source records attributed to L Eckstein.
Heat stress and thermal dehydration: lactacidemia and plasma volume regulation.
This investigation was undertaken to study heat stress and dehydration effects on 1) plasma lactic acid (LA) concentration and 2) plasma LA effect on plasma volume conservation during thermal dehydration. Experiments were performed on conscious nonacclimated and heat-acclimated laboratory rats subjected to various levels of heat stress and/or dehydration (37-42 degrees C with and without drinking water). During the exposures, rectal temperature (Tre), plasma LA pyruvic acids, and hematocrit were measured. From these data, excess LA, indicative of anaerobic metabolism, was calculated. In separate experiments, transvascular protein efflux (half time of Evans blue-labeled albumin) was measured before and after plasma LA elevation, either by LA infusion or thermal dehydration. The results show that elevation of plasma LA was associated with a rise in Tre, with accelerated elevation within a Tre range of 41-42 degrees C. LA concentrations were similar for the same Tre in all experimental groups. In nonacclimated rats, this rise was accompanied by a significant rise in excess LA. In acclimated rats, only a minor rise in excess LA was observed. A positive correlation was found between plasma LA elevation and the increase in plasma protein efflux. It is concluded that there is a temperature threshold for the rise in plasma LA. In nonacclimated rats, local hypoxia may contribute to this rise. The data also suggest that, in nonacclimated rats, lactacidemia accelerates plasma protein and fluid loss, leading to circulatory failure during acute thermal dehydration.
Acclimatization↗
Proteolytic enzymes in human fetal membranes and amniotic fluid. A comparison of normal and premature ruptured membranes.
The amniotic and chorionic membranes obtained at term and term amniotic fluid contain a soluble protease activity which cleaves [14C]-labeled globin at acid pH. In contrast, a salt extract of the pellet fraction obtained from the fetal membranes displays only negligible protease activities at the pH range of 4-8. Specific activities of the proteases in the soluble and salt-extractable fractions of fetal membranes which were intact before onset of labor were not significantly different from the respective activities in cases of premature rupture of fetal membranes (PROM). However, the protease activity of the amniotic fluid was found to increase with advancing gestational age and to reach maximal activity at term. A heat-sensitive and nondializable protease inhibitory activity was found in term amniotic fluid. This inhibitory activity acted on the cytosolic protease of amniotic membranes from control and PROM cases, but not on the soluble protease of chorionic membranes, and had a similar potency in fluids from PROM cases or fluids collected at term. These results do not support a role for fetal membrane proteases, amniotic fluid proteases, or amniotic fluid protease inhibitory activities in the etiology of PROM. However, the observed changes in amniotic fluid protease activity with fetal age suggest a physiological role for the enzyme in normal fetal development.
Amniotic Fluid↗
The mechanism of alpha-adrenergic inhibition of catecholamine release.
1 The effect of alpha-adrenoceptor agonists on membrane adenosine triphosphatase (ATPase) activity was studied in membranes from the bovine adrenal medulla and the rat submaxillary gland. 2 alpha-Adrenoceptor agonists (10(-7) to 10(-5) M) enhanced significantly Na,K-ATPase activity but not Mg-ATPase activity in adrenal medulla. This effect was not observed in membranes from phaeochromyocytoma. Phenylephrine (10(-5) M), naphazoline (10(-5) M) and clonidine (10(-5) M) caused a significant increase of the activity of Na,K-ATPase (but not of Mg-ATPase) in the submaxillary gland. The enhancement became more prominent after ligature of the submaxillary duct but disappeared completely after superior cervical ganglionectomy. Thus, the effect of the alpha-adrenoceptor agonists was due to an action on adrenergic nerve terminals in the submaxillary gland. 3 Phenylephrine and naphazoline did not affect 45Ca uptake but enhanced the rate of 45Ca efflux from adrenal medullary slices in vitro. 4 Phenylephrine enhanced the rate of 45Ca efflux from slices of submaxillary gland (with previous ligation of the duct); this was blocked by phentolamine and sympathetic denervation. Therefore phenylephrine was acting on the adrenergic nerve terminals. 5 It is suggested that the inhibition by alpha-adrenoceptor agonists of the exocytotic release of catecholamines from adrenergic nerve terminals and from chromaffin cells may be due to activation of the sodium pump, which results in enhancement of calcium efflux, causing a reduction of free intracellular Ca2+.
Adrenal Gland Neoplasms↗