HS Infusion Research Articles

Oriented crystal particles of semiconductor PbS on Langmuir monolayer surfaces

Oriented PbS crystal particles have been prepared by the infusion of H2S onto Langmuir monolayers of arachidic acid (AA), [CH3(CH2)18COOH]. The morphology and crystallographic orientation of PbS crystals have been determined by transmission electron microscopy/electron diffraction (TEM/ED) and atomic force microscopy (AFM). Two related morphological types of platelike crystals with narrow size distributions were observed: right-angle and equilateral triangular particles with their [100] and [111] axes perpendicular to the monolayer surface, respectively. The crystallographic relations between PbS and their organic templates were elucidated. Optical spectra and AFM images provided evidence for the formation of one-dimensional quantum-confined semiconductor crystals at the early stages of growth.

Preparation‐dependent rectification behavior of lead sulfide particulate films

Semiconductor particulate films, exhibiting either p‐type or n‐type behavior, have been produced by varying the synthetic method. Infusion of NH3 into arachidic acid (AA) monolayers floating on an aqueous solution of Pb(NO3)2 and CS(NH 2)2 results in p‐type films while the infusion of H2S into AA monolayers on aqqueous Pb(NO3)2 results in n‐type films. The preparation and characterization of the films are described.

Size-quantized semiconductor particles formed at monolayer surfaces

Infusion of H2S onto cadmium arachidate, zinc arachidate, or metal-ion-coated poly(styrenephosphonate diethyl ester) monolayers resulted in the formation of size-quantized semiconductor particles which could be transferred, essentially intact, to solid substrates at different stages of their growth; scanning tunnelling microscopy, transmission electron microscopy, and absorption spectrophotometry established the initial formation of 25–30 A diameter particles which aligned themselves and grew laterally to linked, 50–100 A diameter, 20–30 A thick, disk-shaped polyparticles.

Osmotically released vasopressin augments cardiopulmonary reflex inhibition of the circulation.

Exogenous arginine vasopressin (AVP) has been shown to augment the inhibitory influence of arterial and cardiopulmonary baroreflexes. This study examined the influence of osmotically released AVP on the inhibitory responses to activation of cardiopulmonary receptors by administration of veratrum alkaloids. Three groups of conscious dogs, with carotid sinus intact, with prior sinoaortic denervation (SAD), and with prior lesion of the area postrema (AP), were instrumented for monitoring arterial pressure and heart rate and with left circumflex coronary artery or left atrial catheters for administration of veratrum alkaloids. Conscious dogs were administered veratridine (0.5-1.0 microgram.kg-1.min-1) under control conditions, after infusion of hypertonic saline (HS, 6% NaCl), and after HS in the presence of the AVP vascular (V1) receptor antagonist. In carotid sinus-intact dogs, veratridine reduced arterial pressure (-10 +/- 0.4 mmHg). After HS infusion, the depressor response to veratridine was significantly greater (-18 +/- 0.8 mmHg). The enhanced depressor response during HS infusion was prevented by administration of the AVP antagonist (-8 +/- 0.6 mmHg). Responses to veratrum alkaloids in SAD dogs were similar. In AP-lesioned animals, the depressor effects of veratridine (-9 +/- 0.5 mmHg) were similar to intact animals. However, the response to veratridine during HS was not altered (-9 +/- 0.8 mmHg) in AP-lesioned dogs. Results suggest that osmotically stimulated AVP augments the inhibitory effects of cardiopulmonary reflexes and that this effect is mediated through the area postrema via the V1 receptor.

Maternal fetal osmolar homeostasis: fetal posterior pituitary autonomy.

Summary: After the infusion of a bolus of 225 mEq NaCl (HS) to maternal ewes, we studied fetal plasma sodium, osmolality, total serum solids, plasma arginine vasopressin (AVP) and plasma renin activity (PRA) responses in 16 chronically catheterized, 112–139 days of gestation fetal lambs. To examine the degree to which this might have represented transplacental passage of AVP, we infused a large amount of synthetic AVP into the fetal circulation (protocol 3) and detected no change in maternal plasma AVP. The protocol was designed to allow multiple, frequent blood sampling not possible by infusing the synthetic AVP into the maternal circulation. In order to compare the fetal AVP response elicited by HS in the maternal ewe and that after direct HS into the newborn lamb and fetus, we calculated stimulus response ratio (SRR) as: Log (AVP)1 - Log (AVP)2, divided by Δosmolality. The SRR of lamb fetuses after maternal HS was significantly greater (0.16 ± 0.02) than that after direct fetal HS (0.04 ± 0.01). In comparison, the newborn lamb has a SRR of 0.02 ± 0.01, and the ewe has a SRR of 0.02 ± 0.01 after HS. These data suggest that after maternal HS infusion, both a volume and, to a lesser extent, an osmolar stimulus for AVP secretion occurs after an induced water flux from the fetal to maternal compartments. Maternal plasma sodium concentration rose promptly from a base line of 146 ± 2.2 (mean ± SEM) to 157 ± 2.8 mEq/liter by 1–20 min where it remained throughout the hour observation period. Fetal plasma sodium concentration rose more slowly from base line of 143 ± 1.8 to 149 ± 1.8 mEq/liter by 1 hr. When 85 mCi22Na was additionally infused with the HS, fetal 22Na constituted only 10% of maternal 22Na counts by the end of 1 hr. During the same period fetal PRA rose from a base line of 12.9 ± 3.8 to 32.0 ± 3.6 ng/ml/hr, while maternal renin remained unchanged. Maternal AVP rose modestly, 11 min after the HS, but promptly returned to base line. There was a rapid and sustained rise by fetal AVP from a base line of 0.7 μU/ml to a peak of 8.2 μU/ml by 22 min post HS. A fetal SRR, Log (AVP)1-Log (AVP)2/Δosmolality after maternal HS was greater than that after direct fetal HS or HS to the ewe or newborn lamb. In an additional experiment, using five chronically catheterized fetuses, 10 million μU AVP injected in the fetal circulation failed to produce an increase in maternal AVP. These results demonstrate that: 1) AVP does not cross the placenta; 2) the fetal sheep neurohypophysis is autonomous and responsive to both direct and indirect (maternal) osmolar stimulation; and 3) the relatively slow rate of maternal to fetal sodium transfer, the augmented SRR after maternal HS, and the elevated fetal PRA and AVP concentration suggest that there is a rapid fetal to maternal flow of water after maternal HS and a combined volume and osmolar stimulus to the fetus. Speculation: Infusions of hypertonic saline in pregnant ewes resulted in rapid increases of fetal plasma sodium due to transfer of water from fetus to mother. A marked rise in fetal renin activity and AVP was also observed. The increase in AVP exceeded that seen in the mother and that produced by infusing hypertonic saline in the fetus. Fetal secretion of AVP is stimulated by hyperosmolality and volume contraction. Elevated AVP may help the fetal kidney retain water and, thereby, minimize hypotonic urine formation and volume depletion.