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Biomedical subjects

L A Wade

Publications and source records attributed to L A Wade.

8 recordsLinked to original sources
PubMed1995

Implementing a parent-present induction program.

One of the greatest fears of children undergoing surgery is separation from their parents. Children for whom preoperative sedation is contraindicated often endure the distress of this separation and the beginning of anesthesia surrounded by masked strangers. Those who receive sedation often experience the invasiveness of a medication administered rectally or intramuscularly or the insertion of an IV line. Until recently, the doors to the operating room remained closed to family members. Like other hospitals throughout the country, however, Children's Hospital in Boston has responded to the concerns of parents and staff members by implementing a parent-present anesthesia induction program. As a result, the surgical experience for many children and families has changed significantly for the better.

Anesthesia↗
PubMed1984

A quantitative study of intramembrane changes during cell junctional breakdown in the dystrophic rat retinal pigment epithelium.

Previous electron microscope freeze-fracture and tracer studies have revealed that intercellular junctions in the retinal pigment epithelium (RPE) of Royal College of Surgeons (RCS) rats with inherited retinal dystrophy [5] break down between three and six postnatal weeks [6, 7]. In this study quantitative computer techniques were used to analyze the freeze-fracture changes in the dystrophic RPE. The following parameters were measured: length of tight junctional strands/micron2; number of tight junctional strand anastomoses/micron2; number of gap junctional aggregates/micron2; area of gap junctional aggregates/micron2; and density of background intramembrane particles/micron2. At three postnatal weeks, the dystrophic junctional complex membrane is similar to normal, but at 10 weeks and later there are dramatic decreases in tight junctional strand length/micron2 and number of anastomoses/micron2, as well as in the number/micron2 and area of gap junctions/micron2, while the density of background particles/micron2 is dramatically increased. Correlational analysis revealed that changes in gap and tight junctions were significantly related to each other and to the increase in background particle density. The diameter of background particles within the normal and post-breakdown dystrophic junctions was measured in order to see whether the dispersal of gap and tight junctional particles (8-10 nm) into the surrounding membrane contributes to the increased particle density. These measures showed that background particles in all size ranges were more numerous in the dystrophic RPE, but that the largest increase was in the smallest diameter particles (6-7 nm). Thus, while gap and tight junctional sized particles contribute to the increase, particles from other sources may also be involved. Particle density of apical and basal membranes in the normal and in the 10 week and older dystrophic RPE was analyzed to study the effects of tight junctional breakdown on the distribution of intramembrane particles. These measures showed that particle density was greater basally than apically in the normal RPE and that particle density in both membranes decreased slightly in the dystrophic RPE, but that their ratio remained unchanged. It has been shown previously that even a single intact tight junctional strand is sufficient to maintain differences in particle density between apical and basal surfaces [14, 15] and in the majority of abnormal dystrophic junctional complexes at least one tight junctional strand remains intact.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Blood-brain barrier transport of basic amino acids is selectively inhibited at low pH.

The transport of amino acids across the blood-brain barrier was measured with the single-pass carotid injection method. The pH of the injected bolus varied between 4.5 and 8.5. Arginine and lysine uptakes were inhibited 24% at pH 5.5 and 59% at pH 4.5. The uptakes of 2-aminobicyclo (2,2,1) heptane-2-carboxylic acid and phenylalanine were unaffected at this pH. There were also no changes observed in choline, glucose, or butanol transport. The Ki of arginine transport inhibition by H+ was 2.4 +/- 0.5 microM; i.e., pH 5.6 +/- 0.1. No change with pH occurred in the Km of arginine transport, while a significant decrease (p less than 0.01) was observed in the Vmax (10.2 +/- 2.3 nmol min-1 g-1 and 5.6 +/- 2.3 nmol min-1 g-1 at pH 7.5 and pH 5.5, respectively). This noncompetitive inhibition was found to be transient as arginine uptake at pH 7.5; it was measured by carotid injection 30 sec following a previous bolus which was buffered to pH 4.5, and was not significantly different from the control. This selective inhibition of the blood-brain barrier basic amino acid carrier demonstrates the advantage of the carotid injection approach in exposing the capillary exchange site to extreme alterations in chemical composition which could not be tolerated systemically.

Amino Acids↗
PubMed1981

Osmotically induced increase in cerebrovascular permeability to [3H]sucrose.

The effect of an intracarotid infusion of a 5 M urea solution on the blood--brain barrier of the rat was measured using the carotid injection technique. The urea infusion increased the amount of sucrose penetrating the barrier. This increased uptake of sucrose was first seen 10--25 sec after the 15 sec urea infusion. By 10 min, sucrose uptake had decreased in some animals.

Animals↗
PubMed1981

Cysteine and cystine transport at the blood-brain barrier.

The nature of cysteine and cystine uptake from the cerebral capillary lumen was studied in the rat using the carotid injection technique, [35S]-Cysteine uptake was readily inhibited by the synthetic amino acid 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid (BCH), the defining substrate for the leucine-preferring (L) system in the Ehrlich ascites cell. The addition of nonradioactive alanine or serine, representatives of the alanine, serine, and cysteine-preferring (ASC) system, produced no significant decrease in the uptake of cysteine after cysteine transport by the L system was blocked with BCH. This indicated that the major component of cysteine's transport from the brain capillary lumen was by the L system with no detectable uptake of cysteine by the ASC system. No carrier-mediated transport of cystine, the disulfide form of the amino acid, was detected, nor was there any inhibition by cystine of the transport of the neutral amino acid methionine or the basic amino acid arginine. These results suggest that the ASC system, if present, is not quantitatively important for the transport of neutral amino acids from the brain capillary lumen.

Amino Acids↗
PubMed1975

Rat brain regional uptake and decarboxylation of L-DOPA following carotid injection.

Using the carotid injection technique, the regional uptake and decarboxylation of L-DOPA at the blood-brain barrier in the rat was studied. After a single intracarotid injection in the rat followed by decapitation 15 S later, the uptake of L-DOPA was measured relative to tritiated water injected simultaneously as a diffusible internal standard. Decarboxylation was investigated with an injection mixture of L-[carboxy-14C]DOPA and L-[2,3-3H]DOPA. Uptake of L-DOPA studied over the range of 15-5,076 nmol/ml appeared to be a composite of two separate mechanisms. The saturable component had a half-maximal velocity transport value, K-t, of 336 muG. A diffusional, nonsaturable component had a diffusion constant of 0.018. A regional study showed that uptake operated at approximately the same rate in the various brain areas despite marked regional variation in catecholamine concentration. The decarboxylation of L-DOPA also occurred at a similar rate in all regions. Even when L-DOPA was injected at a concentration of 3 mM, 33-51% was decarboxylated within the 15-S period. These results support the hypothesis that L-DOPA movement into the brain occures via a neutral amino acid transport mechanism common to cerebral capillaries of different regions of the brain.

Animals↗