Date of Award

1985

Document Type

Dissertation - Restricted

Degree Name

Doctor of Philosophy (PhD)

Department

Biomedical Engineering

First Advisor

Smith, George

Second Advisor

Myklebust, Joel B.

Third Advisor

Ackmann, James J.

Abstract

It is generally accepted that Sodium (Na+) in vascular muscle exists not only in a dissolved, osmotically active form, but also in a bound, osmotically inactive, form, presumably associated with the extracellular space (ECS). Although there have been attempts to define it with static studies, investigators have not yet explicitly incorporated the bound Na+ fraction into a kinetic model. A four-compartment (bound extracellular, dissolved extracellular, dissolved intracellular, dissolved subcellular) model consonant with the bound Na+ concept was developed to represent distribution of Na+ in vascular muscle. In vitro washouts of rat aorta segments were performed after incubation in 22Na+. A nonlinear least-squares multiexponential fit to each tracer washout curve was obtained. The multiexponential description having as parameters means of parameters of individual multiexponential fits was used to generate a prototype washout curve which was fit compartmentally. Two groups of aorta segments were studied: 1) those in which uptake and washout temperature was the only variable; 2) those obtained from rats with established dietary magnesium (Mg2+) deficiencies. Four prototype data records can be identified: 1) Low-temperature; 2) Normal-temperature; 3) Mg2+-deficient; 4) Mg2+-sufficient. The four-compartment model not only incorporated the bound fraction, but yielded better fits than a three compartment model. In the temperature perturbation study, quantities of Na+ in extracellular compartments decreased by 15% with decrease in temperature, while intra and subcellular quantities increased by 9 and 530%, respectively. Transport of Na+ from the subcellular compartment to the intracellular compartment increased 700% while transport into the ECS was decreased with decrease in temperature. In the Mg2+-deficiency study, quantities of Na+ in extracellular compartments increased slightly (3%), while intra and subcellular quantities increased by 54 and 150% in aorta from Mg2+-deficient rats. Transport of Na+ from the subcellular compartment to the intracellular compartment increased 330%, as did transport into the ECS in Mg2+-deficient tissues.

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