PubMed Health⌕ Search

Biomedical subjects

H A Massaldi

Publications and source records attributed to H A Massaldi.

9 recordsLinked to original sources
PubMed1993

Glucose effects on oxygen consumption by the arterial wall.

The effect of both D- and L-glucose on the rate of oxygen consumption in rat aorta was determined. Oxygen uptake (V02) was found to decrease when the concentration of D-glucose in the medium was increased, with the same effect being found when L-glucose, rather than D-glucose, was used. Based on these results, it would appear that the decrease in the vascular wall oxygen consumption which results from increased glucose levels is not due to a metabolic effect since one of the isomers (D) is metabolized and the other (L) is not. It is suggested, instead, that these results may be be due to a change in the diffusion of oxygen. Possible implications for atherogenesis are also discussed.

Animals↗
PubMed1991

Haemodynamics and arterial wall metabolism: their possible combined role in atherogenesis.

An integrated model for the genesis of atherosclerosis is proposed on the basis of the evidence reported in the literature from the fields of haemodynamics and arterial wall metabolism. The model is based on the hypothesis of 'localized nutrient shortage' in the arterial wall at critical regions of the vascular tree, such as branchings, bendings, stenosis etc. In particular, it is proposed that a tissue deficit of glucose and oxygen, more pronounced at those regions, may be the main cause of endothelial dysfunction and lesion initiation. LDL-cholesterol level and hypertension are included as strongly interacting risk factors, and new explanations are provided for the effects of smoking and diabetes. For the latter factors, transport limitations in the lumen and/or in the tissue are likely to interact with wall metabolism; in the case of smoking, additional competition of CO and O2 within the tissue is suggested, and for diabetes, the impaired uptake of glucose by the tissue is proposed as the main causal factor. Also, the incorporation of secondary risk factors to the model is shown to be feasible on the basis of their suggested action mechanism. It is concluded that the study of nutrients and LDL transport at regions of complex arterial geometry in connection with wall metabolic requirements can provide a better understanding of the atherogenic process.

Arteries↗
PubMed1990

Improved method for estimating Ca uptake in vascular smooth muscle using compartmental analysis.

A comparative study on the modeling aspects of Ca uptake in vascular smooth muscle is presented with particular emphasis on determination of the influx rate and its standard error for one- and two-compartment models. Experimental data from our laboratory of 45Ca uptake by dog carotid arteries were optimally fitted to a one-compartment model and were used to compare different estimation methods and experiment designs. Reparameterization of the model equation yielded an expression that allows direct estimation of the influx rate and its standard error. Experiment design with replicated sampling at three to four times were found to provide the highest estimation precision and successful comparisons of influx rates under treatment and control conditions. Two-compartment model data reported in the literature for Ca uptake by cells were reprocessed, yielding standard errors for the rate constant of the fast component an order of magnitude larger than the mean estimate. For this case, a three-parameter variant of the one-compartment model was developed that described the data with acceptable standard errors. Overall we found that the choice of the model that fitted Ca uptake data best required consideration of parameter estimate precision comparisons in addition to F tests of significance between alternate models.

Animals↗
PubMed1988

Osmotic fragility model for red cell populations.

A model that predicts the osmotic fragility curve of a red cell population is developed by relating the critical osmotic pressure to the size distribution of the cells, determined by resistive pulse spectroscopy. Two of the parameters involved, namely the normalized osmotic volume correction, B, and the swelling index, k, are previously determined from the experimental average properties of the population. From these values the critical volume of the cell is obtained, and is shown to be 6-12% larger than the first spherical volume, obtained from an independent experiment. A new parameter, n, a measure of the surface area distribution of the cells, is incorporated through a simple function that relates the critical volume to the size of the cells, and is theoretically shown to be linked to parameters k and B. The model is used to fit and interpret fragility data obtained in this laboratory for normal and sickle cell samples. From the values of n obtained for normal samples, the model predicts an essentially constant surface-to-volume ratio within an individual's cell population. For sickle cell samples, instead, the value of index n is negative, thereby supporting an increase in excess surface area as cell size decreases. Both findings are in agreement with direct observations reported in the literature. It is concluded that this set of parameters may be used to develop an index classification of blood disorders.

Anemia, Sickle Cell↗
PubMed1986

Alternative interpretation for the osmotic response of human erythrocytes.

In a recent publication, Heubusch et al. (J Cell. Physiol, 122:266-272, 1985) reported changes of erythrocyte volume measured by the Coulter counter technique over a wide range of osmolalities (160 to 3000 m0sm). Their results showed a partially hindered, nonlinear response, in contrast to classical observations made over more restricted osmolality ranges, using other methods. The authors suggested the underlying cause of this behavior to be a mechanical resistance of the membrane cytoskeleton. In this paper, we wish to offer a different interpretation of their results on erythrocyte osmotic behavior, based on similar experiments carried out in our laboratory, and supported by previous analyses from the literature. In particular, it is shown that the shape-factor correction to the electronic sizing measurement can correctly account for the observed deviations from linearity in the hypotonic range. In contrast, increased chemical nonideality and eventual hemolysis are the likely factors responsible for the behavior in the hypertonic range.

Erythrocytes↗
PubMed1984

The physico-chemical mechanism of mediated transport. II. Osmotic and isosmotic volume flow.

The process of volume change of cells subject to osmotic shocks or isosmotic entrance of permeant solute is formulated on the basis of the accepted structure for the plasma membrane and a physico-chemical approach similar to that recently developed. The effect of relevant parameters is discussed and theoretical equilibrium values for the variables are calculated in connection with water and permeant solute permeability determinations. Although a sorption-diffusional mechanism for solute and/or water volume flow within the membrane is assumed in both cases, the kinetics of volume change is shown to be totally different between them. In the isosmotic process a fixed relationship, given by the total solute concentration, is shown to exist between the permeant solute and volume fluxes to the cell, thereby implying a definite value for the volume fraction of water in the migration pathway, higher than 90%. The bi-phase osmotic regulatory response caused by permeant solute is simulated on the basis of an osmotic and isosmotic processes in series, showing good agreement with general behavior. Finally, an explanation to the problem of volume flow and forces in connection with a diffusional mechanism in biological and artificial membranes, is presented.

Biological Transport↗
PubMed1984

The physico-chemical mechanism of mediated transport. I. Facilitated diffusion.

On the basis of the currently accepted model for the cell membrane structure, a physico-chemical model for mediated transport is developed and solved for the case of polar non-electrolyte migration through the cell membrane. The model considers the interstitial space defined by the transport protein subunits to be the migration pathway for polar solutes. A Langmuir-type adsorption equilibrium is assumed at the interfaces and a multicomponent diffusion mechanism of solute and water is postulated within the migration pathway, where the polar residues of the transport protein represent another component of the system. Membrane selectivity is governed by the adsorption constants, which are shown to affect strongly the kinetics of transport. Isosmotic transport and the volume change of the cell are important features incorporated in the model, which is shown to fulfill the peculiar properties of facilitated diffusion systems. It is concluded that the same type of pathway can be used for the transport of other polar solutes through existing or induced hydrophilic channels, for which a similar approach is suggested.

Adsorption↗
PubMed1983

The dynamics of the stress stage of osmotic haemolysis.

A simple physical model for the dynamics of the stress stage of osmotic haemolysis is presented. An 'elastic restitutive coefficient' for the red cell membrane is defined to relate the increase of internal pressure to the volume change during the stress stage, and it is estimated on the basis of the work of Evans et al. (1976, 1977). It is shown that the time elapsed between complete swelling and the start of haemoglobin leakage can be a substantial part of the total haemolysis time, in accordance with experimental results reported in the literature.

Biomechanical Phenomena↗