Search PubMed⌕ Search

Biomedical subjects

K M Jan

Publications and source records attributed to K M Jan.

At least 37 records · Page 2Linked to original sources
PubMed1987

Influence of reduced red cell deformability on regional blood flow.

The effects of a reduction in red blood cell (RBC) deformability on regional blood flow and RBC distribution were studied in rats anesthetized with pentobarbital sodium. RBCs were subjected to minimum hardening by incubation in a very diluted solution of glutaraldehyde (0.025%). Normal and partially hardened RBCs, labeled with 51Cr or 111In, were injected into the femoral vein, while an equal volume of blood was simultaneously withdrawn from the femoral artery. Approximately 70% of the labeled, partially hardened RBCs disappeared from the circulating blood within 25 min after injection, compared with less than 2% of the labeled normal RBCs. The relative distribution of RBCs with reduced deformability to normal RBCs in tissues was determined from radioactivity counting; this ratio (mean +/- SD) was 7.95 +/- 0.85 in the spleen, 7.44 +/- 0.43 in the sternum, 7.10 +/- 1.09 in the lung, 4.54 +/- 0.31 in the liver, and 3.50 +/- 0.61 in the femur bone. The results indicate a significant degree of trapping of RBCs with reduced deformability in these regions. This ratio of relative distribution of RBCs with reduced deformability as compared with normal RBCs was 1.06 +/- 0.13 in the heart, indicating the absence of preferential trapping of RBCs with reduced deformability in this organ. Regional blood flows were determined with 15-microns microspheres in the control period and after infusion of RBCs with reduced deformability (experimental).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effects of blood viscosity on plasma renin activity and renal hemodynamics.

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

Animals↗
PubMed1986

Roles of surface electrochemistry and macromolecular adsorption in heparin-induced red blood cell aggregation.

Red blood cell (RBC) aggregation in heparin-saline solution was quantified by microscopic observation. The adsorption isotherms of heparin onto normal and neuraminidase-treated RBC surfaces were determined by radioactive heparin labeled with 125I-Bolton-Hunter Reagent. RBC aggregation by heparin requires the presence of sialic acids at cell surface and was enhanced by reduction of ionic strength of the suspending medium. Adsorption of heparin onto RBC surface was increased by removal of sialic acids. These findings not only serve to elucidate the basic mechanism of cell-cell interaction mediated by negatively charged macromolecules, but also provide experimental evidence for the possible conformational change of macromolecules at the charged surface.

Adsorption↗
PubMed1985

Distribution of myocardial stress and its influence on coronary blood flow.

The myocardial stress was analyzed by biomechanical modeling in correlation with experimental findings. The pressure-volume relationship follows the stress-strain relationship of muscle fibers. From the knowledge of fiber orientation and the distribution of sarcomere length, the myocardial stress components including fiber, longitudinal, circumferential and radial stresses were expressed as a function of fraction of wall thickness. The coronary blood flow is influenced by the myocardial radial stress. With the use of vascular waterfall theory, it is possible to correlate the theoretically defined stress distribution with experimentally obtained stress distribution. An elevation of radial stress in myocardium causes a reduction of vessel patency. During both systole and diastole, vessel patency remains constant at epicardium. At endocardium, however, vessel patency undergoes rhythmic changes following the systolic and diastolic influences of the radial stress. The physiological implication is that during systole, the endocardium suffers low blood flow and this transient ischemic state requires compensatory replenishment from diastolic perfusion. Such phenomena become less apparent toward the epicardium.

Biomechanical Phenomena↗
PubMed1985

Mechanism of thallium extraction in pump perfused canine hearts.

Myocardial extraction of Tl has been postulated to depend on the rate of delivery (flow rate) and the metabolic state of tissue (ATPase activity). Experiments were performed to assess the role of these factors. In 22 arrested dog hearts the left anterior descending and circumflex coronary arteries were cannulated and pump perfused with oxygenated blood containing 204Tl. Isotope activity was determined in coronary sinus blood. The myocardial extraction ratio (E) of Tl varied inversely with flow, and the permeability-surface area product (PS) increased with increasing flow rates. These findings indicate that Tl uptake is flow dependent and can be analyzed with Renkin's capillary clearance theory. To assess the role of ATPase in Tl uptake, studies were also performed with blood containing ouabain. After introducing ouabain, coronary sinus blood Tl activity increased, approaching arterial activity, and E fell markedly. It was concluded that myocardial Tl uptake is mediated by ATPase.

Adenosine Triphosphatases↗
PubMed1984

Distribution of plasmalemmal vesicles on arterial endothelial surface as determined by freeze cleavage.

The freeze-fracture technique was used to study the density and distribution of plasmalemmal vesicles at the endothelial surface of canine carotid arteries. The fractured surface of the endothelium can be divided into areas with vesicles (Aves) and areas without vesicles (Anves), the latter being located at the parajunctional zone. With morphometric analysis, Aves and Anves were found to be 75% and 25% of the endothelial surface, respectively. The average width of Anves (distance from the intercellular cleft) is approximately 0.4 micron. In Aves, the density of vesicles is 120 micron-2, and approximately 16% of Aves is covered by the vesicle orifices. The tight junctions appear as long and straight strands, 8-9 nm in width. The number of the strands varies from one to five. The gap junctions consist of closely packed particles 9-10 nm in size which form patches or plaques from 80 to 800 nm in size. These findings provide the quantitative information needed for the theoretical modeling of transendothelial vesicular transport of macromolecules.

Animals↗
PubMed1984

Deformation of leukocytes on a hematological blood film.

Human leukocytes in a blood film exhibit a significantly larger diameter than in the circulation. This is due to the fact that white cells are highly deformed during preparation of a blood film. Instead of having the usual spherical shape, the cells are compressed to "pancake" forms with a thickness of about 1 micron. Hematological investigation is usually performed on these compressed cells, but in the circulation they are not observed. The deformation of the cells on a blood film is due to compression by the glass edge used to spread the blood. After deformation leukocytes do not have enough time to recover since the blood film usually dries in a shorter period than is needed for cell recovery. The shape and size of the leukocyte on the blood film is not only determined by cell volume but also by the cell membrane area. This is shown for each kind of leukocyte by independent prediction of the pancake dimensions from previous measurements of cell volume and membrane area. Leukocytes which are strongly compressed during blood film preparation may exhibit mechanical damage with rupture of membranes.

Blood Specimen Collection↗
PubMed1983

Energy balance in red cell interactions.

Experiments were performed to elucidate the balance of energies involved in the formation of red blood cell (RBC) aggregates and in their disaggregation. In order to achieve a mean stable rouleau formation, the aggregating energy provided by macromolecular binding to the cell membrane must overcome the disaggregation energy of electrostatic repulsion between RBC surfaces and the effects of mechanical shear stress. In a quiescent suspension the net aggregation energy is largely stored in the membrane as a change in strain energy. The alterations in strain energy cause the curvature of the end cells in rouleaux of normal RBCs in Dx 80 to change from concave to convex and back again to concave as [Dx 80] was increased from 1 to 4 to 6 g/dl; computation of net aggregation energy per unit area (gamma) from changes in membrane strain energy yielded values on the order of 10(3) ergs/cm2. The end cells of neuraminidase-treated RBCs remained convex with [Dx 80] above 2 g/dl, and gamma is probably on the order of 10(2) ergs/cm2. The variations in gamma with [Dx 80] and RBC surface charge are similar to variations in reflectometric aggregation index without shear ( RAI0 ), indicating that RAI0 reflects gamma. The difference in gamma between normal and neuraminidase-treated RBCs represents the electrostatic repulsive energy, the magnitude of which varied inversely with dextran molecular size and directly with [Dx]. Moderate shearing in the reflectometer enhanced RBC aggregation by promoting cell-cell encounter, but high shear stresses cause RBC disaggregation. The energy required to disaggregate a unit interacting area of normal RBCs in Dx 80 in a flow channel is on the order of 10(4) ergs/cm2, which is much lower than gamma. These results suggest that the release of the stored membrane strain energy during disaggregation aids in the separation process. The results show that the understanding of RBC aggregation requires the considerations of surface charge, properties of aggregating agents, and the rheology of the cell membrane.

Dextrans↗
PubMed1983

The bulk rheology of close-packed red blood cells in shear flow.

A theoretical analysis is made of the dynamical behavior and bulk rheology of close-packed red blood cell suspensions subjected to simple shear flow. The model for the polyhedral cell shapes and tank-treading membrane motion developed in the companion paper (1) is used. The flow in the thin lubricating plasma layers between cells is analyzed taking into account the mechanical properties of the membrane at the corner regions of sharp membrane curvature. This leads to predictions for the apparent viscosity as a function of hematocrit and shear rate. Good agreement with experimental results is obtained at moderate and high shear rates (above 20 s-1). At lower shear rates, a rapid rise in apparent viscosity has been found experimentally, and the mechanisms leading to this behavior are examined.

Blood Viscosity↗
PubMed1981

Mechanics of Rouleau formation.

The formation of rouleau of red blood cells is considered from the standpoint of adhesion theory. With the use of the elastic properties of the red blood cell membrane obtained from previous work, the strain energy of the red blood cell in rouleau formation has been computed. The surface energy of adhesion for the bonding of two red blood cells is then computed from the variation of this strain energy. Computed cell shapes agree well with experiments.

Cell Adhesion↗
PubMed1980

Coronary hemodynamics and oxygen utilization after hematocrit variations in hemorrhage.

Twenty closed-chest dogs anesthetized with pentobarbital sodium were used for studying coronary hemodynamics and myocardial oxygen utilization during hemorrhagic hypotension, with the mean arterial pressure maintained constant at 50 mmHg. Variations of hematocrit (Hct) were achieved by exchange of blood with plasma or packed cells. Coronary blood flow (133Xe washout) varied inversely with Hct, whereas cardiac output (indicator dilution) showed a peak value at a Hct of approximately 25%. Coronary, systemic, and pulmonary flow resistances varied in the same direction with Hct, and the relationship was attributable to the change of blood viscosity with Hct. Analyses of vascular hindrance (= resistance/viscosity) suggested that during hemorrhagic hypotension, coronary vasodilation was maintained during variations of Hct. In systemic and pulmonary circulations, however, there were marked increases in vasoconstriction after hemodilution. The optimum Hct for maximum O2 transport was 25% for coronary circulatin and approximately 45% for systemic circulation. The O2 consumption (QO2) in the myocardium increased after hemodilution with a peak value at a Hct of approximately 25%. The QO2 in the total body was constant over a wide range of Hct between 25 and 45%, above and below which the QO2 decreased.

Animals↗
PubMed1979

Role of hydrogen bonding in red cell aggregation.

The role of hydrogen bonding in red cell aggregation induced by dextran was studied with the use of urea, an inhibitor for hydrogen bonding. In order to avoid hemolysis of red cells by the high concentration of urea, the studies were performed on human red cells hardened in glutaraldehyde. The degree of red cell aggregation at Hct = 45% was estimated by the use of a coaxial cylinder viscometer. The viscometric aggregation index (VAI) was calculated from viscosity values at shear rates of 52 sec-1 (eta H) and 0.05 sec-1 (eta L); VAI = (eta L - eta H)/eta H. Red cells with surface charge intact and with charge removal by neuraminidase treatment were studied. Urea at high concentrations, e.g., 6 M, significantly inhibited red cell aggregation induced by dextran. These findings indicate that hydrogen bonding plays an important role in dextran-induced red cell aggregation. An understanding of the nature of the forces involved in red cell aggregation serves to establish the physicochemical principles of cell-to-cell interactions induced by macromolecules.

Blood Viscosity↗