Search PubMed⌕ Search

Biomedical subjects

K M Jan

Publications and source records attributed to K M Jan.

52 records · Page 3Linked to original sources
PubMed1979

Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling.

Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.

Adolescent↗
PubMed1977

Effect of hematocrit variations on coronary hemodynamics and oxygen utilization.

Twenty-five closed-chest pentobarbitalized dogs were used for studying coronary flow dynamics and myocardial oxygen utilization following variations of hematocrit (Hct) by isovolumetric exchange of blood with plasma or packed red cells. Coronary blood flow (133Xe washout) and cardiac output varied inversely with Hct. Coronary systemic, and pulmonary flow resistances varied in the same direction with Hct. Blood viscosity played a significant role in determining the flow resistances in these three regions. Analysis of vascular hindrance (vascular resistance/blood viscosity) suggested that coronary vasodilation occurred following Hct changes beyond the range of 20-60%. In systemic and pulmonary circulations, however, there was vasoconstriction following hemodilution. The range of optimum Hct for maximum O2 transport (blood flow X arterial O2 content) was much wider in coronary (20-60% Hct) than in systemic circulation (40-60% Hct). The O2 consumptions in total body and in myocardium were essentially constant over a wide range of Hct (20-60%). The maintenance of total body O2 consumption over the Hct range of 20-40% was attributable to an increase in A-V O2 extraction. The O2 extraction ratio in the coronary circulation was constant over the entire range of Hct studied, suggesting that the myocardial O2 consumption was primarily determined by the coronary O2 transport.

Animals↗
PubMed1975

Observations on blood viscosity changes after acute myocardial infarction.

Serial blood rheologic measurements were made in 25 patients with acute myocardial infarction; measurements included blood and plasma viscosities, hematological data and plasma protein concentrations. The blood viscosity was elevated on admission and for more than 21 days after acute myocardial infarction. However, the cause of the elevated viscosity was changed as a function of time after acute myocardial infarction. During the first three days after admission, the high blood viscosity was mainly attributable to high hematocrit values. Thereafter, the hematocrit fell, but blood viscosity remained high. High blood viscosity after the first three days of acute myocardial infarction can be correlated with increases in plasma viscosity and red cell aggregation, which in turn are explained by elevations of alpha 2 globulin and fibrinogen concentrations. Patients with higher blood viscosity on admission had a significantly higher incidence of complications, i.e., shock, thromboembolism and left ventricular failure.

Alpha-Globulins↗
PubMed1973

Role of surface electric charge in red blood cell interactions.

The role of the surface charge of human red blood cells (RBC's) in affecting RBC aggregation by macromolecules was studied by comparing the behavior of normal RBC's with that of RBC's treated with neuraminidase, which removes the sialic acids from the cell membrane and reduces the zeta potential. RBC aggregation in dextrans with different molecular weights (Dx 20, Dx 40, and Dx 80) was quantified by microscopic observation, measurement of erythrocyte sedimentation rate, and determination of low-shear viscosity. Dx 20 did not cause aggregation of normal RBC's, but caused considerable aggregation of neuraminidase-treated RBC's. Neuraminidase-treated RBC's also showed stronger aggregation than normal RBC's in Dx 40 and 80. Together with the electron microscopic findings that the intercellular distance in the RBC rouleaux varies with the molecular size of dextrans used, the present study indicates that the surface charge of RBC's inhibits their aggregation by dextrans and that the electrostatic repulsive force between cell surfaces may operate over a distance of 20 nm.

Blood Sedimentation↗
PubMed1973

Influence of the ionic composition of fluid medium on red cell aggregation.

The effects of ionic strength and cationic valency of the fluid medium on the surface potential and dextran-induced aggregation of red blood cells (RBC's) were investigated. The zeta potential was calculated from cell mobility in a microelectrophoresis apparatus; the degree of aggregation of normal and neuraminidase-treated RBC's in dextrans (Dx 40 and Dx 80) was quantified by microscopic observation, measurement of erythrocyte sedimentation rate, and determination of low-shear viscosity. A decrease in ionic strength caused a reduction in aggregation of normal RBC's in dextrans, but had no effect on the aggregation of neuraminidase-treated RBC's. These findings reflect an increase in electrostatic repulsive force between normal RBC's by the reduction in ionic strength due to (a) a decrease in the screening of surface charge by counter-ions and (b) an increase in the thickness of the electric double layer. Divalent cations (Ca(++), Mg(++), and Ba(++)) increased aggregation of normal RBC's in dextrans, but had no effect on the aggregation of neuraminidase-treated RBC's. These effects of the divalent cations are attributable to a decrease in surface potential of normal RBC's and a shrinkage of the electric double layer. It is concluded that the surface charge of RBC's plays a significant role in cell-to-cell interactions.

Barium↗
PubMedDate not supplied

Macromolecular transport across arterial and venous endothelium in rats. Studies with Evans blue-albumin and horseradish peroxidase.

Atherosclerotic lesions are characterized by lipid infiltration in regions with high rates of endothelial cell turnover. The present investigation was designed to elucidate the route of macromolecular transport across vascular endothelium. The aorta and vena cava of male Sprague-Dawley rats were perfusion-fixed after the intravenous injection of Evans-blue albumin (EBA) or horseradish peroxidase (HRP). Fluorescence microscopic examination of en face preparation of the aorta stained with hematoxylin allowed the identification of endothelial cells that underwent mitosis, together with the localization and quantification of fluorescent spots for EBA leakage. The HRP specimens were subjected to histochemical treatment, and HRP leakage was seen as brown spots under the light microscope. Silver nitrate stain was added in both EBA and HRP studies to outline cell boundaries and to visualize stigmata, stomata, and dead cells. In the aorta, almost every dividing cell showed junctional leakage to albumin and HRP, with clustering of leaky spots around the branch orifices. Time-dependent studies showed gradual increases in the diameter and number of these heterogeneously sized leaky spots, which finally fused to sizes corresponding to the "blue areas" for EBA or "brown areas" for HRP. Compared with arteries, veins had fewer mitotic cells, but more dead cells and diffuse dye-staining areas, indicating a more rapid transport of macromolecules. The leaky spots in the artery were associated mainly with mitotic cells, dead cells, and stigmata, whereas those in the vein occurred primarily at regions with dead cells. These results suggest that the preferential association of the enhanced transport of macromolecules with mitosis in the arterial as compared to venous endothelium and the differential behavior in transmural transport between arteries and veins may form the basis for the predilection of atherosclerosis in arteries.

Animals↗
PubMedDate not supplied

Role of dying endothelial cells in transendothelial macromolecular transport.

There are focal areas in the aorta with an enhanced endothelial permeability to macromolecules, as indicated by the focal uptake of the protein-binding azo dye Evans blue in vivo. These areas exhibit high rates of endothelial cell turnover and a number of structural characteristics in en face endothelial morphology. To determine the relationship of endothelial cell death to macromolecular leakage at the level of individual endothelial cells, thoracic aortas of 12 adult male Sprague-Dawley rats were studied at 3 to 5 minutes after intravenous administration of Evans blue-albumin (EBA). Leakage of EBA around individual endothelial cells in en face preparations of the aorta was visualized by fluorescence microscopy. Dying or dead endothelial cells were identified by indirect immunoglobulin G (IgG) immunocytochemistry. Although endothelial cell death is uncommon in normal aortic endothedium (i.e., an average frequency of 0.48%), a high percentage (63%) of IgG-containing dying or dead endothelial cells was found to be associated with EBA leakage. These dying or dead endothelial cells were responsible for 37% of total EBA leaky foci. The results suggest that, in addition to mitotic endothelial cells, the dying or dead endothelial cells also make significant contributions to the local enhancement in aortic endothelial permeability. The present findings lend further support to the "cell turnover-leaky junction" hypothesis for the localization of atherosclerosis.

Albumins↗
PubMedDate not supplied

Transendothelial transport of low density lipoprotein in association with cell mitosis in rat aorta.

Atherosclerosis is characterized by focal areas of lipid accumulation and intimal smooth muscle cell proliferation in large arteries. In vivo studies on rat aorta with Evans blue-albumin conjugate (EBA) have shown that there are preferential sites of increased permeability with an increased uptake of the conjugate. It has been shown that these blue areas are associated with a high endothelial cell turnover rate and an enhanced permeability to lipids. In a previous study, we demonstrated that 99% of endothelial cells in the mitotic (M) phase as identified by hematoxylin staining of the dividing nuclei exhibited EBA leakage and that these dividing cells accounted for 30% of all leakage sites. In the present study, experiments were performed on the thoracic aortas of 10 adult male Sprague-Dawley rats to determine the statistical frequency of isolated leaks to Lucifer yellow-low density lipoprotein conjugate (LY-LDL) at the level of individual cells and to assess the relationship of such leaks to the cell turnover processes. Leakage of LY-LDL around individual endothelial cells was visualized by fluorescence microscopy, and cells in mitosis on the same specimens were identified by hematoxylin staining. Although endothelial cell mitosis is infrequent (0.034%), 80% of dividing cells in the M phase were associated with LY-LDL leakage. These dividing cells accounted for 45% of all leakage spots. These findings lend support to our recent hypothesis that transiently open junctions surrounding the endothelial cells undergoing cell turnover provide pathways through which LDL enters the subendothelial space, resulting in lipid accumulation.

Animals↗
PubMedDate not supplied

Spontaneous activation of circulating granulocytes in patients with acute myocardial and cerebral diseases.

Recent animal studies have suggested that there exists an activated subpopulation of circulating granulocytes which plays an important part in microvascular sequestration and tissue injury during shock and ischemia. In this respect, spontaneous granulocyte activation in form of pseudopod formation, a manifestation of actin polymerization, is a high risk for microvascular entrapment. The present investigation was carried out to determine if there is a significant difference in pseudopod formation in vitro between granulocytes obtained from healthy volunteers without symptoms and patients with acute cardiovascular illnesses. Blood samples from 25 healthy volunteers, 12 patients with acute myocardial infarction (AMI) and 12 patients with acute cerebral infarction (ACI) to determine spontaneous pseudopod formation in granulocytes with a high resolution light microscope over a period of several hours. The results revealed that the mean percentage of cells with pseudopod formation in the control group was below 10% in the first 3 hours, and increased to about 50% at 12 hours. In AMI patients, the level of activation within the first hour was not significantly different from the controls, but it rose rapidly to 90% in 4 to 5 hours. Patients with cerebral infarction, however, showed no significant difference from the control group. When the granulocytes of healthy subjects were incubated in plasma of AMI, the cells were activated similar to AMI granulocytes in their own plasma. When AMI plasma was serially diluted with Ringer's solution, the activation curve fell successively. These results indicate that AMI patients' blood contains plasma factor(s) which can activate granulocytes at a more rapid rate than controls.

Cells, Cultured↗