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G D Sloop

Publications and source records attributed to G D Sloop.

24 records · Page 2Linked to original sources
PubMed1998

Opposite effects of low-density and high-density lipoprotein on blood viscosity in fasting subjects.

Given the enlarging body of evidence implicating increased blood viscosity in atherogenesis, the authors hypothesize that lipoproteins modulate the atherogenic process by affecting blood viscosity. In order to define the magnitude of the effect of lipoproteins on blood viscosity, capillary viscometry was performed on blood from 16 healthy, fasting subjects, and results were correlated with lipoprotein-cholesterol levels. Low-density lipoprotein-cholesterol was positively associated with blood viscosity (r = 0.610, p = 0.01). High-density lipoprotein-cholesterol was negatively associated with blood viscosity (r = -0.479, p = 0.06). A multiple regression model was developed with these data, revealing that 54% of variation in blood viscosity was attributable to these lipoproteins. This model was validated on a second dataset, in which these lipoproteins accounted for 28% of variation in blood viscosity. A second model, including hematocrit, serum viscosity, and high-density lipoprotein-cholesterol levels, explained 73% of variation in blood viscosity. By modulating blood viscosity and flow, lipoproteins may affect the residence time of atherogenic particles and atherogenesis.

Adult↗
PubMed1997

The effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis in humans.

1. Increased blood or plasma viscosity has been observed in almost all conditions associated with accelerated atherosclerosis. Cognizant of the enlarging body of evidence implicating increased viscosity in atherogenesis, we hypothesize that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis. 2. Blood viscometry was performed on samples from 28 healthy, non-fasting adult volunteers using a capillary viscometer. Data were correlated with haematocrit, fibrinogen, serum viscosity, total cholesterol, high-density lipoprotein-cholesterol, triglycerides and calculated low-density lipoprotein-cholesterol. 3. Low-density lipoprotein-cholesterol was more strongly correlated with blood viscosity than was total cholesterol (r = 0.4149, P = 0.0281, compared with r = 0.2790, P = 0.1505). High-density lipoprotein-cholesterol levels were inversely associated with blood viscosity (r = -0.4018, P = 0.0341). 4. To confirm these effects, viscometry was performed on erythrocytes, suspended in saline, which had been incubated in plasma of various low-density lipoprotein/high-density lipoprotein ratios. Viscosity correlated directly with low-density lipoprotein/high-density lipoprotein ratio (n = 23, r = 0.8561, P < 0.01). 5. Low-density lipoprotein receptor occupancy data suggests that these effects on viscosity are mediated by erythrocyte aggregation. 6. These results demonstrate that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity in healthy subjects correlate with their association with risk of atherosclerosis. These effects on viscosity may play a role in atherogenesis by modulating the dwell or residence time of atherogenic particles in the vicinity of the endothelium.

Adult↗
PubMed1997

Histopathological studies of staphylococcal alpha-toxin: effects on rabbit corneas.

PURPOSE: Previous studies from this laboratory have demonstrated, in a rabbit model of keratitis, a relationship between the corneal virulence of Staphylococcus aureus and the alpha-toxin activity of the infecting bacteria. This study is a histopathological characterization of the action of purified alpha-toxin on corneal tissue. METHODS: Alpha-toxin was purified by isoelectric focusing and intrastromally injected into rabbit corneas (2 micrograms per cornea). A kinetic analysis of toxin effect was performed following injection. Normal corneas and corneas injected with phosphate buffered saline (PBS) or heat-inactivated alpha-toxin in PBS served as controls. Eyes were examined from 0 to 4 h by slit lamp examination (SLE) and scored on the basis of seven ocular parameters. Corneal tissue was removed and examined for histopathological changes. RESULTS: From 0.5 to 4 h post-injection, alpha-toxin injection induced a significant increase in the SLE score relative to untreated eyes or eyes injected with PBS (P < 0.0001). Histolo-pathological examination of corneas one-half h after alpha-toxin injection revealed edema of the central cornea and death of epithelial cells by both necrosis and apoptosis. Later times showed continued edema and loss of apparently normal epithelial cells. Development of polymorphonuclear (PMN) leukocyte infiltration from the tear film into the central cornea and from limbal vessels into the peripheral cornea was observed. CONCLUSIONS: Purified alpha-toxin mediates cell death by necrosis and apoptosis, sloughing of viable corneal epithelial cells, severe corneal edema, and PMN migration into the cornea from both the tear film and limbal vessels. The pathologic changes revealed by histological studies of corneas injected with purified alpha-toxin included death of cells by necrosis and apoptosis as well as overall changes analogous to that seen by SLE of eyes infected with wild-type, but not alpha-toxin-deficient strains of Staphylococcus aureus.

Animals↗
PubMed1996

A unifying theory of atherogenesis.

The author proposes that all major risk factors, including elevated serum low-density lipoprotein, cause atherosclerosis by increasing viscosity, creating larger areas of decreased blood flow, thereby perpetuating the interaction of atherogenic elements with the endothelium. Low-density lipoprotein causes increased viscosity by fostering erythrocyte aggregation. High-density lipoprotein protects against atherosclerosis by antagonizing erythrocyte aggregation, thereby decreasing viscosity. Implications of this theory are discussed.

Animals↗
PubMed1995

Complications of blood transfusion. How to recognize and respond to noninfectious reactions.

Severe transfusion reactions occur much less often than minor reactions, but it is difficult to discriminate clinically between impending severe reactions and minor reactions. Therefore, whenever a reaction occurs, the transfusion should be discontinued and a laboratory workup initiated to rule out an acute hemolytic transfusion reaction. At a minimum, a direct antiglobulin (Coombs') test should be performed, and specimens obtained before and after transfusion should be assayed for hemoglobinemia and hemoglobinuria. If the product transfused included red blood cells, then typing and crossmatching should be repeated on a posttransfusion blood specimen. Routine premedication with antipyretics is not recommended, since they may mask early signs and symptoms of more severe reactions and their efficacy is questionable. Recent insights into the mechanisms of transfusion reactions have suggested interventions that may help minimize or prevent potentially serious sequelae.

Anaphylaxis↗