J P Doweiko1, B R Bistrian. 1. Division of Infectious Disease, New England Deaconess Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Abstract
BACKGROUND: Albumin has a role in the complicated process of platelet aggregation. Although it is known that quantitative changes in plasma albumin alter platelet aggregation, less is known about the interaction between qualitative changes in plasma albumin and platelets. One common qualitative change in plasma albumin is nonenzymatic glycosylation, which occurs during states of prolonged hyperglycemia. METHODS: Albumin was selectively removed from normal plasma by means of an affinity column. Glycosylated albumin was added to this albumin-poor plasma, and it was used to study platelet aggregation induced by low concentrations of arachidonic acid. Platelet aggregation was determined by light transmittance. RESULTS: As the concentration of glucose in which albumin was incubated was increased, there was progressive augmentation of platelet aggregation. At a plasma glucose of 150 mg/dL, average light transmittance was 9.4%, and at 200 mg/dL, it was 24.6%. These values were significantly different at a p value < .01. At glucose levels of 300 mg/dL and 400 mg/dL, mean light transmittance was 40.6% and 74.4%, respectively, and these values were significantly different with p values of < .01. CONCLUSIONS: Platelet aggregation in response to a relatively low concentration of arachidonic acid is enhanced in the presence of albumin that has been incubated in a medium containing levels of glucose that are higher than would be seen in normal patients but are consistent with those seen in diabetics with less than optimal control. This augmentation of platelet aggregation is statistically significant.
BACKGROUND:Albumin has a role in the complicated process of platelet aggregation. Although it is known that quantitative changes in plasma albumin alter platelet aggregation, less is known about the interaction between qualitative changes in plasma albumin and platelets. One common qualitative change in plasma albumin is nonenzymatic glycosylation, which occurs during states of prolonged hyperglycemia. METHODS:Albumin was selectively removed from normal plasma by means of an affinity column. Glycosylated albumin was added to this albumin-poor plasma, and it was used to study platelet aggregation induced by low concentrations of arachidonic acid. Platelet aggregation was determined by light transmittance. RESULTS: As the concentration of glucose in which albumin was incubated was increased, there was progressive augmentation of platelet aggregation. At a plasma glucose of 150 mg/dL, average light transmittance was 9.4%, and at 200 mg/dL, it was 24.6%. These values were significantly different at a p value < .01. At glucose levels of 300 mg/dL and 400 mg/dL, mean light transmittance was 40.6% and 74.4%, respectively, and these values were significantly different with p values of < .01. CONCLUSIONS:Platelet aggregation in response to a relatively low concentration of arachidonic acid is enhanced in the presence of albumin that has been incubated in a medium containing levels of glucose that are higher than would be seen in normal patients but are consistent with those seen in diabetics with less than optimal control. This augmentation of platelet aggregation is statistically significant.