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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Aorta, Thoracic, Atherosclerosis, Blood Glucose, Cell Adhesion, Cell Communication, Cell Count, Diabetes Mellitus, Experimental, Endothelium, Vascular, Glucose, Hyperglycemia, Immunohistochemistry, Injections, Intravenous, Insulin, Male, Monocytes, Octreotide, Rats, Rats, Sprague-Dawley, Time Factors.
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Does temporary hyperglycaemia provoke monocyte adhesion to endothelial cells in rat thoracic aorta? Context: Several epidemiological data suggest that patients with postprandial hyperglycaemia are at high risk of cardiovascular disease. The aim of this study was to elucidate the effect of a glucose 'spike' on monocyte adhesion to rat aortic endothelial cells. Monocyte adhesion to endothelial cells in vivo was quantitated using an en face method for observation of endothelial surface after immunohistochemical staining for CD68 in the thoracic aortas of Sprague-Dawley rats after several kinds of blood glucose rises. The number of monocytes adhering to endothelial cells increased at 30 min after injection of glucose in 8-week-old Sprague-Dawley rats. The increased adhesion returned to the basal level at 120 min after glucose injection, concomitantly with the return of blood glucose levels to normal. The infusion of octreotide to inhibit endogenous insulin secretion did not prevent the glucose-induced increase in monocyte adhesion to endothelial cells. On the other hand, the number of monocytes adhering to endothelial cells did not increase in rats with streptozotocin-induced diabetes and sustained hyperglycaemia.
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Our data demonstrate that a temporary rise in blood glucose levels can in itself promote a reversible increase in monocyte adhesion to arterial endothelial cells. Final Decision: yes