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Am J Physiol Heart Circ Physiol 281: H2097-H2104, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 5, H2097-H2104, November 2001

Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism

Judy R. Kersten1, Wolfgang G. Toller5, John P. Tessmer1, Paul S. Pagel1,2,4, and David C. Warltier1,2,3,4

Departments of 1 Anesthesiology, Pharmacology, and 2 Toxicology, and 3 Division of Cardiovascular Diseases, Department of Medicine, Medical College of Wisconsin; 4 Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226; and 5 Department of Anesthesiology, University of Graz, A-8036 Graz, Austria

We tested the hypothesis that hyperglycemia alters retrograde coronary collateral blood flow by a nitric oxide-mediated mechanism in a canine Ameriod constrictor model of enhanced collateral development. Administration of 15% dextrose to increase blood glucose concentration to 400 or 600 mg/dl decreased retrograde blood flow through the left anterior descending coronary artery to 78 ± 9 and 82 ± 8% of baseline values, respectively. In contrast, saline or L-arginine (400 mg · kg-1 · h-1) had no effect on retrograde flow. Coronary hypoperfusion and 1 h of reperfusion decreased retrograde blood flow similarly in saline- or L-arginine-treated dogs (76 ± 11 and 89 ± 4% of baseline, respectively), but these decreases were more pronounced in hyperglycemic dogs (47 ± 10%). L-Arginine prevented decreases in retrograde coronary collateral blood flow during hyperglycemia (100 ± 5 and 95 ± 6% of baseline at blood glucose concentrations of 400 and 600 mg/dl, respectively) and after coronary hypoperfusion and reperfusion (84 ± 14%). The results suggest that hyperglycemia decreases retrograde coronary collateral blood flow by adversely affecting nitric oxide availability.

collateral circulation; myocardial ischemia; reperfusion injury


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