期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 281, 期 5, 页码 H2097-H2104出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.281.5.H2097
关键词
collateral circulation; myocardial ischemia; reperfusion injury
资金
- NHLBI NIH HHS [HL-63705, HL-54280, HL-03690] Funding Source: Medline
- NIAAA NIH HHS [AA-12331] Funding Source: Medline
- NIGMS NIH HHS [GM-08377] Funding Source: Medline
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.
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