1 The formation of advanced glycation endproducts (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study was to examine the role of aminoguanidine (AG), an inhibitor of AGEs formation, in the prevention of arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) induced diabetes in rats. 2 Diabetes was induced in animals by a single tail vein injection with 65 mg kg À1 STZ. After confirmation of the development of hyperglycemia (2 days later), rats were treated for 8 weeks with AG (daily peritoneal injections of 50 mg kg À1 ) and compared with the age-matched untreated diabetic controls.3 After exposure to AG, the STZ-diabetic rats showed no alterations in cardiac output, aortic pressure profiles, total peripheral resistance, and aortic characteristic impedance. 4 By contrast, treatment of this experimental diabetes with AG resulted in a significant increase in wave transit time (t), from 20.470.6 to 24.770.5 ms (Po0.05) and a decrease in wave reflection factor (R f ), from 0.7870.04 to 0.5370.02 (Po0.05). The decreased R f associated with the increased t suggest that AG may retard the diabetes-induced augmentation in systolic load of the left ventricle coupled to its arterial system. 5 Meanwhile, the diminished ratio of left ventricular weight to body weight suggests that prevention of the diabetes-related cardiac hypertrophy by AG may correspond to the drug-induced decline in aortic stiffening. 6 Glycation-derived modification on aortic collagen was also found to be enhanced in rats with diabetes ( þ 65.3%, Po0.05) and the advanced glycation process was retarded by AG treatment. 7 We conclude that long-term administration of AG to the STZ-treated rats imparts significant protection against the diabetes-derived deterioration in vascular dynamics, at least partly through inhibition of the AGEs accumulation on collagen in the arterial wall. Abbreviations: AG, aminoguanidine; AGEs, advanced glycation endproducts; BW, body weight (g); C, systemic arterial compliance (ml kg À1 mmHg À1 ); CO, cardiac output (ml kg À1 min À1 ); HR, basal heart rate (beats min À1 ); iNOS, inducible isoform of nitric oxide syntheses; LVW, left ventricular weight (g); NO, nitric oxide; P b , magnitude of the forward pressure (mmHg); P d , diastolic aortic pressure (mmHg); P f , magnitude of the forward pressure (mmHg); P m , mean aortic pressure (mmHg); P s , systolic aortic pressure (mmHg); R f , wave reflection factor; R p , total peripheral resistance (mmHg min kg ml À1 ); SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; STZ, streptozotocin; SV, stroke volume (ml kg À1 beat À1 ); Z c , aortic characteristic impedance (mmHg min kg ml À1 ); Z i , aortic input impedance spectra (mmHg min kg ml À1 ); t, wave transit time (ms)

Long-term administration of AG to the STZ-NA diabetic rats imparts significant protection against the NIDDM-derived impairment in vascular dynamics, at least partly through inhibition of the AGE accumulation on collagen in the arterial wall.

The heavy intensity with early return of the pulse wave reflection may augment systolic load of the left ventricle coupled to the arterial system, leading to cardiac hypertrophy in the rats at 8 weeks after following STZ and NA administration.

We studied whether the 27 base pair (bp) tandem repeat polymorphism in intron 4 of the endothelial nitric oxide synthase (eNOS) gene was associated with coronary artery disease (CAD) in a hospital-based Taiwanese population. We included 219 consecutive patients who underwent coronary angiography at our institution. Two alleles, containing 4 (eNOS4a) and 5 repeats (eNOS4b), were identified after polymerase chain reaction amplifying intron 4 of the eNOS gene. The genotype frequencies for eNOS4b/b, eNOS4a/b and eNOS4a/a were 77.9, 21.5 and 0.6% in CAD subjects, and 80, 20 and 0% in control subjects (Fisher’s exact test, p = 0.90), respectively. The odds ratio (OR) for CAD in patients with at least one eNOSa allele was 1.2 (0.5–2.9) after adjustment for classical CAD risk factors. The eNOS4a allele was not associated with the severity of CAD (Fisher’s exact test, p = 0.90) and the occurrence of acute myocardial infarction (AMI) or unstable angina (adjusted OR 0.6, 0.3–1.6) in patients with CAD. In conclusion, the 27-bp repeat polymorphism of the eNOS gene was not associated with CAD and the occurrence of AMI or unstable angina in a hospital-based Taiwanese population.

Acetyl-L-carnitine, but not oxfenicine, attenuates aortic stiffening and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived MDA/TBARS in the rats with insulin deficiency.