Erectile dysfunction(ED) is a common disease in males, and
vascular disorder is the most common cause. ED is considered
to be the earliest clinical manifestation of cardiovascular diseases
(CVD), so ED can be seen as an early warning factor of
cardiovascular events. Endothelial dysfunction is the initial triggering factor and most important in the pathogenesis of ED and
CVD. Glycometabolism markers significantly correlate with ED.
Glucose can be slowly combined with serum proteins and then
transformed into glycosylated products, which is the process of
non-enzymatic glycosylation reaction. Once glycometabolism is
disordered, high level glycated products will increase significantly
and impair systemic microvascular tissue. In diabetic patients,
abnormally high-levels of advanced glycation end products
(AGEs) cause the cardiovascular complications. Glycosylated
serum protein (GSP) is an early glycated product which may
appear before the occurrence of diabetes. Thus, serum levels of
GSP may significantly increase when a potential glycometabolic
disorder occurs. Some studies have demonstrated that GSP may
damage the biological function of endothelial cells, which may
accelerate the development of cardiovascular disease.
To studied the impaired role of glycated serum albumin on
vascular endothelium-dependent relaxation in vitro. In clinical
study, young ED patients without obvious causes for ED were
selected to evaluate the state of glycometabolism and endothelial
function and investigate the influence of glycosylated serum protein
on vascular erectile dysfunction.
Male SD rats were selected and killed with dislocation. Aorta
was cut into vascular rings with a length of 3-4 mm in each. The
vascular rings were fixed with steel hook in different constant
perfusion tanks, respectively. The vascular rings were divided
into three groups including control, BSA and GBSA group. Two
tanks were selected to add BSA and GBSA to incubate vascular
rings for 60min, respectively. Phe and ACh were used to stimulate
the pre-contraction and relaxation of vascular rings, and
then a maximum contraction value (Emax0) and diastolic value
(Emax1) were marked, respectively.
ED patients aged 20-40 years were screened, and control
group which is age-matched with case group were screened from
health population. All the participants need to accept systemic
data collection. We made the uniform standards for screening
and inclusion including IIEF-5 <21 without obvious causes for
ED in ED group, and IIEF-5 ≥22 without risk factors of ED in
control group. Ultimately, the participants met the screening and
inclusion criteria were enrolled in the research cohort. The target
patients were then divided into groups for analysis according to
the severity of erectile dysfunction determined by IIEF-5 scores.
In vitro, GBSA significantly impaired endothelium-dependent
vasodilation. Before treatment, no significant differences were
found in maximum expansion rate among three groups of vascular
rings. After treatment, the maximum expansion rate of control
and BSA groups had no significant difference compared with before
treatment. The maximum expansion rate of the GBSA group
was significantly lower than before treatment (10.7 ± 8.0 vs. 58.5 ± 0.08, P<0.05), control group (10.7±8.0 vs. 49.1±21.6, P<0.05),
and BSA group (10.7±8.0 vs. 45.8±19.2, P<0.05), respectively.
Compared with control group, case group had significantly
lower IIEF-5 score. Clinical parameters in two groups showed no
significant difference. FBG level of case group was higher than
of control group, and GSP level in case group was significantly
higher than in control group. In ED group, FMD was significantly
lower than that in control group. FMD values decreased
and GSP values increased with the increasing severity of ED.
FMD value was positively correlated with IIEF-5 score, and GSP
level was negtively correlated with IIEF-5 score. There was a significantly
negative correlation between GSP and FMD. Multiple
linear regression analysis showed FMD and GSP can be used as
independent predictors of ED.
Glycosylated serum albumin can impair endotheliumdependent
dilation of rat aorta in vitro. Potential endothelial
dysfunction and glycometabolism disorder may present in young
ED patients without obvious causes. Glycosylated serum protein
significantly correlates with endothelial dysfunction and erectile
dysfunction, and it may be an early predictor of endothelial dysfunction
and erectile dysfunction.