Effects of Cholesterol Feeding Periods on Blood Haematology
and Biochemistry of Rabbits Fed High Cholesterol Diet
Authors: Dr. Mohamed A. K. Abdelhalim and Dr. Hisham A. Alhadlak, King Saud
University, College of Sciences, Department of Physics and Astronomy, Riyadh, Saudi
Arabia
Corresponding Author: Dr. Mohamed A. K. Abdelhalim
E-mail: abdelhalimmak@yahoo.com
Phone: 009660509649633
Fax: 0096614673656
P.O. Box 2455, Riyadh 11451
Saudi Arabia
Abstract
An increasing number of studies report altered haematological and biochemical
parameters to be associated with hyperlipoproteinemia, adverse dietary habits and other
life-style factors. Moreover, controversy still remains as to the relevance of blood
haematology and biochemistry to the development of arteriosclerosis; some investigators
suggested that some haematological and biochemical parameters of blood plasma of
rabbits fed high cholesterol diet increased in oppose to control rabbits, while others
suggested the opposite. The effects of cholesterol feeding periods on blood haematology
and biochemistry of rabbits fed high cholesterol diet have not been well documented. The
aim of the present study was to elucidate these haematological and biochemical
abnormalities in rabbits fed high cholesterol and saturated fat diet for feeding periods of
5, 10 and 15 weeks, i.e., to elucidate the abnormalities in total cholesterol (TC), lowdensity lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC),
triglyceride (TG), fibrinogen, haemoglobin, hematocrit, white blood cells (WBC), red
blood cells (RBC), platelet, lymphocytes, neutrophils, monocytes, and eosinophils levels.
For this purpose, fifty five 12-week-old New Zealand white male rabbits were purchased,
individually caged, and divided into either control group or cholesterol-fed group. The
control-fed rabbits were subjected to blood analyses at feeding period of 15 weeks. The
cholesterol-fed rabbits were subjected to blood analysis at feeding periods of 5, 10 and 15
weeks. It became evident from the results of the present study that TC, LDLC, TG, and
platelets were significantly (p < 0.05) increased in cholesterol-fed rabbits as compared
with control rabbits. WBC count was NOT significantly different between the cholesterol
feeding periods 5 and 10 weeks and the control group, but it significantly increased at the
cholesterol feeding period of 15 weeks as compared with the control rabbits. On the
contrary, haemoglobin, hematocrit, and RBC count were significantly decreased in the
cholesterol-fed rabbits as compared with the control rabbits. HDLC levels were
significantly decreased in cholesterol-fed rabbits at the feeding periods 5 and 10 weeks as
compared with control rabbits. However, it was NOT significantly different at the
cholesterol feeding period 15 weeks. The fibrinogen levels increased at the feeding
period 5 weeks, it decreased at the feeding period 10 weeks, and it showed no change at
the feeding period of 15 weeks. Fibrinogen levels were NOT significantly different in
cholesterol-fed rabbits as compared with the control rabbits. Lymphocytes percentage
decreased at the feeding period of 5 weeks, and significantly increased at the cholesterol
feeding periods 10 and 15 weeks as compared with the control rabbits. Neutrophils
percentage increased at the cholesterol feeding period of 5 weeks, and significantly
decreased at the cholesterol feeding periods 10 and 15 weeks as compared with the
control rabbits. Monocytes percentage was NOT significantly different in cholesterol-fed
group of rabbits as compared with the control rabbits. Eosinophils percentage
significantly increased at the cholesterol feeding period 5 and 10 weeks, and it
significantly decreased at the feeding period of 15 weeks of cholesterol. The present
study demonstrates that the haematological and biochemical parameters in rabbits fed
high cholesterol and saturated fat diet play the most important role during the
development of atherosclerosis.
Abbreviations used - total cholesterol (TC); low-density lipoprotein cholesterol
(LDLC); high-density lipoprotein cholesterol (HDLC); triglyceride (TG); white blood
cells (WBC); red blood cells (RBC); adenosine diphosphate (ADP).
Keywords: blood haematology; blood biochemistry; cholesterol feeding periods; rabbits;
atherosclerosis.
Introduction
Atherosclerosis is the disease of large and medium-sized arteries, i.e., carotid artery,
coronary artery and arteries of lower extremities. It is characterized by focal lesions of
one of the following types; fatty streak, fibrous plaque and complicated lesion. A vast
number of hypotheses to elucidate pathogenesis of atherosclerosis have been published.
Some of them are lipid hypothesis, thrombogenic hypothesis and endothelial cell injury
hypothesis. A great numbers of epidemiological studies have revealed that chronically
elevated lipids levels and cholesterol levels are associated with an increased incidence of
atherosclerosis (Abdelhalim et al., 1994). Evidence from experimental, clinical and
epidemiological studies suggest, that several hemostatic and hemorheological factors
(e.g., fibrinogen, plasma viscosity, hematocrit, red blood cell aggregation, total white cell
count) might not only play an important role in the evolution of acute thrombotic events,
but may also take part in the pathophysiology of atherosclerosis (Wolfgang and Edzard,
1992). High TC and LDLC have been correlated with the increased risk of atherosclerosis
(Martin et al., 1986). Triglyceride-rich lipoproteins of both intestinal and liver origin
were considered atherogenic factor (Philips et al., 1993; Zilversmit, 1995). Activation of
leukocytes is obligatory for inflammation and atherogenesis by adhering to the
endothelium via specific ligands. There is a TG-specific increase of neutrophil counts and
increased activation of monocytes and neutrophils, i.e., a pro-inflammatory situation that
may correspond with increased adhesive capacity of these cells contributing to the
inflammatory component of atherosclerosis (Van Oostrom et al., 2004). It has been
hypothesized that higher neutrophil counts are associated with an increased incidence of
major adverse cardiovascular events in patients with clinically advanced atherosclerosis
(Markus et al., 2005). In patients with peripheral artery disease, only neutrophils counts,
but not eosinophils, basophils, monocytes, lymphocytes, or the total WBC count
indicated a substantially increased risk for major adverse cardiovascular events (Markus
et al., 2005). Although the underlying mechanisms of atherosclerosis and intimal
hyperplasia remain unclear, the basal adherence of monocytes only was significantly
elevated in atherosclerosis, resulting in increased adherence to endothelial cells (Dovgan
et al., 1994). Fibrinogen concentration has been identified as independent atherosclerotic
risk factors during the development of atherosclerotic plaques and thrombi (Ernst and
Resch 1993; Danesh et al., 1998). Angiographic evidence of coronary artery disease was
correlated with WBC, RBC count, and cholesterol and triglyceride concentrations in
patients who underwent coronary arteriography and who did not have evidence of
infection or recent myocardial infarction (John et al., 1984). Elevated plasma fibrinogen
level is known to progress atherosclerosis and to be one of the risk factors for the
occurrence of cardiovascular diseases (Yoshiyasu et al., 1996). Dietary cholesterol
increased blood total leucocytes count, serum and liver total cholesterol concentrations,
low-density lipoprotein concentration and induction of atherosclerotic plaques in the
aorta and coronary arteries (Meijer et al., 1996). Thus, the effects of cholesterol feeding
periods on the changes of blood hematology and biochemistry in rabbits fed a high
cholesterol and saturated fat diet are considered to play the most important role during the
development of arteriosclerosis.
Materials and methods:
Rabbits
Twenty five 12 week-old, New Zealand white male rabbits, were purchased from
Kitayama Lab. Ltd., Kyoto, Japan, individually caged, and divided into either control
group or cholesterol-fed group. The control group (n = 10) was fed 100 g/day of normal
diet, ORC-4 (Oriental Yeast Co. Ltd., Tokyo, Japan) for feeding period of 15 weeks. The
cholesterol-fed group (n = 15) was fed high cholesterol and saturated fat diet of ORC-4
containing 0.5% cholesterol plus 0.5% olive oil (100 g/day) for feeding periods of 5, 10
and 15 weeks.
Collection of blood
Blood samples (2 ml) were obtained from the rabbits via venepuncture of an antecubital
vein. Blood was collected into two polypropylene tubes viz., one for serum and one for
plasma. The blood for plasma was collected in heparin. Serum was prepared by allowing
the blood to clot at 37 0C and centrifugation at 3000rpm for ten minutes. Fibrinogen
concentration was measured by the thrombin clotting method using a Coagulex 700
analyzer (International Reagents, Kobe, Japan). Haemoglobin, RBC, WBC, platelet,
lymphocytes, neutrophils, monocytes, and eosinophils levels were measured with
ADVIA 120 Hematology System (Bayer Medical, Tarrytown, New York, USA). Serum
TC and TG levels were analyzed by the enzymatic method used in the clinical laboratory
centre of King Khaled Hospital. HDLC and LDLC concentrations were determined by
the previously reported method (Lee et al., 1998 and Koenig et al., 1992).
Statistical analysis
The results of the present study were expressed as mean ± SE, statistical analysis for
significant differences between the control group and the cholesterol-fed group was done
with an ANOVA for repeated measurements and the significance was assessed at 5%
confidence level.
Concentration of total cholesterol (TC; mg/dl)
Results
TC (mg/dl), LDLC (mg/dl), HDLC (mg/dl) and TG (mg/dl) data of control and
cholesterol-fed rabbits are summarized in Figs. 1, 2, 3 and 4. Fig. 1 represents TC
concentration in control and cholesterol-fed rabbits. Fig. 2 represents LDLC
concentration in control and cholesterol-fed rabbits.
1000
*
(15)
*
(15)
800
* (15)
600
TC; Mean ± SE; (* P < 0.05)
(n) number of rabbits
400
200
(10)
0
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 1 represents TC (mg/dl) concentration in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Concentration of LDLC (mg/dl)
800
*
700
(15)
* (15)
*
600
(15)
500
400
300
LDLC; Mean ± SE; (* P < 0.05)
(n) number of rabbits
200
100
(10)
0
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 2 represents LDLC (mg/dl) concentration in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Fig. 3 represents HDLC concentration in control and cholesterol-fed rabbits. Fig. 4
represents TG concentration in control and cholesterol-fed rabbits. In Figs. 1, 2 and 4,
TC, LDLC and TG levels were significantly increased in cholesterol-fed rabbits as
compared with control rabbits.
Concentration of HDLC (mg/dl)
140
*
(15)
HDLC; Mean ± SE; (* P < 0.05)
(n) number of rabbits
120
* (15)
100
80
60
40
(15)
(10)
20
0
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 3 represents HDLC (mg/dl) concentration in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Concentration of triglyceride (TG; mg/dl)
550
TG; Mean ± SE; (* P < 0.05)
(n) number of rabbits
*
500
*
450
(15)
(15)
400
350
300
250
(15)
*
200
150
100
50
(10)
0
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 4 represents TG (mg/dl) concentration in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
In Fig. 3, HDLC levels were significantly decreased in cholesterol-fed rabbits at the
feeding periods 5 and 10 weeks as compared with the control rabbits. However, it was
NOT significantly different at the cholesterol feeding period 15 weeks. Fig. 5 represents
hematocrit (%) levels in control and cholesterol-fed rabbits. In Fig. 5, hematocrit (%)
levels were significantly decreased in the cholesterol-fed rabbits as compared with the
control rabbits.
46
(5)
44
Hematocrit; Mean ± SE; (* P < 0.05)
(n) number of rabbits
Hematocrit (%)
* (15)
42
*
40
(15)
*
(15)
38
36
34
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 5 represents hematocrit (%) in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Platelets (K/UL) levels
Platelets; Mean ± SE; (* P < 0.05)
(n) number of rabbits
580
560
540
520
500
480
460
440
420
400
380
360
340
320
300
280
260
* (15)
*
(15)
*
(15)
(10)
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 6 represents platelet (K/UL) levels in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Fig. 6 represents platelet (K/UL) levels in control and cholesterol-fed rabbits. In Fig. 6,
platelet (K/UL) levels were significantly increased in the cholesterol-fed rabbits as
compared with the control rabbits. Fig. 7 represents the concentration of fibrinogen
(mg/dl) levels in control and cholesterol-fed rabbits. In Fig. 7, although the fibrinogen
levels increased at the feeding period 5 weeks, it decreased at the feeding period 10
weeks, and it showed no change at the feeding period of 15 weeks. Fibrinogen levels
were NOT significantly different in cholesterol-fed group of rabbits as compared with the
control rabbits.
Concentration of fibrinogen (mg/dl)
360
(15)
340
Fibrinogen; Mean ± SE; (* P < 0.05)
(n) number of rabbits
320
300
280
(15)
(10)
260
240
220
200
180
(15)
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 7 represents fibrinogen (mg/dl) in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Concentration of haemoglobin (g/dl)
14.0
(5)
Hemoglobin; Mean ± SE; (* P < 0.05)
(n) number of rabbits
13.5
*
13.0
*
(15)
(15)
12.5
*
(15)
12.0
11.5
11.0
10.5
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 8 represents haemoglobin (g/dl) levels in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
White blood cells count (WBC; (K/UL)
Fig. 8 represents haemoglobin (g/dl) levels in control and cholesterol-fed rabbits. In Fig.
8 concentration of haemoglobin were significantly decreased in cholesterol-fed group of
rabbits as compared with the control rabbits. Fig. 9 represents WBC count (K/UL) in
control and cholesterol-fed groups of rabbits. In Fig. 9, WBC count was NOT
significantly different between the cholesterol feeding periods 5 and 10 weeks and the
control group, but it was significantly increased at the cholesterol feeding period of 15
weeks as compared with the control group.
27
26
25
24
23
22
21
20
19
18
17
16
15
14
13
12
11
(15)
*
WBCs count; Mean ± SE; (* P < 0.05)
(n) number of rabbits
(15)
(15)
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 9 represents WBCs (K/UL) count in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Red blood cells count (RBCs; (M/UL)
6.5
(10)
RBCs count; Mean ± SE; (* P < 0.05)
(n) number of rabbits
6.0
(15)
5.5
(15)
*
*
(15)
5.0
4.5
4.0
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 10 represents RBCs (M/UL) count in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Fig. 10 represents RBC count (M/UL) in control and cholesterol-fed rabbits. In Fig. 10,
RBC count (M/UL) was significantly decreased in the cholesterol feeding periods 5, 10
and 15 weeks as compared with the control rabbits.
85
80
75
(15)
Lymphocytes; Mean ± SE; (* P < 0.05)
(n) number of rabbits
*
Lymphocytes %
70
65
(15)
*
60
55
50
45
(10)
(15)
40
35
30
25
Control
5 weeks
10 weeks 15 weeks
Cholesterol feeding periods (weeks)
Fig. 11 represents Lymphocytes % in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Fig. 11 represents lymphocytes % in control and cholesterol-fed rabbits. In Fig. 11,
Lymphocytes decreased at the feeding period of 5 weeks, and significantly increased at
the cholesterol feeding periods 10 and 15 weeks as compared with the control rabbits.
70
65
(10)
(15)
Neutrophils; Mean ± SE; (* P < 0.05)
(n) number of rabbits
Neutrophils %
60
(15)
55
*
50
(15)
45
*
40
35
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 12 represents neutrophils % in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
Fig. 12 represents neutrophils % in control and cholesterol-fed rabbits. In Fig. 12,
neutrophils % increased at the cholesterol feeding period 5 weeks, and significantly (* p
< 0.05) decreased at the cholesterol feeding periods 10 and 15 weeks as compared with
the control rabbits. Fig. 13 represents monocytes % in control and cholesterol-fed rabbits.
In Fig. 13, monocytes %, monocytes % decreased at the feeding period 5 and 10 weeks,
and it showed no change at the feeding period of 15 weeks. Monocyte % was NOT
significantly different in cholesterol-fed group of rabbits as compared with the control
rabbits. Fig. 14 represents eosinophils % in control and cholesterol-fed rabbits. In Fig. 14,
eosinophils % significantly increased at the cholesterol feeding period 5 and 10 weeks,
and it significantly decreased at the cholesterol feeding period of 15 weeks.
3.4
3.2
Monocytes; Mean ± SE; (* P < 0.05)
(n) number of rabbits
3.0
Monocytes %
2.8
2.6
2.4
2.2
2.0
1.8
1.6
1.4
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 13 represents monocytes % in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
3.2
3.0
Eosinophils; Mean ± SE; (* P < 0.05)
(n) number of rabbits
(15) *
2.8
Eosinophils %
2.6
2.4
(10)
(15)
2.2
2.0
1.8
1.6
(15)
*
1.4
1.2
Control
5W
10 W
15 W
Cholesterol feeding periods (weeks)
Fig. 14 represents Eosinophils % in control and cholesterol-fed
rabbits versus cholesterol feeding periods 5, 10 and 15 weeks.
All data of Figs (1~ 14) are summarized in Table 1.
Table 1 – Changes in TC, LDLC, HDLC, TG, hematocrit, platelets, fibrinogen,
hemoglobin, WBC, RBC, lymphocytes, neutrophils, monocytes, and eosinophils in the
blood of control rabbits fed on normal diet for feeding period of 15 weeks, and
cholesterol fed rabbits fed on high cholesterol diet for feeding periods of 5, 10 and 15
weeks.
Group
Control
15 weeks (10)
Group (1)
5 weeks (15)
Group (2)
10 weeks (15)
Group (3)
15 weeks (15)
Total Cholesterol
(TC; mg/dl)
Low density
lipoprotein (LDLC;
mg/dl)
High density
lipoprotein (HDLC;
mg/dl)
Triglyceride (TG;
mg/dl)
Hematocrit (%)
54.625 ± 16.4
841.3 ± 45.4*
837.4 ± 21.5*
708.7 ± 14.8*
36 ± 10.1
677.7 ± 38.5*
677.2 ± 11.01*
608.7 ± 24.1*
18 ± 6.6
131.3 ± 5.0*
77.8 ± 26.09*
26 ± 4.0
50.1 ± 3.6
161.5 ± 4.2*
410.2 ± 54.9*
406.0 ± 120.03*
43.82 ± 1.04
38.74 ± 1.7*
40.225 ± 2.6*
35.5 ± 5.1*
Platelets
(K/UL)
Fibrinogen (mg/dl)
358.79 ± 85.75
471.0 ± 27.5*
490.75 ± 60.5*
419.66 ± 78.8*
248.33 ± 30.8
347.0 ± 0.0
186.0 ± 8.0
264.66 ± 35.02
Hemoglobin (g/dl)
13.36 ± 0.3
12.22 ± 0.5*
12.55 ± 0.7*
10.83 ± 1.5*
WBC (K/UL) count
13.78 ± 1.76
13.34 ± 2.52
13.75 ± 3.21
20.93 ± 4.51*
RBC (K/UL) count
6.21 ± 0.12
5.7 ± 0.28*
4.90 ± 0.30*
4.28 ± 0.93*
Lymphocytes %
39.4 ± 8.96
34.8 ± 5.54
57.75 ± 3.27*
60 ± 2.0*
Neutrophils %
57.8 ± 9.94
62.4 ± 6.79
41 ± 4.88*
36.33 ± 18.83*
Monocytes %
2.33 ± 0.33
2.12 ± 0.11
1.5 ± 0.64
2.33 ± 0.88
Eosinophils %
2.0 ± 0.57
2.15 ± 0.3
2.66 ± 0.66*
1.33 ± 0.66*
(
) is the number of rabbits; Mean ± SE (* P < 0.05)
Discussion
The effects of hypercholesterolemia are not only confined to the deposition of lipids in
the atherosclerotic lesions and produce primary endothelial injury, but it produced
abnormalities in blood haematology and biochemistry of rabbits fed high cholesterol diet.
A high-cholesterol diet elevated level of plasma TC and LDLC to be incorporated into
the atherosclerotic plaques. When LDLC is oxidized by macrophages in lesions, it
becomes toxic to the endothelium, and thereby could injure endothelial cells. Serum
LDLC and HDLC levels have effects on blood viscosity and correlate with increased risk
of atherogenesis (Sloop and Garber, 1997). The present study demonstrated that TC,
LDLC and TG levels significantly increased in cholesterol-fed rabbits as compared with
control rabbits. On the contrary, HDLC levels significantly decreased in cholesterol-fed
rabbits at the feeding periods of 5 and 10 weeks. Low HDLC levels are associated with
an elevated blood viscosity, and this rheological abnormality contributes to
cardiovascular risks (Thomas et al., 1999). It has been reported that serum
hypercholesterolemia accelerates atherogenesis and contributes to symptomatic
atherosclerosis by increasing blood viscosity and disturbing the mechanical fragility of
atherosclerotic plaques making them vulnerable to rupture and thrombosis (Gregory,
1999). The Hemorheological-hemodynamic theory suggests that the increased blood
viscosity associated with serum hypercholesterolemia accelerates atherogenesis (Sloop,
1996). Hemorheological or haemostatic mechanisms that might promote
thromboatherogenesis include the predisposition to thrombosis via a hypercoagulable
state, the enhancement of atherosclerosis by fibrinogen and its metabolites, and finally
the reduction of blood flow through various rheological effects (e.g., increase in plasma
viscosity and red cell aggregation, or leukocyte activation). Deeper insight into the
mechanisms involved might lead to new preventive strategies as well as to therapeutic
procedures in the management of atherosclerosis and associated thrombotic events
(Wolfgang and Ernst, 1992). Hypercholesterolemia modulates homeostasis by altering
the expression and/or function of thrombotic, fibrinolytic and rheologic factors
(Rosenson et al., 1998). Platelet aggregation studies in vitro demonstrated that
hypercholesterolemic patients were more sensitive to aggregatory agents than platelets
from normocholesterolemic (Corash et al., 1981; Di et al., 1986). LDL bonded directly to
the platelet glycoprotein receptor which serves as the binding site for several agonists
including fibrinogen, fibronectin, thrombospondin and vitronectin (Hantgan et al., 1990;
Plow et al., 1985; Parise et al., 1986). The present study demonstrated that fibrinogen
levels were NOT significantly different in cholesterol-fed rabbits as compared with
control rabbits. Fibrinogen levels are elevated in familial hypercholesterolemia patients
(Di et al., 1986), and in a population study, fibrinogen concentration is weakly, but
positively associated with LDLC (Koenig et al., 1992). Adenosine diphosphate (ADP)induced fibrinogen binding to platelets is increased in a dose-dependent manner by LDL
(0.5-2.0 mg/dl protein), and resulting in faster aggregation and formation of larger
platelet aggregates without a change in thromboxane B2 production (Di et al., 1986). The
present study demonstrated significantly increase in WBC count at the cholesterol
feeding period of 15 weeks as compared with the control group, this lead to the adherence
of leukocyte to the endothelium which represents one of the early responses to injury.
Among the cells, the basal adherence of monocyte only was significantly elevated in
atherosclerosis, resulting in increased adherence to endothelial cells (Dovgan et al.,
1994). This study suggested that monocyte level was NOT significantly different in the
cholesterol-fed group of rabbits as compared with the control rabbits. Moreover,
lymphocytes significantly increased at the cholesterol feeding periods of 10 and 15 weeks
as compared with the control rabbits and eosinophils level significantly increased at the
cholesterol feeding period of 5 and 10 weeks, but it significantly decreased at the
cholesterol feeding period of 15 weeks. On the contrary, neutrophils level significantly
decreased at the cholesterol feeding periods of 10 and 15 weeks as compared with the
control rabbits. In conclusion, these results strongly suggested that rabbits fed high
cholesterol and saturated fat diet have impaired blood rheology and elevated circulating
TC and LDLC and TG concentrations compared with control rabbits The elevation of TC
and LDLC and TG concentrations may be associated with the pathophysiology of the
atherosclerotic process in hypercholesterolemic rabbits and may be responsible for the
risk of cardiovascular diseases. The progress of atherosclerosis may be related to the
changes in cholesterol metabolism, increased rheology of blood and/or, most likely, free
iron concentration and oxidized lipoproteins are a major contributing factor in
atherosclerosis. 15-Lipoxygenase is the principal enzyme that can oxidize polysaturated
fatty acids present in intact lipoproteins, and in membrane phospholipids in situ. It has
reported that 15-Lipoxygenase levels in heart, aortic adventitia, and lung, but not in liver,
were increased up to 100-fold in rabbits fed an atherogenic diet containing 1%
cholesterol for 14 weeks above controls (Martin et al., 1986; Bailey et al., 1995). The
elevation of plasma viscosity is considered a predictor of atherosclerotic vascular disease
as well as a potential mechanism for increasing the risk of cardiovascular diseases.
Further studies are required to investigate whether lipid lowering therapies may improve
impaired rheology in rabbits with hypercholesterolemia to prevent cardiovascular
disorders.
Acknowledgements
This research work was kindly supported by College of Science-Research center project
(Phys/2006/41), College of Science, King Saud University.
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