High sugar intake exacerbates cardiac reperfusion injury in perinatal taurine depleted adult rats.

Abstract

Perinatal taurine depletion and high sugar diets blunted baroreflex function and heightens sympathetic nerve activity in adult rats. Cardiac ischemia/reperfusion also produces these disorders and taurine treatment appears to improve these effects. This study tests the hypothesis that perinatal taurine exposure predisposes recovery from reperfusion injury in rats on either a basal or high sugar diet. Female Sprague-Dawley rats were fed normal rat chow with 3% beta-alanine (taurine depletion, TD), 3% taurine (taurine supplementation, TS) or water alone (control, C) from conception to weaning. Male offspring were fed normal rat chow and water containing 5% glucose (G) or water alone (W) throughout the experiment. At 7-8 weeks of age, all rats were anesthetized and their trachea clamped until cardiac arrest occurred and mean arterial pressure fell below 60 mm Hg. The clamp was immediately released and cardiopulmonary resuscitation was performed with cardiac function returning within 4 min. Twenty-four hours later, arterial pressure, heart rate, and baroreflex function were measured in conscious and one day later in anesthetized conditions. Basic blood chemistry and circulating markers of cardiac injury were also measured. Baroreflex sensitivity was depressed moderately in CG and TDW, and severely in TDG. TSW displayed increased baroreflex and high sugar intake returned it to CW. Sympathetic nerve activity increased and parasympathetic decreased in TDW but not TSW and these effects were exacerbated sharply in TDG and slightly in TSG. Arterial pressure and heart rate increased in all groups but to a lesser degree in TDG. Plasma aspartate aminotransferase increased in all groups except TSW, but the increase was nearly 3X greater in TDG vs. any other group. Creatine kinase-MB increased in all groups except TSG and was far greater in TD than other groups. Troponin-T and brain natriuretic peptide were greatly increased in TDG compared to all other groups. Thus, perinatal taurine depletion increases injury from cardiac ischemia/reperfusion, and in adult rats on a high sugar diet, these effects are greatly exacerbated.

Full text

Page 1

REVIEWOpen Access
High sugar intake exacerbates cardiac reperfusion
injury in perinatal taurine depleted adult rats
Supaporn Kulthinee1, J Michael Wyss2, Dusit Jirakulsomchok1, Sanya Roysommuti1*
From 17thInternational Meeting of Taurine
Fort Lauderdale, FL, USA. 14-19 December 2009
Abstract
Perinatal taurine depletion and high sugar diets blunted baroreflex function and heightens sympathetic nerve
activity in adult rats. Cardiac ischemia/reperfusion also produces these disorders and taurine treatment appears to
improve these effects. This study tests the hypothesis that perinatal taurine exposure predisposes recovery from
reperfusion injury in rats on either a basal or high sugar diet. Female Sprague-Dawley rats were fed normal rat
chow with 3% beta-alanine (taurine depletion, TD), 3% taurine (taurine supplementation, TS) or water alone (con-
trol, C) from conception to weaning. Male offspring were fed normal rat chow and water containing 5% glucose
(G) or water alone (W) throughout the experiment. At 7-8 weeks of age, all rats were anesthetized and their tra-
chea clamped until cardiac arrest occurred and mean arterial pressure fell below 60 mm Hg. The clamp was imme-
diately released and cardiopulmonary resuscitation was performed with cardiac function returning within 4 min.
Twenty-four hours later, arterial pressure, heart rate, and baroreflex function were measured in conscious and one
day later in anesthetized conditions. Basic blood chemistry and circulating markers of cardiac injury were also mea-
sured. Baroreflex sensitivity was depressed moderately in CG and TDW, and severely in TDG. TSW displayed
increased baroreflex and high sugar intake returned it to CW. Sympathetic nerve activity increased and parasympa-
thetic decreased in TDW but not TSW and these effects were exacerbated sharply in TDG and slightly in TSG. Arter-
ial pressure and heart rate increased in all groups but to a lesser degree in TDG. Plasma aspartate aminotransferase
increased in all groups except TSW, but the increase was nearly 3X greater in TDG vs. any other group. Creatine
kinase-MB increased in all groups except TSG and was far greater in TD than other groups. Troponin-T and brain
natriuretic peptide were greatly increased in TDG compared to all other groups. Thus, perinatal taurine depletion
increases injury from cardiac ischemia/reperfusion, and in adult rats on a high sugar diet, these effects are greatly
exacerbated.
Introduction
Myocardial ischemia is the leading cause of death
among people around the world [1,2]. Cardiac arrest
also accounts for 20% of deaths following myocardial
infarction, primarily in the first 1-7 days (75%) [3]. Myo-
cardial ischemia has a close relation to the autonomic
nervous system dysregulation; particularly heighten sym-
pathetic nerve activity before symptoms and during
recovery. In myocardial infarction patients, sympathetic
nerve activity is elevated by a few days after ischemia
(2–4 days) and remains high for 3-6 months [4]. Barore-
ceptor reflex control of heart rate is also blunted or
resetting in these patients [5-8]. b-blockers are often
prescribed for the treatment of patients with chronic
heart failure [9] and myocardial infarction [10,11].
Taurine has been reported to improve cardiac func-
tion in many disorders. Plasma taurine increases in
patients with acute myocardial ischemia and increases
with the severity of the infarction [12]. Its source seems
to be mainly from the myocardium. In this case, other
cardiac peptides also increase, e.g., B-type natriuretic
peptide [13]. The circulating taurine concentration in
these patients increases for up to three days, paralleling
the increased creatine kinase levels [12]. Taurine appears
* Correspondence: sanya@kku.ac.th
1Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon
Kaen 40002, Thailand
Full list of author information is available at the end of the article
Kulthinee et al. Journal of Biomedical Science 2010, 17(Suppl 1):S22
http://www.jbiomedsci.com/content/17/S1/S22
© 2010 Roysommuti et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.

Page 2

to be able to inhibit sympathetic nerve overactivity in
these patients [14,15], and thus taurine may retard the
rise in sympathetic nerve activity during ischemia and
post cardiac reperfusion and protect the heart from
adverse effects of sympathetic nerve hyperactivity and
its consequences [16,17].
Taurine plays an important role in animals and
humans at all age periods especially at the early life
[18,19]. Prenatal taurine deficiency induces low birth
weight in animals and the adult offspring are at high
risk of cardiovascular diseases, diabetes mellitus, and
renal damage [20]. Perinatal taurine supplementation, in
contrast, attenuates hypertension in spontaneously
hypertensive rats [21,22]. Previous experiments indicated
that either taurine depletion or supplementation in early
life altered renal function [23] and autonomic nervous
control of arterial pressure [24] in adult rats. Their renal
hemodynamics and excretory function are also modified
by altered perinatal taurine exposure [23].
Perinatal taurine depletion depresses the autonomic
function and blunts baroreflex function in adult male
rats [24]. If these animals are treated by high sugar
intake since weaning, the blunted baroreflex function
will be exacerbated and sympathetic nerve activity is in
turn heightened. Perinatal taurine supplementation does
not possess this action. Blunted baroreflex function and
sympathetic nerve overactivity are also observed in car-
diac ischemia/reperfusion, and these changes appear to
be reduced by taurine treatment [16,17]. Whether peri-
natal taurine over or under exposure predisposes the
autonomic nervous system function and cardiac injury
in this abnormality has not been established. The pre-
sent study tests the hypothesis that perinatal taurine
exposure increases the efficiency of autonomic nervous
system control of arterial pressure at the early phase of
recovery from cardiac arrest (2-5 days) in adults. Perina-
tal taurine supplementation or deficiency effects are
compared to lifetime normal taurine diet control off-
spring. Their interactions with high sugar intake since
weaning were also investigated.
Materials and methods
Animal preparation
Sprague-Dawley (SD) rats were bred at the animal unit of
Faculty of Medicine, Khon Kaen University and main-
tained at constant humidity (60 ± 5%), temperature (24 ±
1oC), and light cycle (06.00-18.00 h). Female SD rats
were fed normal rat chow with 3% beta-alanine (taurine
depletion, TD), 3% taurine (taurine supplementation, TS)
or water alone (Control, C) from conception to weaning.
Thereafter, the male offspring were fed normal rat chow
and tap water ad libitum. Further, the male offspring
drank either 5% glucose in tap water (TD with glucose,
TDG; TS with glucose, TSG; C with glucose, CG) or tap
water alone (TDW, TSW, and CW) throughout the
experiment. 5% glucose was previously reported to alter
renal function before hypertension and diabetes mellitus
[25] and to increase the sympathetic nerve activity in
TDG rats [24]. All experimental procedures were preap-
proved by the Khon Kaen University Animal Care and
Use Committee and were conducted in accordance with
the National Institutes of Health guidelines.
Experimental protocol
At 7-8 weeks of age, rats were anesthetized with thio-
pental sodium (50 mg/kg, i.p.). After catheterization of
femoral artery for arterial measurement and blood sam-
pling and femoral vein for infusions, arterial pressure
was continuously monitored (BIOPAC, Goleta, CA,
USA). A tracheal tube was slowly and carefully inserted
through the mouth. After a 15-20 min acclimation and
while still under deep anesthesia, cardiac arrest was
induced by a direct tracheal tube clamping. When the
heart arrested and mean arterial pressure went below
60 mm Hg, the clamp was released and cardiopulmon-
ary resuscitation (CPR) was immediately performed by
manual chest compression at 60 times/min. Ventilation
was continuously controlled by a ventilator through the
tracheal tube. The return of arterial pressure pulse and
voluntary respiration indicated the success of CPR
(within 4 min). Two days later, arterial pressure pulses
were continuously recorded in a conscious condition
before and during infusion of phenylephrine (increased
arterial pressure) or sodium nitroprusside (decreased
arterial pressure) to assess the baroreflex sensitivity.
One-day later, male rats were anesthetized with thio-
pental sodium, tracheostomized, and arterial pulse
recorded continuously. Body temperature was servo-
controlled at 37±0.5°C by a rectal probe connected to a
temperature regulator controlling an overhead heating
lamp. Laparotomy was done by longitudinal incision on
the mid line area of abdomen. Then, the right renal
artery was exposed and a stainless steel electrode (12 M
Ω, 0.01 Taper, A-M system, FL, USA) was slowly
inserted to the renal nerve, using a gold-plated electrode
holder connected to a micromanipulator. A second elec-
trode was attached to the snipped abdominal muscle
close to the recording site. Both electrodes were con-
nected to a DAM-80 differential amplifier (WPI, USA)
which amplified (1000x) a band pass (500-1000 Hz) sig-
nal via a UM100, MP100, and a computer, respectively
(BIOPAC). All data were continuously recorded (sam-
pling rate = 5,000 sample/sec). After these experiments,
animals were rested for 30 min. Then, arterial blood
samples were obtained and sodium (Na), potassium (K),
hematocrit (Hct), blood sugar, creatine kinase–MB (CK-
MB), troponin T (Trop-T), aspartate aminotransferase
(AST), and N-Terminal prohormone Brain Natriuretic
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Peptide (NT-proBNP) determinations were made.
Finally, all animals were sacrificed and kidney and heart
weights were measured.
Data analyses
All data were analyzed by using the Acknowledge Soft-
ware (BIOPAC). Changes in renal nerve activity and
heart rate per changes in arterial pressure following
sodium nitroprusside or phenylephrine infusion were
used to measure baroreceptor reflex control of renal
nerve activity (BSRN) and heart rate (BRHR). The auto-
nomic nervous system control of arterial pressure was
estimated by analyzing the power spectrum density of
low (LF, 0.3-0.5 Hz; the sympathetic nerve activity
dominant) and high (HF, 0.5-4.0 Hz; the parasympa-
thetic nerve activity dominant) frequency components of
arterial pulse (Fourier analysis). The absolute values
were normalized by the total power (LF+HF). In addi-
tion, all blood chemistry parameters were specifically
measured by the Khon Kaen University hospital
laboratory.
All data were expressed as mean ± SEM. Statistical
comparisons among groups were performed by using
one-way ANOVA followed by post hoc tests. Duncan’s
Multi-Range and paired t-tests were used to indicate
significant differences among groups and within groups,
respectively (Statmost version 3.5, DataMost, USA). The
significant criterion was p< 0.05.
Results
Compared to CW, body, heart, and kidney weights sig-
nificantly decreased only in TDW groups. Kidney to
body but not heart to body weight ratios also were
decreased in TDW (Table 1). This decrement was
restored to CW levels by high sugar intake. TSG (com-
pared to CG and TSW rats) displayed slightly increased
body and heart weights. At the end of experiment,
plasma sodium concentration slightly decreased in
TSW, but not in any other group (Table 2). Compared
to CW, CG, TDW and TDG displayed significantly
higher plasma potassium concentrations but TSW and
TSG did not differ from CW rats in this measure.
Plasma glucose concentration varied within the normal
range for non-fasting rats (75-100 mg/dl) in most
groups, but compared to the other groups, TDW and
TDG displayed lower and higher values, respectively.
Compared to other groups, TDG displayed a sharp rise
in BUN and a lower hematocrit. Plasma creatinine levels
significantly increased in all perinatal taurine depleted
and supplemented rats, those of TDW were lowest, but
they were partially restored to control levels by glucose
supplementation. All plasma cardiac injury markers dis-
played higher concentrations in TD, compared to the
other groups of the same dietary sugar status (Table 3).
Prior to the cardiac arrest procedure, MAP of all
groups varied between 100 to 120 mm Hg (Table 4);
TD rats displayed significantly higher arterial pressure
than controls, while TS rats displayed significantly lower
arterial pressure than controls. Three days after cardiac
arrest resuscitation recovery, all groups displayed signifi-
cantly increased arterial pressure, and no longer dis-
played any group differences, except for TSG, which
was about 5 mm Hg lower than the arterial pressures in
all other groups. Among the groups, TDG displayed a
significantly decreased post-reperfusion increase in
arterial pressure (3.3% compared to 7-20%). Tachycardia
responses to the reperfusion were very similar to the
MAP changes, including the finding that TDG displayed
the least change (1.4% compared to 6-18%). Baroreflex
sensitivity of heart rate and renal sympathetic nerve
activity were significantly blunted in TDW and TDG
when compared to CW or CG (Table 5). High sugar
intake exacerbated this disorder. In contrast, a signifi-
cant increase in baroreflex sensitivity was observed in
perinatal taurine supplemented rats, a condition that
was attenuated by high sugar intake. It is worth noting
that high glucose intake alone slightly and significantly
depressed the baroreflex sensitivity in the CG group.
Three days after cardiac arrest, sympathetic nerve
activity (indirectly estimated by low frequency compo-
nent of arterial pulse) in CG and TSW was unchanged
and was not influenced by glucose. Both glucose and
control diet TD rats displayed a significantly elevated
low frequency component (Fig. 1). Parasympathetic
Table 1 Body (BW), heart (HW), and kidney (KW) weights among groups
TreatmentBW
(g)
HW
(g)
KW
(g)
HW/BW
(%)
KW/BW
(%)
CW
CG
TDW
TDG
TSW
TSG
190 ± 1
192 ± 1
169 ± 1*
190 ± 2£
191 ± 2
204 ± 2#,€
0.78 ± 0.01
0.82 ± 0.02
0.67 ± 0.01*
0.83 ± 0.01£
0.82 ± 0.01*
0.89 ± 0.01#,€
0.97 ± 0.01
0.91 ± 0.02
0.76 ± 0.01*
0.98 ± 0.01£
1.05 ± 0.02
0.96 ± 0.10
0.41 ± 0.01
0.43 ± 0.01
0.40 ± 0.01
0.44 ± 0.01£
0.43 ± 0.00
0.43 ± 0.00
0.51 ± 0.01
0.47 ± 0.01
0.45 ± 0.0*
0.52 ± 0.01£
0.55 ± 0.01
0.47 ± 0.05€
Data are mean SEM (n = 10 each groups). *,#,€,£P < 0.05 when compared to CW*, CG#,
TSW€, and TDW£; see text for abbreviations.
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(high frequency) nerve activity was not altered by the
high sugar diet, but it was decreased in the TD groups
compared to all other groups. In TS rats, the parasym-
pathetic nerve activity was significantly higher than CW
or CG, while the sympathetic nerve activity was
remained at CW levels and slightly increased by the
high sugar intake.
Discussion
Previous experiments indicate that perinatal taurine
depletion depresses baroreflex sensitivity and the auto-
nomic nervous system activity in adult male rats [24]. A
high sugar diet would be expected to exacerbate this
baroreflex impairment and increase sympathetic nerve
activity. The present data indicate that, three days after
cardiac arrest, these abnormal responses are present and
markedly amplified. In addition, the present data are the
first to demonstrate that perinatal taurine supplementa-
tion improves baroreceptor reflex function and main-
tainsnearnormal autonomic
Moreover, perinatal taurine depletion alone increased
cardiac injury, a condition that is markedly exacerbated
by a high sugar diet.
The decreased (compared to CW) body weight in
TDW and the high sugar diet ability to restore body
weight in TDG are similar to that previously reported
[24]. While the lower body weight in TDW is unlikely
to play a major role in post-cardiac arrest changes in
this group, since TDG rats had a normal body weight
but displayed exacerbated adverse effects of the cardiac
nervous activity.
arrest/resuscitation. Taurine influences growth and
development in the early life. Its perinatal deficiency
induces low birth weight and injuries to several body
organs [18,19]. The low body weight at birth has been
shown to underline a high risk of obesity, diabetes melli-
tus, hypertension and coronary vascular diseases in the
mature life [26-29]. One possible mechanism is due to
the body’s propensity to prefer anabolism over catabo-
lism; this is supported by changes in metabolic enzymes
in adipose tissues, muscle and liver. This may partially
explain why TDG display normal weight as adults. How-
ever, the existence of baroreflex sensitivity dysregulation
implies that perinatal taurine depletion leads to long-
term changes in rats. In contrast, perinatal taurine sup-
plemented rats display changes in baroreflex that are
not related to body weight. Thus, low birth weights may
not play a key role of cardiovascular system dysregula-
tion following perinatal taurine under- or over-exposure.
Acute cardiac arrest produces hypotension. Resuscita-
tion, while saving the organism, leads to reperfusion,
which initiates mechanisms that damage the heart
[30-32]. These mechanisms likely include increased cal-
cium entry into cardiac myocytes, sympathetic nerve
hyperactivity, superoxide generation, and release of
adverse enzymes. Taurine content increases early in the
cardiac recovery period and taurine supplementation
before or after cardiac ischemia has been shown to pro-
tect the ischemia/reperfusion injury [12,16,17]. Barore-
flex sensitivity also blunted while arterial pressure rises
probably as a result of sympathetic nerve hyperactivity
Table 2 General blood chemistry profiles in anesthetized animals
TreatmentPlasma Na
(mEq/L)
Plasma K
(mEq/L)
Blood sugar
(mg/dl)
BUN
(mg/dl)
Plasma Cr
(mg/dl)
Hct
(%)
CW
CG
TDW
TDG
TSW
TSG
137.30±1.25
135.80±0.74
138.30±0.70
136.30±0.72
132.30±0.75*
136.00±0.83€
4.42±0.11
5.21±0.15*
5.47±0.10*
5.60±0.13*,#
4.73±0.08
4.57±0.10
94.30±1.08
91.40±0.85*
78.10±1.29*
98.70±0.82*,#,£
88.30±0.99*
85.80±0.76*,#
15.61±0.79
15.58±0.59
17.44±0.83
27.77±2.31#,£
14.00±0.80
16.10±0.73
0.61±0.06
0.47±0.05
0.37±0.03*
0.52±0.06*,£
0.46±0.04*
0.46±0.05*
37.80±0.76
37.30±0.47
35.90±0.55*
33.90±0.53*,#
39.30±0.63
39.30±0.47#
Data are mean SEM (n = 10 each groups). *,#,€,£P < 0.05 when compared to CW*, CG#,
TSW€, and TDW£; see text for abbreviations.
Table 3 Blood cardiac injury markers in anesthetized animals
TreatmentAST
(u/l)
CK–MB
(u/l)
Trop T
(ng/ml)
NT-proBNP
(pg/ml)
CW
CG
TDW
TDG
TSW
TSG
162.10±5.41
714.00±51.47*
491.50±9.84*
1471.50±110.24*,#,£
171.00±4.44#
544.60±65.32*,#,€
275.00±25.53
410.50±28.50*
621.10±37.87*
1084.40±30.12*,#,£
477.20±25.17*
286.00±29.38#,€
<0.01
<0.01
<0.01
0.07±0.04
<0.01
<0.01
<5
<5
<5
7.8±0.41
<5
<5
Data are mean SEM (n = 10 each groups). *,#,€,£P < 0.05 when compared to CW*, CG#,
TSW€, and TDW£; see text for abbreviations.
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and subsequently increased total peripheral resistance
[32,33]. Although all these common phenomena were
also observed in the present experiment, some amplifi-
cation was significantly noted.
We previously reported that perinatal taurine deple-
tion alone depressed autonomic nerve activity in adult
male rats and this was reversed and over activated by a
high sugar diet [24]. The high sugar treatment alone
does not have any effect on the nerve activity or barore-
flex sensitivity. In the present study, TD rats displayed
sympathetic nerve overactivity, suggesting that these
changes are related to ischemia/reperfusion. Blunted
baroreflex function was also exacerbated by TD, as sup-
ported by a consistent decrease in baroreflex sensitivity
control of both heart rate and renal nerve activity tested
by either phenylephrine or sodium nitropusside. Non
cardiac ischemia/reperfusion TDW depressed mainly
that control of heart rate while that control of renal
nerve activity significantly decreased only that tested by
sodium nitroprusside infusion [24]. In addition, the high
sugar intake exaggerated sympathetic nerve hyperactivity
in the present study. The cardiovascular responses to
ischemia/reperfusion recovery are thus amplified by
perinatal taurine depletion. Interestingly, TD decreased
parasympathetic nerve activity while it increased sympa-
thetic nerve activity.
All cardiac injury markers increased in TDG animals
when compared to CW and other groups, suggesting
increased myocardial damage in these animals [34-37].
These largest increases also suggest that a combination
of high sugar intake and perinatal taurine depletion has
the greatest impact on ischemia/reperfusion-induced
myocardial damage. Elevated troponin-T and NT-
proBNP confirmed significant ventricular injury in these
animals compared to all other groups. These markers
are released mainly from the cardiac ventricle [36,37].
The rise in plasma potassium levels in TDG also may
indicate that myocardial damage and metabolic acidosis
during the early phase of ischemia/reperfusion recovery,
are potentiated in these animals [38]. In contrast to
perinatal taurine depletion, perinatal taurine supplemen-
tation appears to have negligible effect on myocardial
injury. It is noted that AST and CK-MB are not specific
markers for myocardial injury; liver or muscle damage
can also elevate their plasma levels [34,35]. Troponin-T
and NT-proBNP are much more specific markers for
cardiac damage [39,40].
Three days after cardiac arrest/resuscitation recovery,
MAP and HR significantly increased in all rats. These
changes are not consistent with blunted baroreflex and
heightened sympathetic nerve activity in the TD com-
pared to CG or TSG rats. The rise in arterial pressure
in response to ischemia/reperfusion appears to be
initiated by cardiac sympathetic afferent nerve from the
ischemic or infracted heart tissue [32]. Increased vascu-
lar resistance and heart rate determines arterial pressure
in this condition. Further, sympathetic nerve hyperactiv-
ity is related to the size of the ischemia or infract
Table 5 Baroreflex sensitivity control of heart rate (BSHR) and renal nerve activity (BSRA) in conscious animals
TreatmentBSHR (bpm/mm Hg) BSRA (spikes/mm Hg)
PhenylephrineNitroprussidePhenylephrine Nitroprusside
CW
CG
TDW
TDG
TSW
TSG
2.40±0.02
2.24±0.01*
1.99±0.05*
1.96±0.02*,#
2.89±0.04*
2.46±0.01#,€
3.66±0.02
3.27±0.25*
3.12±0.12*
2.94±0.01*
3.94±0.08
3.84±0.01#
10.56±0.57
7.37±0.02*
8.79±0.58*
6.35±0.03*,£
12.36±0.67*
9.55±0.02#,€
13.75±1.05
13.70±0.04
10.41±0.74*
5.72±0.02*,#,£
14.20±0.77
12.42±0.02
Data are mean SEM (n = 10 each groups). *,#,€,£P < 0.05 when compared to CW*, CG#,
TSW€, and TDW£; see text for abbreviations.
Table 4 Mean arterial pressure and heart rate before and after cardiac arrest in anesthetized animals
Treatment Mean arterial pressure (mm Hg)Heart rate (bpm)
Pre-arrestRecovery
122 ± 1π
123 ± 1π
123 ± 1π
124 ± 1π
123 ± 1π
117 ± 1*,€,π
%Pre-arrest Recovery
422 ± 1π
483 ± 2*,π
437 ± 4*,π
423 ± 2#,£
427 ± 2,π
434 ± 2*,#,€,π
%
CW
CG
TDW
TDG
TSW
TSG
110 ± 2
112 ± 2
115 ± 2*
120 ± 1*,#,£
102 ± 1*,#
103 ± 1*,#
10.9
9.8
7.0
3.3
20.6
13.6
395 ± 5
411 ± 2*
408 ± 3*
417 ± 1*
392 ± 3#
409 ± 1*,€
6.8
17.5
7.1
1.4
8.9
6.1
Data are mean SEM (n = 10 each groups). *,#,€,£P < 0.05 when compared to CW*, CG#,
TSW€, and TDW£; see text for abbreviations,πP< 0.05 paired Student t-test of same groups; see text for abbreviations.
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[30-33]. In the present study, the increased plasma car-
diac injury marker levels suggest that TDG animals
develop more myocardial damage or larger infarct size
than other groups. Thus, this injury likely activates sym-
pathetic nerve hyperactivity more than in other groups.
The high glucose intake significantly increased BUN in
TD rats more than other groups. This might be due to
tissue damage rather than severe renal glomerular
damage since plasma creatinine levels were not different
from those of CW or CG groups. In general, the plasma
creatinine increases in case of decreased glomerular fil-
tration and/or muscle damage [41]. Non-fasting blood
sugar concentrations remained within normal range (70-
110 mg/dl) and the minor differences among groups did
not correlate with changes in cardiovascular responses.
Conclusions
Taurine is the main free amino acid in cardiac muscle
and plays many protective roles for the heart. The pre-
sent study indicates that perinatal taurine depletion and
high sugar intake exacerbates ischemia/reperfusion
induced cardiovascular dysregulation in adult male rats,
and the depletion appears to predispose these animals
to increased myocardial damage and decreased recovery.
List of abbreviations used
CW: control with water intake alone; CG: control with high sugar intake;
TDW: perinatal taurine depletion (TD) with water intake alone; TDG: perinatal
taurine depletion with high sugar intake; TSW: perinatal taurine
supplementation (TS) with water intake alone; TSG: perinatal taurine
supplementation with high sugar intake; BW: body weight; HW: heart
weight; KW: kidney weight; SD: Sprague Dawley; i.p.: intraperitoneal; BSRA:
baroreceptor reflex sensitivity control of renal nerve activity; BSHR:
baroreceptor reflex sensitivity control of heart rate; SEM: standard error of
means; BUN: blood urea nitrogen; Hct: hematocrit; K: potassium: Na: sodium;
Cr: creatinine; CK-MB: creatine kinase-MB: Trop-T: troponin-T; CPR:
cardiopulmonary resuscitation; AST: aspartate aminotransferase; NT-proBNP:
N-Terminal prohormone Brain Natriuretic Peptide; HF: high frequency; LH:
low frequency; bpm: beat per minute.
Acknowledgements
This study was supported in part by a grant from the Faculty of Medicine,
Khon Kaen University, Khon Kaen 40002, Thailand and by the USA National
Institutes of Health (NIH) grant AT 00477 (JMW).
This article has been published as part as part of Journal of Biomedical
Science Volume 17 Supplement 1, 2010: Proceedings of the 17th
International Meeting of Taurine. The full contents of the supplement are
available online at http://www.jbiomedsci.com/supplements/17/S1.
Author details
1Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon
Kaen 40002, Thailand.2Department of Cell Biology, School of Medicine,
University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Authors’ contributions
1. Supaporn Kulthinee: research proposal preparation, data collection and
analysis, article preparation
2. J. Michael Wyss: research consult, article preparation
3. Dusit Jirakulsomchok: research consult, article preparation
4. Sanya Roysommuti: research proposal design, data analysis, article
preparation, correspondence
Competing interests
The authors declare that they have no competing interests.
Published: 24 August 2010
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doi:10.1186/1423-0127-17-S1-S22
Cite this article as: Kulthinee et al.: High sugar intake exacerbates
cardiac reperfusion injury in perinatal taurine depleted adult rats.
Journal of Biomedical Science 2010 17(Suppl 1):S22.
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