20 / 102
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 3, May/June 2016
142
AFRICA
Our data suggest that hypertrophic indices decline from four
to six weeks post surgery, with myocardial hypertrophy reaching
its peak at four weeks in rats. This observation may be associated
with acute pressure overload within four weeks post surgery, and
then LV pressure decreases slightly (data not shown), leading to
alleviation of myocardial hypertrophy, as previously shown.
18
As an important biological marker, BNP concentrations in
the plasma may increase in line with increased haemodynamic
stress, or ventricular cavity expansion in the case of cardiac
hypertrophy and heart failure.
14,19-21
In the present study, plasma
BNP concentrations were associated with the duration of
AAC. As the duration extended, BNP levels were progressively
elevated, for example, 307, 396 and 474% higher than in the sham
groups at three, four and six weeks, respectively.
Some limitations of this study should be considered. E and
A waves were not isolated due to the high heart rates of rodents.
In addition, the longest time point studied (six weeks) was
not long enough to observe the transition from concentric to
eccentric hypertrophy. Echocardiographic measurements were
performed under anaesthesia, which is known to alter cardiac
and respiratory function, even if the doses used were the
minimum necessary.
Conclusion
This study demonstrated that constriction of the abdominal
aorta between the branches of the coeliac and anterior
mesenteric arteries, to a diameter of 0.55 mm in young rats
represents an excellent experimental animal model of pressure
overload-induced myocardial hypertrophy. This model induces
hypertrophy that occurs at three weeks or earlier, developing to a
peak at four weeks, and recovering slightly at six weeks. Changes
in cardiac structure and function during the development of
cardiac hypertrophy were monitored using a standard ultrasound
probe. LVm was determined using echocardiography and was
consistent with the actual tissue weights. By using this animal
model, we aim to provide a theoretical and experimental
foundation for the application of novel drugs, for example, high-
specificity and high-affinity receptor antagonists or agonists to
intervene in the pathogenesis of clinical LVH.
This study was supported by grants from the National Natural Science
Foundation of China (No.30440053) and the Natural Science Foundation of
Guang Dong Province, China (No. S2011010004269 and 9151018201000029).
References
1.
Boluyt MO, Robinson KG, Meredith AL,
et al
. Heart failure after long-
term supravalvular aortic constriction in rats.
Am J Hypertens
2005;
18
(2 Pt 1): 202–212.
2.
Molina EJ, Gupta D, Palma J,
et al
. Novel experimental model of pres-
sure overload hypertrophy in rats.
J Surg Res
2009;
153
(2): 287–294.
3.
Cantor EJ, Babick AP, Vasanji Z, Dhalla NS, Netticadan T. A compara-
tive serial echocardiographic analysis of cardiac structure and func-
tionin rats subjected to pressure or volume overload.
J Mol Cell Cardiol
2005;
38
(5): 777–786.
4.
Xu R, Lin F, Zhang S, Chen X, Hu S, Zheng Z. Signal pathways
involved in reverse remodeling of the hypertrophic rat heart after pres-
sure unloading.
Int J Cardiol
2010;
143
(3): 414–423.
5.
Kompa AR, Wang BH, Phrommintikul A,
et al.
Chronic urotensin II
receptor antagonist treatment does not alter hypertrophy or fibrosis
in a rat model of pressure-overload hypertrophy.
Peptides
2010;
31
(8):
1523–1530.
6.
Shah KB, Duda MK, O’Shea KM,
et al
. The cardioprotective effects of
fish oil during pressure overload are blocked by high fat intake: role of
cardiac phospholipid remodeling.
Hypertension
2009;
54
(3): 605–611.
7.
Kokubo M, Uemura A, Matsubara T, Murohara T. Noninvasive
evaluation of the time course of change in cardiac function inspontane-
ously hypertensive rats by echocardiography.
Hypertens Res
2005;
28
(7):
601–609.
8.
Pandey KN. Biology of natriuretic peptides and their receptors.
Peptides
2005;
26
(6): 901–932.
9.
Phrommintikul A, Tran L, Kompa A,
et al
. Effects of a rho kinase
inhibitor on pressure overload induced cardiac hypertrophy and associ-
ated diastolic dysfunction.
Am J Physiol Heart Circ Physiol
2008;
294
(4):
H1804–1814.
10. Ono K, Masuyama T, Yamamoto K,
et al
. Echo Doppler assessment of
left ventricular function in rats with hypertensive hypertrophy.
J Am Soc
Echocardiogr
2002;
15
(2): 109–117.
11. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regard-
ing quantitation in M-mode echocardiography: results of a survey of
echocardiographic measurements.
Circulation
1978;
58
(6): 1072–1083.
12. Doser TA, Turdi S, Thomas DP, Epstein PN, Li SY, Ren J. Transgenic
overexpression of aldehyde dehydrogenase-2 rescues chronic alcohol
intake-induced myocardial hypertrophy and contractile dysfunction.
Circulation
2009;
119
(14): 1941–1949.
13. Shen YT, Malik FI, Zhao X,
et al
. Improvement of cardiac function by
a cardiac myosin activator in conscious dogswith systolic heart failure.
Circ Heart Fail
2010;
3
(4): 522–527.
14. Nader L, Lahoud L, Chouery E, Aftimos G, Bois P, Fares NA. B-type
natriuretic peptide receptors in hypertrophied adult rat cardiomyocytes.
Ann Cardiol Angiol (Paris)
2010;
59
(1): 20–24.
15. Ruetten H, Dimmeler S, Gehring D, Ihling C, Zeiher AM. Concentric
left ventricular remodeling in endothelial nitric oxide synthaseknockout
mice by chronic pressure overload.
Cardiovasc Res
2005;
66
(3): 444–453.
16. Heyen JR, Blasi ER, Nikula K,
et al
. Structural, functional, and molec-
ular characterization of the SHHF model of heartfailure.
Am J Physiol
Heart Circ Physiol
2002;
283
(5): H1775–1784.
17. Namba T, Tsutsui H, Tagawa H,
et al.
Regulation of fibrillar collagen
gene expression and protein accumulation involume-overloaded cardiac
hypertrophy.
Circulation
1997;
95
(10): 2448–2454.
18. Cantor EJ, Babick AP, Vasanji Z, Dhalla NS, Netticadan T. A compara-
tive serial echocardiographic analysis of cardiac structure and function
in rats subjected to pressure or volume overload.
J Mol Cell Cardiol
2005;
38
(5): 777–786.
19. Beeri R, Chaput M, Guerrero JL,
et al
. Gene delivery of sarcoplasmic
reticulum calcium ATPase inhibits ventricularremodeling in ischemic
mitral regurgitation.
Circ Heart Fail
2010;
3
(5): 627–634.
20. Yoon PO, Lee MA, Cha H,
et al.
The opposing effects of CCN2 and
CCN5 on the development of cardiac hypertrophyand fibrosis.
J Mol
Cell Cardiol
2010;
49
(2): 294–303.
21. Nader L, Smayra V, Jebara V, Bois P, Potreau D, Fares N. Brain natriu-
retic peptide secretion in adult rat heart muscle cells: the role of calcium
channels.
Arch Cardiovasc Dis
2008;
101
(7–8): 459–463.