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Cardiac remodeling in chronic hypertension during murine pregnancy
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Chronic hypertension affects 3-5% of pregnancies, presenting a
combination of pressure and volume overload with opposing effects on cardiac
function [1]. However, the influence of these competing forces on cardiac
remodeling in hypertensive pregnancy remains unclear. Using a murine model,
we aimed to characterize cardiac remodeling, hypothesizing that pregnancy
may counteract hypertension-related declines in cardiac function.
Nulliparous female C57Bl6/J mice (10-13 weeks old) were implanted with
42-day mini-osmotic pumps (Azlet Durect) loaded with angiotensin II (1000
ng/kg/min) to induce hypertension. Animals were randomly assigned into
hypertensive control (AngII, n=7) and hypertensive pregnancy (AngII+Preg,
n=5) groups. We collected tail-cuff blood pressure, and 2D and 4D
high-frequency ultrasound (MX550D, 40 MHz center frequency, Vevo3100,
VisualSonics) images of the left ventricle at baseline, 14 days after pump
implantation, gestational (e) days 6.5, 12.5, 15.5, 18.5, and on postpartum
(p) day 1. Statistical significance was assessed by two-way ANOVA ( p
<0.05). Ejection fraction was maintained across both animal groups
throughout the experimental timeline. Stroke volume (SV), however, decreased
in the AngII group and increased in the AngII+Preg group compared to
baseline, and by gestational day (e) 15 was significantly higher in the
AngII+Preg group (30.4 ± 7.4 uL vs. 21.5± 6.1 uL, AngII+Preg vs. AngII).
Similar to SV, cardiac output decreased in the AngII group and increased the
AngII+Preg group (12.0 ± 3.6 uL vs. 16.3 ± 4.3 uL, AngII vs AngII+Preg, eday
15). Excised heart mass was greater in the AngII group at 190.7 ± 21.1 mg
compared to 158.0 ± 10.7mg in the AngII+Preg group on pday 1. These results
suggest that adaptations during pregnancy may alter cardiac remodeling in
the settings of hypertension. Ongoing histology and 4D strain mapping may be
helpful to further identify related changes in tissue geometry and
biomechanics. Findings from this work could provide insight into the
pathophysiology of chronic hypertension in pregnancy and set the foundation
for future efforts in identifying patient risk factors, ultimately improving
standard of care for both mother and child. [1] Lawler, et al., Hypertens
Pregnancy. 2007.
This abstract was presented at the American Physiology Summit 2025 and
is only available in HTML format. There is no downloadable file or PDF
version. The Physiology editorial board was not involved in the peer review
process.
American Physiological Society
Title: Cardiac remodeling in chronic hypertension during murine
pregnancy
Description:
Chronic hypertension affects 3-5% of pregnancies, presenting a
combination of pressure and volume overload with opposing effects on cardiac
function [1].
However, the influence of these competing forces on cardiac
remodeling in hypertensive pregnancy remains unclear.
Using a murine model,
we aimed to characterize cardiac remodeling, hypothesizing that pregnancy
may counteract hypertension-related declines in cardiac function.
Nulliparous female C57Bl6/J mice (10-13 weeks old) were implanted with
42-day mini-osmotic pumps (Azlet Durect) loaded with angiotensin II (1000
ng/kg/min) to induce hypertension.
Animals were randomly assigned into
hypertensive control (AngII, n=7) and hypertensive pregnancy (AngII+Preg,
n=5) groups.
We collected tail-cuff blood pressure, and 2D and 4D
high-frequency ultrasound (MX550D, 40 MHz center frequency, Vevo3100,
VisualSonics) images of the left ventricle at baseline, 14 days after pump
implantation, gestational (e) days 6.
5, 12.
5, 15.
5, 18.
5, and on postpartum
(p) day 1.
Statistical significance was assessed by two-way ANOVA ( p
<0.
05).
Ejection fraction was maintained across both animal groups
throughout the experimental timeline.
Stroke volume (SV), however, decreased
in the AngII group and increased in the AngII+Preg group compared to
baseline, and by gestational day (e) 15 was significantly higher in the
AngII+Preg group (30.
4 ± 7.
4 uL vs.
21.
5± 6.
1 uL, AngII+Preg vs.
AngII).
Similar to SV, cardiac output decreased in the AngII group and increased the
AngII+Preg group (12.
0 ± 3.
6 uL vs.
16.
3 ± 4.
3 uL, AngII vs AngII+Preg, eday
15).
Excised heart mass was greater in the AngII group at 190.
7 ± 21.
1 mg
compared to 158.
0 ± 10.
7mg in the AngII+Preg group on pday 1.
These results
suggest that adaptations during pregnancy may alter cardiac remodeling in
the settings of hypertension.
Ongoing histology and 4D strain mapping may be
helpful to further identify related changes in tissue geometry and
biomechanics.
Findings from this work could provide insight into the
pathophysiology of chronic hypertension in pregnancy and set the foundation
for future efforts in identifying patient risk factors, ultimately improving
standard of care for both mother and child.
[1] Lawler, et al.
, Hypertens
Pregnancy.
2007.
This abstract was presented at the American Physiology Summit 2025 and
is only available in HTML format.
There is no downloadable file or PDF
version.
The Physiology editorial board was not involved in the peer review
process.
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