Perinatal aortic growth in lambs: relation to blood flow changes at birth

1990 ◽  
Vol 259 (4) ◽  
pp. H1247-H1253 ◽  
Author(s):  
B. L. Langille ◽  
R. D. Brownlee ◽  
S. L. Adamson

We have examined aortic growth and aortic hemodynamics in lambs in the perinatal period. Morphometry of histological cross sections indicated that abdominal aortic circumference decreased by 31% between 131 days of gestation and 2-3 wk postpartum. In contrast, the internal circumference of the thoracic aorta increased by 34% over the same time interval; thus size reduction of the abdominal aorta was not part of a generalized arterial response to ex utero life. We also determined medial cross-sectional area as an index of medial tissue mass. In the perinatal period (120 days gestation to 21 days postpartum), this index increased by 144% for the thoracic aorta but only by 69% in the abdominal aorta. Differences in rate of medial tissue accumulation were much greater postpartum than in utero. The relationship between abdominal aortic growth and hemodynamic changes was examined by instrumenting fetal lambs with blood pressure catheters, abdominal aortic blood velocity transducers, and sonomicrometer diameter crystals mounted on the abdominal aorta. Parturition, and the consequent loss of the placental circulation, caused a 73% reduction in abdominal aortic blood velocity. Abdominal aortic external diameter in the period between 4 and 14 days postpartum was reduced significantly compared with in utero values. These data are consistent with the hypothesis that blood flow changes at birth significantly influence arterial growth postpartum.

1994 ◽  
Vol 267 (6) ◽  
pp. H2268-H2279 ◽  
Author(s):  
M. P. Bendeck ◽  
F. W. Keeley ◽  
B. L. Langille

We compared arterial growth to hemodynamic changes in the perinatal period in lambs. Blood pressure did not change significantly from 120 days gestation to 3 days postpartum, when it was 45.4 +/- 1.9 mmHg; however, pressure rose to 64.8 +/- 2.5 mmHg at 21 days postpartum. Thoracic and abdominal aortic and iliac and carotid arterial blood flows fell > 50% after birth but returned to fetal levels except in the abdominal aorta by 21 days postpartum. Blood flows in mesenteric (BFm) and renal (BFr) arteries increased between 120 days gestation (BFr = 13.4 +/- 1.4; BFm = 41.8 +/- 3.5 ml/min) and 140 days gestation (BFr = 25.9 +/- 1.8; BFm = 189 +/- 18 ml/min) and between 3 and 21 days postpartum (to BFr = 71.1 +/- 14.3; BFm = 334 +/- 59 ml/min). Elastin accumulation accelerated at 140 days gestation in all arteries except the thoracic aorta, in which elastin accumulation was always rapid. Collagen but not DNA accumulation also accelerated in most arteries. Postpartum dexamethasone (0.1 mg/kg twice a day) did not affect abdominal aortic elastin by 10 days of age (23.9 +/- 2.7 vs. 26.4 +/- 4.1 mg for controls); however, dexamethasone upregulated tropoelastin mRNA in fetuses. We hypothesize that cortisol stimulates elastin accumulation in late gestation. Postnatal elastin but neither collagen nor DNA correlated with blood flow changes at birth (r = 0.855, P < 0.05). We infer that accumulation of elastin is sensitive to blood flow rates during perinatal development.


1997 ◽  
Vol 272 (2) ◽  
pp. H851-H858 ◽  
Author(s):  
A. Ben Driss ◽  
J. Benessiano ◽  
P. Poitevin ◽  
B. I. Levy ◽  
J. B. Michel

The effects of chronic increase in aortic blood flow on arterial wall remodeling were investigated in vivo with the use of an aortocaval fistula (ACF) model in rats. Phasic hemodynamics and aortic wall structure upstream and downstream in 30 male Wistar rats with ACF and 30 sham-operated rats were compared immediately and 2 mo after the ACF was opened in anesthetized rats. Opening the ACF upstream acutely decreased aortic pressure (-30%, P < 0.001) and increased aortic blood velocity (x12, P < 0.001), blood flow (x9, P < 0.001), wall shear stress (x10, P < 0.001) and guanosine 3',5'-cyclic monophosphate (cGMP) wall content (+50%, P < 0.01). After 2 mo, aortic pressure decreased (-22%, P < 0.001) and aortic blood velocity, diameter, and blood flow increased (+114%, P < 0.001; +60%, P < 0.001; and +250%, P < 0.001; respectively) compared with the control group. Aortic wall shear stress and cGMP wall content dropped over time and tended to recover control values; aortic wall tensile stress was higher than in the control group (P < 0.05). Medial cross-sectional area and elastin and collagen contents increased (+38%, P < 0.01; +50%, P < 0.01; and +30%, P < 0.05, respectively) and were associated with smooth muscle cell hypertrophy) (+23%, P < 0.05), despite a decrease in arterial wall thickness (-13%, P < 0.01). Opening the ACF downstream acutely decreased aortic pressure (-30%, P < 0.001) without any change in aortic blood velocity, diameter, blood flow, shear stress, and cGMP wall content. After 2 mo, pressure, blood velocity, shear stress, and cGMP wall content decreased (-22%, P < 0.001; -31%, P < 0.01; -46%, P < 0.02; and -50%, P < 0.05; respectively) and diameter and blood flow were unchanged; smooth muscle cell hypertrophy and hypoplasia were the only observed changes in the aortic wall structure. These results suggest that both shear and tensile stresses are involved in the aortic wall remodeling. Increase in shear stress likely induces expansive remodeling in relation to flow-dependent vasodilation, whereas increase in tensile stress is responsible for medial hypertrophy and fibrosis.


1995 ◽  
Vol 268 (1) ◽  
pp. H499-H505 ◽  
Author(s):  
C. J. Hartley ◽  
L. H. Michael ◽  
M. L. Entman

Mice are useful models in numerous research protocols, but monitoring cardiovascular parameters in small animals is difficult. Therefore we evaluated the use of 20-MHz pulsed Doppler ultrasound to measure ascending aortic blood velocity in intact anesthetized mice. Using a 0.5-mm-diameter 20-MHz transducer applied to the right sternal border, we recorded audio Doppler signals from the ascending aorta of 31 mice [24.4 +/- 1.5 (SD) g body wt]. The signals were played back at speed into a fast Fourier transform analyzer from which we measured heart rate (453 +/- 96 beats/min), ejection time (38 +/- 3%), peak velocity (90 +/- 11 cm/s), mean velocity (23 +/- 4 cm/s), rise time (7.3 +/- 2 ms), stroke distance (29 +/- 7 mm), and acceleration (163 +/- 63 m/s2) from the spectral envelopes. We determined aortic diameter (1.2 +/- 0.2 mm) and Doppler angle (0–20 degrees) in six mice by molding the aortic root and major systemic vessels with casting resin infused at 100 mmHg pressure. For an aortic diameter of 1.2 mm, cardiac output was estimated to be 14.8 ml/min and stroke volume to be 33 microliters. To verify the origin of the signals and to test responsiveness to known stimuli, we measured velocity signals from the aorta and other nearby vessels and varied heart rate and aortic velocity by warming or by infusion of isoproterenol in three open-chest animals. For the noninvasive applications, acoustic coupling was adequate through the moistened fur, and aortic velocity signals were obtained in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 29 (12) ◽  
pp. 2255-2265 ◽  
Author(s):  
Rafael Knuesel ◽  
Stephan M. Jakob ◽  
Lukas Brander ◽  
Hendrik Bracht ◽  
Andreas Siegenthaler ◽  
...  

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