Changes in blood flow distribution during the perinatal period in fetal sheep and lambs

1992 ◽  
Vol 70 (12) ◽  
pp. 1576-1582 ◽  
Author(s):  
Michelle P. Bendeck ◽  
B. Lowell Langille

We have measured total blood flows and blood flows per 100 g tissue to major tissues at 120 and 140 days gestation in fetal sheep and at 3 and 21 days of age in lambs (gestation period = 144 ± 2 days). Between 120 and 140 days gestation, flow per 100 g tissue increased by 74, 150, and 317% in the renal, intestinal, and hepatic arterial beds, but no further significant change in flow was observed at 3 or 21 days postpartum. Blood flows per 100 g to cerebral hemispheres and cerebellar tissues also increased dramatically during late gestation (142 and 121%, respectively), but declined sharply by 3 days postpartum (73 and 75%, respectively). Brain blood flows at 21 days postpartum remained substantially below late gestational levels. Adrenal blood flows per 100 g more than doubled during late gestation, fell by more than half at birth, and only partially recovered by 21 days of age. Blood flows to carcass tissues did not change in late gestation, fell at birth, then partially recovered. Pre- and post-natal increases in brain blood flows were almost entirely attributable to increased perfusion rather than tissue growth, whereas large perinatal increases in flow to the diaphragm paralleled tissue growth. Tissue growth and increased perfusion per 100 g contributed almost equally to increased blood flows to kidneys postnatally, and to adrenal glands and the gastrointestinal tract prenatally.Key words: blood flow, perinatal, birth, fetus, sheep.

1998 ◽  
Vol 274 (5) ◽  
pp. R1331-R1337 ◽  
Author(s):  
Joseph J. Smolich

It is unknown if nitric oxide (NO) influences the relative level of the left (LV) and right ventricular (RV) outputs, the blood flow distribution between the body and placenta, or whole body O2extraction and O2 consumption in the fetus. To address these questions eight fetal lambs were chronically instrumented at 128–134 days gestation (term 147 days), and blood flows were measured with radioactive microspheres 3–4 days later at baseline and after inhibition of NO synthesis with N ω-nitro-l-arginine (l-NNA, 10 and 25 mg/kg iv).l-NNA progressively reduced the combined ventricular output ( P < 0.005) but did not alter the relative levels of the LV and RV outputs. Fetal body blood flow fell by 31% after 10 mg/kgl-NNA ( P < 0.005), but a reduction in placental blood flow ( P < 0.005) was smaller (20%) and not observed until 25 mg/kgl-NNA. Whole body O2 extraction increased by 71% after 10 mg/kg l-NNA ( P < 0.005) and did change further at 25 mg/kg l-NNA, whereas whole body O2 consumption rose by 15% at 10 mg/kg l-NNA ( P < 0.05) and returned to baseline at 25 mg/kg l-NNA. These results suggest that, as well as reducing the combined ventricular output, inhibition of fetal NO synthesis redistributes systemic blood flow toward the placenta and increases fetal body O2 extraction. The latter initially increases whole body O2consumption and then maintains it at near baseline levels after a fall in placental perfusion.


1986 ◽  
Vol 250 (4) ◽  
pp. E441-E448 ◽  
Author(s):  
J. Gorski ◽  
D. A. Hood ◽  
R. L. Terjung

Aerobic muscle metabolism during concentrations requires adequate blood flow and oxygen delivery. Since the perfused rat hindquarter (HQ) has become widely used for muscle stimulation, we examined the blood flow distribution, using 15 microns radiolabeled microspheres, and oxygen consumption of the HQ, using different commonly used perfusion protocols. Perfusion via the abdominal aorta resulted in well-matched (r = 0.90) blood flows between tissues of both hindlimbs that were proportional to total perfusion inflow. Blood flows to the high-oxidative fast-twitch and slow-twitch red muscle sections were three- to fourfold greater than flows to sections of low-oxidative fast-twitch white muscle. However, a large fraction (28%) of the total inflow went to the trunk region, even though all apparent arterial branches to the trunk region were ligated. This trunk mass accounts for at least 40% of the total metabolic responses of the HQ and diverts a large blood flow that is often presumed to supply the hindlimbs. As a result, muscle performance of the distal hindlimb muscle during stimulation can be inordinately poor. Ligation of the iliac artery to the contralateral limb improves blood flow to the remaining hindlimb but does not eliminate trunk blood flow. In contrast, perfusion via the femoral artery restricted 95% of the inflow to the single hindlimb, thereby reducing the tissue mass perfused. Blood flow to the distal limb musculature was high, resulting in an enhanced muscle performance. Thus single hindlimb perfusion provides a preparation where the contracting muscle is a large fraction of the total tissue, and the venous effluent better reflects the metabolic events in the contracting muscle.(ABSTRACT TRUNCATED AT 250 WORDS)


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.


2001 ◽  
Vol 280 (4) ◽  
pp. R1016-R1022 ◽  
Author(s):  
Joseph J. Smolich

It is unknown if nitric oxide (NO) modulates the relative levels of left (LV) and right (RV) ventricular output, fetal O2 consumption, or blood flow distribution between the body and placenta at midgestation. To address these questions, six fetal lambs were instrumented at 89–96 days gestation (term 147 days), and blood flows were measured with radioactive microspheres 3–4 days later at baseline and after inhibition of NO synthesis with 10 mg/kg (l-NNA10) and 25 mg/kg (l-NNA25) N ω-nitro-l-arginine. LV output fell by 74 ± 15 ml · min−1 · kg−1 atl-NNA10 ( P < 0.005), whereas RV output decreased by 90 ± 18 ml · min−1 · kg−1 atl-NNA10 ( P < 0.02) and by a further 80 ± 22 ml · min−1 · kg−1 atl-NNA25 ( P < 0.05). As a result, RV output exceeded LV output at baseline ( P = 0.03) and l-NNA10 ( P < 0.02) but not at l-NNA25. Fetal body blood flow fell by 95 ± 25 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01), but because placental blood flow decreased by 70 ± 22 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01) and a further 71 ± 21 ml · min−1 · kg−1 atl-NNA25 ( P < 0.01), the fetal body-to-placental blood flow ratio was near unity at baseline andl-NNA10 but rose to 1.5 ± 0.3 atl-NNA25 ( P < 0.05). In association with these flow changes, fetal O2 consumption declined by 1.4 ± 0.3 ml · min−1 · kg−1 atl-NNA10 ( P < 0.05) and by a further 1.5 ± 0.6 ml · min−1 · kg−1 atl-NNA25 ( P < 0.02). These findings suggest that, in midgestation fetal lambs, NO supports an RV flow dominance, whole body O2 utilization, and the maintenance of a near-equal fetoplacental blood flow distribution.


1978 ◽  
Vol 234 (6) ◽  
pp. H706-H710 ◽  
Author(s):  
T. Anzai ◽  
M. D. Turner ◽  
W. H. Gibson ◽  
W. A. Neely

Blood flow distribution in tissues of mongrel dogs during hypothermia was studied with radionuclide-tagged microspheres. The animals were cooled at 21 degrees C and rewarmed under thiamylal sodiuni anesthesia. During hypothermia, cardiac output fell to 20% of the control; the highest rate of blood flow relative to normothermic values was observed in the subendocardium of the left ventricle, and the lowest in the hypophysis. Each tissue showed specific reactions to hypothermia. During hypothermia the myocardial and brain-stem blood flows were about 40% of the control; almost all of the digestive tract, striated muscle, adrenal gland, and hypophysis blood flows were maintained at 20% or less of the control. After rewarming, cardiac output recovered to values significantly lower than control. The myocardium, brain, renal cortex, and striated and smooth muscle recovered to control levels; however, blood flow to the digestive organs, bronchial artery flow to the lung, and flow to the endocrine organs did not completely recover by 2 after rewarming.


1990 ◽  
Vol 68 (1) ◽  
pp. 241-247 ◽  
Author(s):  
K. I. Norton ◽  
M. T. Jones ◽  
R. B. Armstrong

The purpose of this study was threefold: 1) to determine whether untrained rats that refused to run on treadmill would climb on a laddermill (75 degrees incline); 2) to determine O2 consumption (VO2) in untrained rats as a function of laddermill climbing speed; and 3) to determine whether the circulatory response of untrained rats to laddermill climbing is similar to that previously reported for treadmill running at an equivalent VO2. Eighteen female Sprague-Dawley rats that would not perform on a treadmill as part of another study were used to measure VO2 as a function of laddermill speed (5-17 m/min). Data were obtained from all 18 rats; VO2 increased linearly as a function of laddermill speed (r = 0.83, y = 3.0 x + 63.2). Twenty-four female Sprague-Dawley rats that also refused to run on a treadmill were used to measure mean arterial pressure, heart rate, and blood flow distribution (with microspheres) during climbing at 5 and 10 m/min. These exercise intensities were metabolically equivalent to level treadmill running at 45 and 60 m/min (VO2 approximately 78 and 93 ml.min-1.kg-1, respectively). Of the 24 animals, 23 were willing to climb. Mean arterial pressures were higher (approximately 10%) during laddermill climbing than during equivalent treadmill running, but heart rates were the same. General blood flow distribution among muscles as a function of fiber type (with red muscles receiving higher flows) and between muscles and visceral tissues (muscle blood flow increased as a function of exercise intensity while visceral blood flows decreased) were similar to data for rats running on the level.(ABSTRACT TRUNCATED AT 250 WORDS)


1998 ◽  
Vol 275 (3) ◽  
pp. H731-H743 ◽  
Author(s):  
Ronald R. Magness ◽  
Terrance M. Phernetton ◽  
Jing Zheng

Prolonged 17β-estradiol (E2β) infusion decreases mean arterial pressure (MAP) and systemic vascular resistance (SVR) while increasing heart rate (HR) and cardiac output (CO). It is unclear, however, which systemic vascular beds show increases in perfusion. The purpose of this study was to determine which reproductive and nonreproductive vascular beds exhibit alterations in vascular resistance and blood flow during prolonged E2β infusion. Nonpregnant, ovariectomized sheep received either vehicle ( n = 6) or E2β (5 μg/kg iv bolus followed by 6 μg/kg over 24 h for 10 days; n= 9), and blood flow distribution was evaluated using radiolabeled microspheres at control and 120 min and 3, 6, 8, and 10 days of infusion. During E2β infusion MAP (87 ± 5 mmHg; mean ± SE) decreased 3–9% and HR (83 ± 5 beats/min) increased 4–31%. The combined baseline (control) perfusion to the uterus, broad ligament, oviducts, cervix, vagina, and mammary gland (reproductive blood flows) was 49 ± 9 ml/min; at 120 min, E2β increased flow ( P < 0.001) to 605 ± 74 ml/min (1,263%) and it remained elevated, but at a reduced rate, on day 3 (218 ± 44 ml/min; 399%), day 6 (144 ± 23; 217%), day 8(181 ± 19; 321%), and day 10 (204 ± 48; 454%), accounting for only 3–17% of the E2β-induced increase in CO. During this E2β treatment, there also were significant decreases in vascular resistances leading to increases ( P < 0.05) in blood flows to several nonreproductive (systemic) vascular beds including skin (32–113%), coronary (32–190%), skeletal muscle (25–133%), brain (21–292%), bladder (128–524%), spleen (87–180%), and pancreas (35–137%) vascular beds. Responses of these combined nonreproductive blood flows represent the major percentage (21–67%) of the E2β-induced increase in CO. Vehicle infusion was without effect. We conclude that prolonged E2β infusion increases reproductive and nonreproductive tissue blood flows. The latter appears to principally be responsible for the observed rise in CO and decrease in SVR.


1963 ◽  
Vol 18 (2) ◽  
pp. 233-243 ◽  
Author(s):  
K. T. Fowler ◽  
John Read

A relationship has been developed between the amplitudes of cardiogenic oscillations of expired gas tensions and the ratio of blood flows through upper and lower zones of the erect human lung. Instrumental methods have been devised for the accurate measurement of the amplitudes of these oscillations. A theoretical and experimental study was made of the sources of error. The ratio of upper- to lower-zone blood flow could be determined with a reproducibility of ±20% so that changes in this ratio of greater than 20%, attendant upon a stimulus, could be identified. Submitted on July 16, 1962


1994 ◽  
Vol 267 (3) ◽  
pp. H912-H917
Author(s):  
N. Imai ◽  
M. Kashiki ◽  
P. D. Woolf ◽  
C. S. Liang

We have shown previously that right heart failure (RHF) in dogs is associated with activated endogenous opiate systems, and that administration of the opioid receptor antagonist, naloxone, increases arterial pressure, cardiac contractile function and organ blood flows. To study whether the cardiovascular effects of naloxone are mediated via the mu- or delta-opioid receptors, we administered ICI-154,129, a delta-receptor antagonist, and naloxonazine, a mu-receptor antagonist, to 10 conscious dogs with RHF on 2 separate days. Like naloxone, ICI-154,129 increased mean aortic pressure, cardiac output, peak positive first derivative of left ventricular pressure, and blood flows to the myocardium, kidneys, splanchnic beds, and skeletal muscle. These changes were associated with increases in plasma epinephrine and norepinephrine. In contrast, naloxonazine had no effects on systemic hemodynamics, regional blood flow distribution, and plasma catecholamines in RHF. These findings suggest that the increased endogenous opioids during heart failure act on the delta-opioid receptors to decrease myocardial mechanical performance and alter regional blood flow distribution. Opioid receptor-blocking agents may exert beneficial cardiovascular effects in heart failure.


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