Regional adrenal blood flow responses to adrenocorticotropic hormone in fetal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. E264-E269 ◽  
Author(s):  
A. M. Carter ◽  
B. S. Richardson ◽  
J. Homan ◽  
M. Towstoless ◽  
J. R. Challis
Keyword(s):  
Blood Flow ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Isotonic Saline ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Regional Blood Flows ◽  
Acth Concentration

To determine whether adrenocorticotropic hormone (ACTH) at plasma concentrations measured during mild hypoxemia and at term affects adrenal blood flow, we measured regional blood flows in five unanesthetized normoxemic fetuses (125–130 days gestation) during a 24-h intravenous infusion of ACTH-(1–24) in isotonic saline solution. Another five fetuses received an infusion of vehicle. Blood flows were determined before the infusion, at 2 and 24 h from its onset, and 24 h afterward using radionuclide-labeled microspheres. Blood flow to the adrenal medulla was fivefold greater than that to the adrenal cortex. Adrenal blood flow rose 99% at 24 h of the ACTH infusion. There was a large increase in adrenal cortical blood flow of 272% at this time but medullary blood flow did not change significantly during ACTH infusion. The rise in cortical blood flow was attributable to decreased vascular resistance. No significant alterations occurred in fetal arterial blood pressure and heart rate, or in blood flow to other lower body organs of the fetus or to the placental cotyledons. These findings are consistent with the hypothesis that the increase in adrenal blood flow observed during fetal hypoxia is associated with changes in plasma ACTH concentration. They are also indicative of selective regulation of cortical and medullary blood flows in the sheep fetus at this stage of gestation.

Regional adrenal blood flow responses to adrenocorticotropic hormone after chronic embolization of the fetal placental circulation in sheep

1996 ◽  
Vol 148 (3) ◽  
pp. 517-522 ◽  
Author(s):  
A M Carter ◽  
J R G Challis ◽  
P Svendsen
Keyword(s):  
Blood Flow ◽  
Adrenal Cortex ◽  
Adrenocorticotropic Hormone ◽  
Maternal Blood ◽  
Arterial Oxygen ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Arterial Oxygen Content ◽  
Blood Flows ◽  
Placental Blood

Abstract To ascertain whether repeated hypoxic stress would alter the response of the adrenal cortex to adrenocorticotropic hormone (ACTH), by premature activation of the hypothalamic–pituitary–adrenal axis, we studied fetal sheep subjected to daily reduction of arterial oxygen content by embolization of the fetal placental circulation with 15 μm microspheres for 8 days from about day 124 of gestation (term ∼147 days) and sham-embolized controls. Starting before the final embolization (or shamembolization) on day 8, and continuing for 24 h, the fetus was given an intravenous infusion of ACTH1–24 (0·5 μg/h) or vehicle. Fetal and maternal blood samples were taken for determination of immunoreactive cortisol, and regional adrenal and fetal placental blood flows were measured by the microsphere technique at three time points: 1 h before infusion, 3 h after the start of the infusion (1 h after embolization), and after 24 h of infusion. Prior to infusion of ACTH or vehicle, fetal placental blood flow was lower in microsphere-embolized fetuses than in sham-embolized controls (199 ± 15 vs 292 ± 25 ml/min per 100 g tissue; mean ± s.e.; P<0·01). However, plasma cortisol and adrenal cortical blood flow did not differ between embolized fetuses and controls. Adrenal vascular responses to the 24-h infusion of ACTH were similar in embolized and shamembolized fetuses. Adrenal cortical blood flow increased 3-fold (P<0·05) due to decreased vascular resistance (P<0·01), with no change in adrenal medullary blood flow. Thus, while daily embolization of the fetal placental circulation caused a sustained decrease in cotyledonary blood flow, no evidence of altered responsiveness of the adrenal cortex to ACTH was found in these experiments. Journal of Endocrinology (1996) 148, 517–522

Inhibition of ACTH secretion blocks hypoxia-induced increase of adrenal cortical blood flow in fetal sheep

1995 ◽  
Vol 269 (3) ◽  
pp. E598-E604 ◽  
Author(s):  
A. M. Carter ◽  
J. Homan ◽  
M. Fraser ◽  
B. S. Richardson ◽  
J. R. Challis
Keyword(s):  
Blood Flow ◽  
Plasma Concentrations ◽  
Fetal Hypoxia ◽  
Control Groups ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Blood Flows ◽  
Fetal Plasma

To examine the role of endogenous adrenocorticotropic hormone (ACTH) in adrenal blood flow responses to hypoxia, we studied unanesthetized ovine fetuses during an intravenous infusion of cortisol or vehicle. Fetal hypoxia was induced after 5 h of cortisol or vehicle infusion. Control fetuses were not made hypoxic. Blood flows were determined before and at three time points during the infusions. At 2 and 6 h of hypoxia, in vehicle-infused fetuses, fetal plasma concentrations of immunoreactive ACTH (irACTH) had risen from 9 +/- 3 (SE) pg/ml to 68 +/- 25 and 127 +/- 37 pg/ml, respectively. No significant change in fetal plasma irACTH occurred in the other groups. Adrenal cortical blood flow rose three- to fourfold during hypoxia in vehicle-infused fetuses but did not change from prehypoxia levels in cortisol-infused fetuses (P < 0.005). Medullary flow rose with hypoxemia, and this was not affected by concurrent cortisol infusion. Adrenal blood flows did not change in the control groups. Thus prior infusion of cortisol suppressed the rise in fetal plasma ACTH during hypoxia and selectively blocked the increase in adrenal cortical blood flow.

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

Age-related changes in regional blood flow in the rat

1985 ◽  
Vol 249 (3) ◽  
pp. H485-H491 ◽  
Author(s):  
R. F. Tuma ◽  
G. L. Irion ◽  
U. S. Vasthare ◽  
L. A. Heinel
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Index ◽  
Regional Blood Flow ◽  
Adult Rats ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Regional Blood Flows ◽  
Central Hemodynamic

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.

Responses to acute hypoxemia in fetal sheep at 0.6-0.7 gestation

1989 ◽  
Vol 256 (3) ◽  
pp. H613-H620 ◽  
Author(s):  
H. S. Iwamoto ◽  
T. Kaufman ◽  
L. C. Keil ◽  
A. M. Rudolph
Keyword(s):  
Blood Flow ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Arterial Blood ◽  
Regulatory Systems ◽  
Group I ◽  
Placental Blood ◽  
Placental Blood Flow ◽  
Sheep Fetus ◽  
I 31

A majority of previous studies of fetal responses to acute hypoxemia has focused on the response of the sheep fetus greater than 120 days of gestation when many regulatory systems have been established. To assess the response of younger, less well-developed fetuses, we exposed two groups of fetal sheep (I, 84-91 days; II, 97-99 days gestational age) to acute hypoxemia by giving the ewe a gas mixture containing 9% O2 to breathe. We decreased descending aortic PO2 in both groups of fetuses [I, 24 +/- 6 to 14 +/- 3 (SD) Torr; II, 23 +/- 3 to 12 +/- 4 Torr] by a degree similar to that achieved in previous studies of fetuses greater than 120 days of gestation. Mean arterial blood pressure (I, 31 +/- 6; II, 40 +/- 3 Torr) did not change significantly from control values, and heart rate (I, 224 +/- 27; II, 203 +/- 16 beats/min) increased significantly in group II fetuses with hypoxemia. In group I and II fetuses, as in older fetuses, cerebral, myocardial, and adrenal blood flows, measured by the microsphere technique, increased, and pulmonary blood flow decreased. These responses mature early and are likely local vascular responses to decreases in oxygen content. Combined ventricular output and umbilical-placental blood flow decreased significantly in both groups. Unlike the response of the fetus greater than 120 days, acute hypoxemia did not decrease blood flow to the musculoskeletal and cutaneous circulations (group I only), gastrointestinal, or renal circulations.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of Thiopental on Regional Blood Flows in the Rat

1996 ◽  
Vol 84 (3) ◽  
pp. 596-604 ◽  
Author(s):  
Russell D. Wada ◽  
Hideyoshi Harashima ◽  
William F. Ebling ◽  
Eileen W. Osaki ◽  
Donald R. Stanski
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Concentrations ◽  
Brain Blood Flow ◽  
Blood Gas ◽  
Fat Tissue ◽  
Blood Flows ◽  
Hypnotic Effect ◽  
Regional Blood Flows ◽  
Arterial Plasma

Background The goal of this investigation was to characterize the effects of thiopental on cardia output and regional blood flows in the rat. Blood flows influence thiopental pharmacokinetics. Acquisition of these data may ultimately permit evaluation of the contribution of thiopental-induced alterations in regional blood flows to the disposition and hypnotic effect of this drug. Methods Chronically instrumented unrestrained Wistar rats (n=20) aged 3-4 months received either a dose of thiopental sufficient to induce a brief period of unconsciousness (20 mg.kg(-1)) or a larger dose achieving electroencephalographic burst suppression (45 mg.kg(-1)). Cardiac output and blood flows to 14 tissues were determined at 4 times in each rat for a period of 420 min using injections of radioactive microspheres (expressed as mean +/- SD). Mean arterial pressure, heart rate, and blood gas tensions were determined at all measurement times. Arterial plasma concentrations were sampled at postinfusion times. Results No important changes in systemic cardiovascular measurements were detected after the smaller dose of thiopental. One minute after the larger dose, cardiac output decreased from baseline (123 +/- 14 to 84 +/- ml.min (-1), P&lt; 0.01), flow to muscle and fat decreased, and muscle and fat resistance increased. At 5 min, compared to baseline, no difference in cardiac output was detected (123 +/- vs. 119 +/- ml.min (-1)), intestinal flows increased and intestinal resistances decreased. Cardiac output was again depressed at 30, 90, and 180 min. Brain blood flow decreased 25 +/- 19 % (P&lt; 0.01) from baseline for the duration of the study. Conclusions Thiopental acutely decreases cardiac output, and blood flows to muscle and fat tissue. The temporary return of cardiac output to baseline may be related to intestinal vasodilation. These blood flow alterations may influence the pharmacokinetics of thiopental.

Cerebral blood flow in intoxicated newborn piglets

1987 ◽  
Vol 65 (1) ◽  
pp. 92-95 ◽  
Author(s):  
Cara J. MacIntyre ◽  
Bill Y. Ong ◽  
Daniel S. Sitar
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Basal Ganglia ◽  
Brain Regions ◽  
Ethanol Exposure ◽  
Blood Flows ◽  
Arterial Blood ◽  
Regional Blood Flows ◽  
Blood Pressures ◽  
And Control

Ethanol exposure in the neonatal period causes impaired brain growth and altered adult behaviour in rats. One possible mechanism may be altered cerebral perfusion caused by ethanol intoxication. We assessed the effects of ethanol on cerebral blood flow and its autoregulation in 2-day-old piglets. Piglets received ethanol (1.4 g/kg) or an equivalent volume of dextrose 5% in water over 30 min. One hour later, cerebral blood flow was measured using the microsphere technique at resting, elevated, and decreased mean arterial blood pressure. Ethanol-treated piglets had total cerebral blood flows of 88 ± 14, 82 ± 10, and 82 ± 12 mL∙100 g−1∙min−1 (mean ± SE) at mean arterial blood pressures of 12.4 ± 1.1, 15.7 ± 1.5, and 8.2 ± 0.9 kPa. Corresponding values in control piglets were 82 ± 14, 78 ± 4, and 82 ± 7 mL∙100 g−1∙min−1 at mean arterial blood pressures of 10.5 ± 1.5, 14.0 ± 1.2, and 7.7 ± 1.1 kPa. At resting arterial blood pressures, regional blood flows to basal ganglia, cortex, brainstem, and cerebellum in ethanol-treated piglets were 123 ± 21, 90 ± 16, 94 ± 17, and 77 ± 12 mL∙100 g−1∙min−1, respectively. Corresponding regional blood flows for the control piglets were 118 ± 16, 85 ± 15, 76 ± 16, and 76 ± 16 mL∙100 g−1∙min−1. Blood flow to basal ganglia was greater than to other brain regions in both ethanol-treated and control piglets (P < 0.01). Total and regional blood flows remained unchanged with altered mean arterial blood pressures, indicating normal autoregulation of cerebral blood flow in both ethanol-treated and control piglets.

Acidemia stimulates ACTH, vasopressin, and heart rate responses in fetal sheep

1989 ◽  
Vol 257 (2) ◽  
pp. R344-R349 ◽  
Author(s):  
C. E. Wood ◽  
H. G. Chen
Keyword(s):  
Heart Rate ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Highly Correlated

Adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hemorrhage are highly correlated to the hemorrhage-induced decreases in arterial pH. The present study was designed to test the responses of these three systems to acute fetal acidemia, produced by intravenous infusion of H+. HCl was infused into chronically catheterized fetal sheep at rates of 0.02 (n = 5), 0.10 (n = 6), and 0.50 (n = 5) meq/min. Infusions at rates of 0.10 and 0.50 meq/min significantly decreased fetal arterial pH and increased arterial PCO2. Fetal heart rate and plasma concentrations of ACTH, cortisol, and AVP were significantly increased during infusion of HCl at 0.5 meq/min. Neither fetal plasma renin activity nor fetal arterial blood pressure was significantly altered by any of the infusions. The results of these experiments suggest that fetal ACTH, AVP, and heart rate are stimulated by decreases in arterial pH and/or increases in arterial PCO2. We speculate that these responses are chemoreceptor mediated, although we cannot distinguish the apparent relative roles of peripheral and central chemoreceptors on the basis of the present study.

Dose-dependent effects of arginine vasopressin on endocrine and blood gas responses of fetal sheep during the last third of pregnancy

1987 ◽  
Vol 65 (11) ◽  
pp. 2291-2296 ◽  
Author(s):  
Laurie J. Norman ◽  
John R. G. Challis
Keyword(s):  
Arginine Vasopressin ◽  
Time Course ◽  
Plasma Concentrations ◽  
Blood Gas ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Acth Concentration ◽  
High Concentrations ◽  
Dose Dependent

Arginine vasopressin (AVP) is released in fetal sheep in response to various intrauterine stresses such as hypoxaemia, hypotension, and haemorrhage. We have examined the effects of exogenous AVP injected at two doses (200 ng and 2 μg) on the plasma concentrations of ACTH and cortisol, and on arterial blood [Formula: see text], [Formula: see text], and pH in chronically catheterized fetal sheep at d110–115, d125–130, and at d135–140 of pregnancy. AVP (2 μg) provoked a significant elevation in the plasma ACTH and cortisol concentration at all three stages of gestation, whereas the administration of 200 ng AVP raised plasma ACTH and cortisol only at d110–115 and at d 125–130. The increment in plasma cortisol after 200 ng AVP at the two earlier stages of pregnancy was similar to that after 2 μg AVP, despite a dose-dependent difference in the change in ACTH concentration. AVP stimulated a rise in [Formula: see text] at each time of study, although the time course of response was shorter at d135–140 than at the previous stages of pregnancy. The effect of AVP on [Formula: see text] was more variable, showing a transient decrease at +5 min after injection in the two oldest groups of fetuses. pH fell after AVP at dl 10–115 and at d125–130, but it rose transiently in the oldest fetuses. We conclude that at high concentrations systemic administration of AVP provokes endocrine and blood gas changes in fetal sheep. ACTH was consistently elevated by AVP. [Formula: see text] also rose at each stage of pregnancy, but the effects on [Formula: see text] and pH varied as a function of fetal age. Our results support other studies that suggest a role for AVP in the responses of the fetus to intrauterine stresses such as hypoxia.

Lack of evidence for impaired preload or Bezold-Jarisch activation during brief umbilical cord occlusions in fetal sheep

2021 ◽  
Author(s):  
Christopher A. Lear ◽  
Laura Bennet ◽  
Benjamin S. A. Lear ◽  
Jenny A. Westgate ◽  
Alistair Jan Gunn
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Cardiovascular Responses ◽  
Diastolic Filling ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Rapid Fall ◽  
Filling Time ◽  
Cervical Vagotomy ◽  
Femoral Blood

Impaired cardiac preload secondary to umbilical cord occlusion (UCO) has been hypothesized to contribute to intrapartum decelerations, brief falls in fetal heart rate (FHR), through the activation of the Bezold-Jarisch reflex. This cardioprotective reflex increases parasympathetic and inhibits sympathetic outflows triggering hypotension, bradycardia and peripheral vasodilation but its potential to contribute to intrapartum decelerations has never been systematically examined. In this study we performed bilateral cervical vagotomy to remove the afferent arm and the efferent parasympathetic arm of the Bezold-Jarisch reflex. 22 chronically instrumented fetal sheep at 0.85 of gestation received vagotomy (n=7) or sham-vagotomy (control, n=15), followed by three 1-min complete UCOs separated by 4-min reperfusion periods. UCOs in control fetuses were associated with a rapid fall in FHR and reduced femoral blood flow mediated by intense femoral vasoconstriction, leading to hypertension. Vagotomy abolished the rapid fall in FHR (p<0.001), and despite reduced diastolic filling time, increased both carotid (p<0.001) and femoral (p<0.05) blood flow during UCOs, secondary to carotid vasodilation (p<0.01) and delayed femoral vasoconstriction (p<0.05). Finally, vagotomy was associated with an attenuated rise in cortical impedance during UCOs (p<0.05), consistent with improved cerebral substrate supply. In conclusion, increased carotid and femoral blood flows after vagotomy are consistent with increased left and right ventricular output, which is incompatible with the hypothesis that labor-like UCOs impair ventricular filling. Overall, the cardiovascular responses to vagotomy do not support the hypothesis that the Bezold-Jarisch reflex is activated by UCO. The Bezold-Jarisch reflex is therefore mechanistically unable to contribute to intrapartum decelerations.

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