scholarly journals Effects of infusions of ACTH in the chronically catheterized pregnant ewe and her fetus

1998 ◽  
Vol 274 (2) ◽  
pp. R445-R452 ◽  
Author(s):  
Eugenie R. Lumbers ◽  
C. Bernasconi ◽  
J. H. Burrell
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Blood Gases ◽  
The Other ◽  
Blood Gas ◽  
Fetal Blood ◽  
Fetal Plasma ◽  
Induced Hypertension ◽  
Cortisol Levels ◽  
Pregnant Ewe

To study the effects of elevated maternal levels of adrenocorticotropic hormone (ACTH) on the fetus, nine chronically catheterized pregnant ewes (132 ± 0.9 days of gestation) were infused intravenously for 3 days with Synacthen (5 μg ⋅ kg−1 ⋅ day−1). Four ewes were given 0.15 M saline intravenously over the same period. ACTH induced hypertension in the ewe. Mean arterial pressure (MAP) increased from 101 ± 4.4 to 114 ± 3.9 mmHg at 48 h ( P < 0.05); cardiac output increased from 8.6 ± 0.5 to 10.4 ± 1.0 l/min after 24 h ( P < 0.05). Within 2–4 h, maternal cortisol levels increased from 24.6 ± 6.3 to 287 ± 30 nM ( P < 0.05) and remained high. Fetal plasma cortisol levels increased from 20 ± 4.5 to 60 ± 4.5 nM ( P < 0.05) within 2–4 h and then increased further. Fetal MAP was increased at 24 h. There was no effect on fetal blood gases or pH. Ewes became hyperglycemic and lactacidemic by 24 h ( P < 0.05), and the fetuses were also hyperglycemic and lactacidemic ( P < 0.05) at this time. There were no changes in fetuses carried by saline-infused ewes. Both ewes and fetuses had raised plasma osmolalities and, since hematocrit fell, retained fluid. Ewes became hypokalemic; the fetuses did not, but there was an increase in fetal K excretion. Thus ACTH-induced hypertension in the ewe had minimal effects on fetal MAP, fetal blood gas status, and pH. The fetus, however, did show many of the other effects of maternal glucocorticoid and mineralocorticoid excess, partly because its cortisol levels were increased but also as a consequence of metabolic and endocrine changes in the ewe.

Stress response of cougars to nonlethal pursuit by hunters

1992 ◽  
Vol 70 (1) ◽  
pp. 136-139 ◽  
Author(s):  
Henry J. Harlow ◽  
Frederick G. Lindzey ◽  
Walter D. Van Sickle ◽  
William A. Gern
Keyword(s):  
Stress Response ◽  
Treatment Group ◽  
Physiological Response ◽  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
The Other ◽  
Response Test ◽  
Felis Concolor ◽  
Adrenal Response ◽  
Cortisol Levels

Five cougars (Felis concolor) were captured and an adrenal response test was administered by injecting synthetic adrenocorticotropic hormone and monitoring plasma cortisol levels at 15-min intervals for 120 min. Three were selected for treatment and chased 5 or 6 more times to simulate the stress they might experience during a pursuit-only season; the other two served as controls and were chased only once more, at recapture. The adrenal response test was administered again at recapture. The cougars in the treatment group had a lowered plasma cortisol profile after the simulated pursuit season, indicating an altered physiological response of the adrenals to the stress of repeated chases.

Biological activity of adrenocorticotropic hormone precursors on ovine adrenal cells

1995 ◽  
Vol 268 (4) ◽  
pp. E623-E629 ◽  
Author(s):  
J. Schwartz ◽  
F. Kleftogiannis ◽  
R. Jacobs ◽  
G. D. Thorburn ◽  
S. R. Crosby ◽  
...  
Keyword(s):  
Biological Activity ◽  
Plasma Cortisol ◽  
Inhibitory Action ◽  
Adrenocorticotropic Hormone ◽  
Physiological Role ◽  
Cortisol Response ◽  
Adrenal Cells ◽  
Fetal Cells ◽  
Fetal Plasma ◽  
Cortisol Responses

Adrenocorticotropic hormone (ACTH) is synthesized in the corticotrophs as a precursor, pro-opiomelanocortin (POMC), which is processed via proACTH to ACTH. Both precursors and ACTH are secreted. Although the steroidogenic activity of ACTH is well characterized, that of the precursors is not. This study assessed the capacity of POMC and proACTH to alter cortisol synthesis. POMC and proACTH were prepared by subjecting medium, conditioned by exposure to DMS-79 cells, to Sephadex chromatography, and the bioactivity was assessed in cultured-dissociated ovine adrenal cells. Alone neither POMC (< or = 2.6 nM) nor proACTH (< or = 0.7 nM) showed any consistent acute (6 h) stimulatory or inhibitory action on cortisol in either fetal or adult cells. In contrast, in fetal cells the precursors inhibited steroidogenic response to ACTH-(1-24). POMC at 2.6 nM, but not lower concentrations, decreased the cortisol responses to 0.01, 0.1, and 1 nM ACTH by at least 50%. ProACTH (0.70 and 0.23 nM) decreased the responses to ACTH at 0.01 nM by 89 and 67%, respectively, and at 0.1 nM by 49 and 34%, respectively. At 1 nM ACTH only 0.7 nM proACTH decreased the response to ACTH (by 69%). In contrast, in adult adrenal cells, the precursors did not significantly reduce the response to ACTH (range 0.01-1 nM). Therefore, these data indicate that POMC and proACTH can inhibit the cortisol response to ACTH in fetal adrenal cells, an effect that is concentration dependent. The data suggest that precursors may play a physiological role, possibly regulating fetal plasma cortisol concentrations.

The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. R324-R330 ◽  
Author(s):  
H. G. Chen ◽  
C. E. Wood
Keyword(s):  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Bilateral Vagotomy ◽  
Pregnant Ewe

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.

Cortisol infusion depresses the ratio of bioactive to immunoreactive ACTH in adrenalectomized sheep fetuses

1998 ◽  
Vol 274 (3) ◽  
pp. E391-E396 ◽  
Author(s):  
Timothy J. Zehnder ◽  
Nancy K. Valego ◽  
Jeffrey Schwartz ◽  
Jennifer Green ◽  
James C. Rose
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Basal Plasma

We examined the effects of exogenous cortisol on plasma immunoreactive adrenocorticotropic hormone (iACTH), bioactive ACTH (bACTH), and ACTH-(1—39) in nine adrenalectomized fetuses at 126–130 and 136–140 days of gestation. Fetuses received 4 h of cortisol (2 μg ⋅ kg−1 ⋅ min−1) or saline infusions on consecutive days. Blood was obtained before and at intervals during infusions. Arterial blood gases and hematocrits were normal and did not change with age. Plasma cortisol did not change during saline infusions but increased significantly (range 30–70 ng/ml) during cortisol infusions. Basal plasma iACTH, bACTH, ACTH-(1—39), and bACTH-to-iACTH and ACTH-(1—39)-to-iACTH ratios were significantly higher in the older fetuses. Cortisol infusions decreased plasma iACTH, bACTH, and ACTH-(1—39) in both groups, and the suppression as a percent of the baseline was similar. The bACTH-to-iACTH ratio declined to the same level at 126–130 (0.201 ± 0.040 to 0.051 ± 0.002) and 136–140 (0.389 ± 0.088 to 0.046 ± 0.002) days of gestation. These data suggest that physiological concentrations of cortisol selectively inhibit bACTH secretion, and the ACTH response to cortisol inhibition is not different between 126 and 140 days of gestation in adrenalectomized sheep fetuses.

Does the ovine placenta secrete ACTH under normoxic or hypoxic conditions?

1991 ◽  
Vol 260 (2) ◽  
pp. R389-R395 ◽  
Author(s):  
M. Keller-Wood ◽  
C. E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Late Pregnancy ◽  
Maternal Plasma ◽  
Late Gestation ◽  
Fetal Circulation ◽  
Fetal Plasma ◽  
Hypoxic Conditions ◽  
Ovine Placenta ◽  
Arterial Po2

In the sheep, maternal plasma cortisol is increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone (ACTH) rise precipitously in late gestation. In many species, the placenta contains ACTH. These experiments were designed to test whether the ovine placenta contains ACTH and whether there is net secretion of ACTH by the uteroplacental unit into either the maternal or fetal circulation. Pregnant ewes and their fetuses were prepared with maternal and fetal arterial and uterine and umbilical venous catheters. Arterial and venous samples were taken from both sides of the placenta before and during hypoxia induced by the ewe breathing 9-11% O2, and arteriovenous (a-v) differences in ACTH, PO2, PCO2, and progesterone were analyzed. A positive a-v difference in PO2 (48.2 +/- 3.4 mmHg) and negative a-v differences in PCO2 and progesterone (-3.5 +/- 0.7 mmHg and -25 +/- 5 ng/ml, respectively) were found across the placenta in the ewe, and a positive a-v difference in PCO2 (4.8 +/- 0.9 mmHg) and negative a-v differences in PO2 and progesterone (-8.1 +/- 1.5 mmHg and -13 +/- 3 ng/ml, respectively) were found across the placenta in the fetus, indicating that the umbilical and uterine venous catheters were properly placed. Hypoxia decreased fetal and maternal arterial PO2 from 22.8 +/- 1.3 to 13.8 +/- 0.7 and from 98.8 +/- 3.3 to 37.0 +/- 2.6 mmHg, respectively, and increased fetal and maternal arterial ACTH immunoreactivity from 95 +/- 60 to 2,676 +/- 795 and from 149 +/- 21 to 275 +/- 88 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Are fetal adrenocorticotropic hormone and renin secretion suppressed by maternal cortisol secretion?

1988 ◽  
Vol 255 (3) ◽  
pp. R412-R417 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Maternal Plasma ◽  
Renin Secretion ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Adrenal Secretion

Previous studies from this laboratory have demonstrated that intravenous infusions of hydrocortisone (cortisol) into fetal sheep at rates that produce plasma concentrations achieved during fetal stress inhibit fetal adrenocorticotropic hormone (ACTH) and renin secretion. The present study was designed to test for inhibition of fetal renin and ACTH after maternal adrenal secretion of cortisol. ACTH-(1-24) or saline infusion into 12 pregnant ewes (120-132 days gestation) at rates of 0, 1, 5, or 20 ng ACTH.kg-1.min-1 for 5 h produced dose-related increases in maternal plasma ACTH and cortisol concentrations and fetal plasma cortisol concentration. In the 20-ng.kg-1.min-1 group, increases in fetal plasma cortisol of 8.0 ng/ml (to 24.3 +/- 3.7 ng/ml) did not suppress basal fetal plasma renin activity. One hour after the end of the maternal vehicle or ACTH infusion, fetal ACTH secretion was stimulated by fetal intravenous infusion of sodium nitroprusside. In the 0-, 1-, and 5-ng.kg-1.min-1 groups, fetal ACTH responses to nitroprusside were suppressed in animals infused with ACTH. Together, these results indicate that the maternal adrenal secretion of cortisol inhibits stimulated secretion of ACTH but not renin in 120- to 132-day-gestation fetal sheep.

Corticotropin-releasing factor in the ovine fetus and pregnant ewe: role of placenta

1991 ◽  
Vol 261 (4) ◽  
pp. R995-R1002 ◽  
Author(s):  
M. Keller-Wood ◽  
C. E. Wood
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Late Pregnancy ◽  
Maternal Plasma ◽  
Corticotropin Releasing Factor ◽  
Late Gestation ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Arterial Plasma ◽  
Pregnant Ewe

In the sheep, maternal plasma adrenocorticotropic hormone and cortisol are increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone rise precipitously in late gestation. To test whether the ovine placenta secretes corticotropin-releasing factor (CRF) into either the maternal or fetal circulation, pregnant ewes and their fetuses were prepared with femoral arterial catheters and uterine and umbilical venous catheters. Samples were taken from all sites before and during hypoxia. There was no difference in CRF concentration across the placenta in the mothers or the fetuses under resting or hypoxemic conditions, but maternal and fetal arterial plasma CRF concentrations increased between 128 and 145 days. In a second study, maternal and fetal femoral venous plasma CRF concentrations were measured 1-19 days before spontaneous parturition. The mean concentration increased 8.6 +/- 0.6 pg/ml 11-19 days before parturition to 13.0 +/- 1.0 and 13.2 +/- 1.4 pg/ml in fetuses 4-8 and 1-3 days before parturition, respectively. Maternal plasma concentrations did not significantly increase in the days closer to parturition. These studies demonstrate that there are low but measurable CRF concentrations in fetal and maternal sheep plasma but that these are not the result of tonic placental secretion of CRF.

Reliability of point-of-care hematocrit, blood gas, electrolyte, lactate and glucose measurement during cardiopulmonary bypass

Perfusion ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 33-37 ◽  
Author(s):  
J Steinfelder-Visscher ◽  
P W Weerwind ◽  
S Teerenstra ◽  
M HJ Brouwer
Keyword(s):  
Cardiopulmonary Bypass ◽  
Linear Trend ◽  
Point Of Care ◽  
Blood Gases ◽  
Systematic Difference ◽  
The Other ◽  
Glucose Measurement ◽  
Prospective Clinical Study ◽  
Blood Gas ◽  
Downward Bias

Background: Recently, the GEM Premier blood gas analyser was upgraded to the GEM Premier 3000. In addition to pH, pCO2, pO2, Na+, K+, Ca2+, and hematocrit measurement, glucose and lactate can be measured on the GEM Premier 3000. In this prospective clinical study, the analytical performance of the GEM Premier 3000 was compared with the Ciba Corning 865 analyser for blood gas/electrolytes/metabolites, and for hematocrit with the Sysmex XE 2100 instrument. Methods: During a 6-month period, 127 blood samples were analysed on both the GEM Premier 3000 analyser and our laboratory analysers (Ciba Corning 865/Sysmex 2100 instrument), and compared using the agreement analysis for quantitative data. Results: With the exception of K+, the other parameters (pCO2, pO2, Na+, Ca2+, hematocrit, glucose, and lactate) can be described in terms of the mean and standard deviation of the differences. For K+ measurement, a clear linear trend (r=0.79, p<0.001) in the deviation of the GEM Premier 3000 from the Ciba Corning was noticed, ie, in the lower or upper K+ reference range, the GEM Premier 3000 measured systematically too low or too high, respectively. Furthermore, in comparison with the other parameters, a therapeutically unacceptable systematic difference (mean of difference: -2.2%, p =0.05) in hematocrit measurement on the GEM Premier 3000 was observed for hematocrit values below 30%. The variance of the readings for the GEM Premier 3000 measurements was at clinically acceptable levels. Conclusion: The GEM Premier 3000 analyser seems to be suitable for point-of-care testing of electrolytes, metabolites, and blood gases during cardiopulmonary bypass. However, its downward bias in hematocrit values below 30% suggests that using the GEM Premier 3000 as a transfusion trigger leads to overtreatment with packed red cells.

Ontogeny of endocrine (ACTH, vasopressin, cortisol) responses to hypotension in lamb fetuses

1981 ◽  
Vol 240 (6) ◽  
pp. E656-E661 ◽  
Author(s):  
J. C. Rose ◽  
P. J. Meis ◽  
M. Morris
Keyword(s):  
Plasma Cortisol ◽  
Feedback Regulation ◽  
Late Gestation ◽  
Negative Feedback Regulation ◽  
Hormonal Responses ◽  
Fetal Plasma ◽  
Age Related ◽  
Basal Plasma ◽  
Cortisol Responses ◽  
Cortisol Levels

We studied the ACTH, vasopressin (AVP), and cortisol responses to nitroprusside-induced hypotension in 27 chronically cannulated lamb fetuses between 0.53 and 0.98 gestation. Age-related differences in the hormonal responses to hypotension were found. Hypotension was associated with peak AVP levels of 7.8 +/- 2.7 pg/ml (mean +/- SE) in animals less than 0.68 gestation and 63.5 +/- 20 pg/ml in animals 0.89–0.98 gestation (P less than 0.05). The peak ACTH response was 95 +/- 20 pg/ml in the youngest animals and 380 +/- 111 pg/ml in animals 0.83–0.88 gestation (P less than 0.05). These observations suggest that maturation of the systems (possibly neuroendocrine) subserving the hormonal responses occurs in utero. Fetal plasma cortisol levels did not increase in response to the increase in ACTH except in animals 0.89–0.98 gestation. At this time, the basal plasma cortisol levels were high (58.8 +/- 16.8 pg/ml) and the ACTH response to hypotension was attenuated. Taken together, these findings suggest functional negative feedback regulation of ACTH by cortisol in the late gestation fetus.

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