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Biomedical subjects

J C Rose

Publications and source records attributed to J C Rose.

At least 73 records · Page 4Linked to original sources
PubMed1989

Intravenous clonidine hydrochloride toxicity in pregnant ewes.

Administration of intravenous clonidine hydrochloride has been advocated to rapidly control blood pressure in severe preeclampsia. To examine clonidine's acute maternal and fetal effects were intravenously injected 300 micrograms clonidine in eight chronically prepared normotensive near term ewes. Unlike intravenous saline solution injection, clonidine produced significant toxicity--intraamniotic pressure increased 97 +/- 27% (p less than 0.05), uterine blood flow decreased 55 +/- 7% (p less than 0.001), maternal and fetal serum glucose increased 158 +/- 23% and 249 +/- 91%, respectively (p less than 0.001), and maternal and fetal Po2 decreased to 44 mm Hg +/- 4 mm Hg and 13 mm Hg +/- 1 mm Hg, respectively (p less than 0.05). Maternal and fetal blood pressure and serum cortisol were unaffected by clonidine, whereas heart rate decreased. No adverse maternal or fetal effects were noted with serum clonidine concentrations less than 1.0 ng/ml. Direct fetal infusion of clonidine did not lower fetal arterial Po2 levels, although heart rates decreased and serum glucose levels increased. The multiple effects of clonidine infusion are best explained by actions on alpha 2-adrenergic receptors. These results suggest that intravenous administration of clonidine may adversely affect the fetus by direct actions and by alterations in maternal physiology.

Animals↗
PubMed1989

Atrial natriuretic factor maternal and fetal concentrations in severe preeclampsia.

There is a reduction in intravascular volume in patients with preeclampsia. Since the secretion of atrial natriuretic factor by human atrial myocytes is stimulated by increased intraatrial pressure or atrial distention, we sought to determine whether circulating maternal plasma atrial natriuretic factor concentrations were lower in patients with preeclampsia compared to normal pregnant women. The level of alpha-human atrial natriuretic factor was measured by a specific radioimmunoassay. Maternal venous concentrations of a alpha-human atrial natriuretic factor were higher in patients with severe preeclampsia (116.12 +/- 13.37 pg/ml) than in normal pregnant women (80.30 +/- 4.02 pg/ml). Umbilical artery alpha-human atrial natriuretic factor concentrations were higher in fetuses born to patients with severe preeclampsia (197.68 +/- 29.10 pg/ml) than normal control subjects (118.00 +/- 12.52 pg/ml). Umbilical artery alpha-human atrial natriuretic factor concentrations were higher than umbilical or maternal venous concentrations. In cases of severe preeclampsia, despite the presumed volume changes, maternal atrial natriuretic factor concentrations are higher than in normal pregnant women. The fetus appears to produce its own atrial natriuretic factor. Umbilical artery atrial natriuretic factor concentrations in fetuses born to preeclamptic mothers are higher than those seen in normal control subjects.

Adolescent↗
PubMed1989

Epidural clonidine analgesia in obstetrics: sheep studies.

Epidural clonidine administration produces analgesia by a nonopiate, spinal mechanism, and offers advantages over other epidural agents for labor analgesia. To examine clonidine's acute maternal and fetal effects, the authors injected clonidine, 300 micrograms, epidurally in seven chronically prepared, near term ewes. Unlike epidural saline injection, clonidine increased maternal and fetal serum glucose (by 178 +/- 30% and 190 +/- 30%, respectively; mean +/- SEM, P less than .01) 1 h following injection. Maternal and fetal serum cortisol and arterial blood gas tensions were unchanged following clonidine. Epidural clonidine injection produced minor decreases (10-15%) in heart rate in ewe and fetus, without altering maternal and fetal blood pressure, intra-uterine pressure, or uterine blood flow. Maternal and fetal serum clonidine concentrations peaked at 58 +/- 8 and 73 +/- 5 min following injection, respectively, and declined with similar half-lives. Heart rate correlated negatively with serum clonidine concentration in both ewe and fetus (P less than .05). Apart from hyperglycemia, which does not occur in humans, these results in sheep suggest that epidurally administered clonidine does not adversely affect the fetus and may be evaluated as an analgesic in obstetrics.

Analgesia, Epidural↗
PubMed1989

Blood volume restitution after hemorrhage in the newborn lamb.

Blood volume restitution after hemorrhage was investigated in lambs in the first week of life. Two groups of nonsplenectomized lambs were bled 10 and 20% of their blood volume at 2%/min while being suspended horizontally in a sling with their legs dependent, and a third group was bled 20% while lying down. Blood pressure fell 8% in the lambs bled both 10 and 20% while lying down and 44% in those bled 20% while being suspended. Blood volume was completely restored in all three groups by 5 h after the hemorrhage, the rate of restitution being equal among the groups. The initial phase of restitution was slower when the lambs were bled while lying down. Vasopressin levels were increased only in the lambs bled 20% of their blood volume while being suspended. Plasma renin activity increased similarly in all groups. Hemorrhage increased plasma glucose but did not change plasma protein and serum osmolality. We conclude that lambs bled up to 20% of blood volume restitute relatively quickly at a rate independent of the volume shed. The position of the animal affects the degree of hypotension, the levels of vasopressin, and the rate of the initial phase of volume restoration.

Animals↗
PubMed1989

Effect of cortisol on vasopressin response to hypertonic saline in fetal sheep.

To determine the effect of cortisol on vasopressin responses to hyperosmolality, we infused hypertonic saline (HS) (12 meq/kg NaCl) into nine chronically cannulated fetal sheep ranging from 110 to 132 days of gestation. The experiment was performed twice on each fetus, once during a continuous cortisol infusion and once during a vehicle infusion. Administration of HS resulted in a prompt increase in serum osmolality from 292.1 +/- 1.8 to 310.4 +/- 2.5 mosmol/kg. Decreases were seen in pH, partial pressure of O2, and hematocrit from 7.37 +/- 0.01 to 7.31 +/- 0.01, from 22.5 +/- 1.6 to 20.0 +/- 2.0 mmHg, and from 35.6 +/- 1.7 to 32.6 +/- 1.6, respectively. Mean arterial pressure increased from 41.3 +/- 1.4 to 48.9 +/- 2.0 mmHg (P less than 0.01). Arginine vasopressin (AVP) rose from base line after HS (P = 0.11 vehicle experiments, P = 0.04 cortisol experiments), and AVP responses were greater in the cortisol experiments than in the vehicle experiments (delta AVP = 21.9 +/- 10.9 vs. 3.1 +/- 0.9 pg/ml, P = 0.05). Also there was a correlation noted between differences in AVP response and cortisol levels (P less than 0.04). We conclude that cortisol exerts a positive influence on the AVP response to HS in fetal sheep.

Animals↗
PubMed1989

Comparison of high-dose opioid antagonist effects on ovine fetal cardiovascular function.

The opioid antagonists, naloxone (NOX) and naltrexone (NTX), were found to produce dose-dependent increases in fetal mean arterial pressure over a dose range of 5-80 mg/kg. There was a concomitant decrease in fetal heart rate up to 40 mg/kg. Above this dose, NOX and NTX caused an increase in heart rate as well as blood pressure. NTX produced similar effects in maternal ewes, although at lower doses (mg/kg) than those needed for fetal lambs. There were no age-related differences in antagonist effects in two fetal age groups studied (100-116 and 124-144 days of gestation). The partial antagonist, levallorphan (LVL), produced effects which were qualitatively similar to those produced by NOX and NTX in doses up to 20 mg/kg. These effects were not stereospecific, as the enantiomer of LVL, dextrallorphan, produced similar effects at equal doses. Pretreatment with the alpha 1-adrenoreceptor antagonist, prazosin, abolished the opioid antagonist effects on fetal blood pressure. We postulate that high doses of opioid antagonists activate sympathetic systems to increase fetal blood pressure through mechanisms which do not involve interactions with mu, delta or kappa opioid receptors.

Animals↗
PubMed1988

Endocrine responses of fetal lambs to hemorrhage after alpha 1-adrenergic receptor blockade.

To determine the importance of alpha 1-adrenergic receptors in the endocrine responses of fetal lambs to hemorrhage, eight chronically instrumented fetal lambs were bled of 20% of their measured blood volume after pretreatment with prazosin (24.8 +/- 2.1 days' gestation) or inert vehicle (124.2 +/- 2.2 days' gestation) according to a randomized, crossover protocol. Cortisol levels increased threefold with prazosin injection and remained elevated after hemorrhage but did not change with hemorrhage after vehicle infusion. Plasma renin activity was unaffected by the injection of prazosin but increased in both groups after hemorrhage. Vasopressin levels were unchanged in the control group throughout the experiment but increased tenfold with hemorrhage after pretreatment with prazosin. alpha 1-Adrenergic receptor blockade removes adrenergic inhibition of cortisol secretion and changes the hypotensive threshold for the secretion of vasopressin.

Adrenergic alpha-Antagonists↗
PubMed1988

Gestational diabetes reverses the circadian variation of plasma insulin response to intravenous glucose.

Both healthy third-trimester pregnant women and a group of women with gestational diabetes failed to show a difference in glucose clearance rates when given an intravenous glucose bolus at 8 AM compared with 4 PM. The plasma insulin response in the healthy pregnant women was greater at 8 AM. In the diabetic group, the peak insulin response was greater at 4 PM, but it was more prolonged after the 8 AM tests. These alterations in plasma insulin response were especially striking in the subgroup of obese women with gestational diabetes, who demonstrated metabolic differences compared with their nonobese counterparts.

Blood Glucose↗
PubMed1988

Arginine vasopressin infusion stimulates adrenocorticotropic hormone and cortisol release in the ovine fetus.

Arginine vasopressin may play a role in the control of adrenocorticotropic hormone release during stress in the adult animal. Arginine vasopressin is also considered an important stress hormone in the fetus. The effect of arginine vasopressin infusion on adrenocorticotropic hormone release in the fetus was investigated in 14 chronically cannulated ovine fetuses with normal blood gas and pH values between 103 and 137 days' gestation. There was a significant increase in adrenocorticotropic hormone and cortisol levels during a 30-minute infusion of arginine vasopressin. Plasma renin activity was unchanged. The corticotropin-releasing activity of arginine vasopressin was not blocked by pretreatment with a V1-receptor antagonist and was not significantly different when the pressor response was attenuated by sodium nitroprusside infusion.

Adrenocorticotropic Hormone↗
PubMed1988

Ovine fetal adrenal gland and cardiovascular function.

Given the necessity of the adrenal gland in maintaining cardiovascular function in adults of various species, these experiments were conducted to determine if fetal bilateral adrenalectomy results in altered resting heart rate, hypotension, and decreased basal blood volume as well as a diminished ability of the fetus to maintain arterial pressure and restore blood volume in response to hemorrhage. We studied heart rate, arterial blood pressure, and blood volume changes in response to hemorrhage of 20% of blood volume at 2%/min in seven adrenalectomized and six intact chronically cannulated unanesthetized lambs between 119 and 133 days of gestation. Blood volumes and percent restitution of shed volume were determined using 51Cr-tagged red blood cells and changes in hematocrit. There was no significant difference between groups in basal heart rate, mean arterial pressure, hematocrit, and blood volume. The two groups were similar to hemorrhage-induced changes in these and restitution of volume. Therefore, fetal adrenal glands are not necessary for basal cardiovascular function or regulation subsequent to moderate hemorrhage in the late gestation ovine fetus.

Adrenal Glands↗
PubMed1988

Comparison of hormonal responses to hypotension in mature and immature fetal lambs.

We studied norepinephrine (NE) and plasma renin activity (PRA) responses to sodium nitroprusside (NP)-induced hypotension in seven chronically catheterized fetal lambs 0.79-0.94 gestation (mature) and in seven fetuses 0.64-0.72 gestation (immature) 4 or 5 days after surgery. We infused intravenously 5% dextrose in water (DW) or NP in DW to reduce arterial pressure 30% in fetuses for 10 min. Initial infusion choice was random, and the two infusions were separated by 24-48 h. In both groups, basal NE levels were similar and doubled in response to hypotension. In mature fetuses, PRA basal levels were 6.89 +/- 1.80 ng.ml-1.h-1 and increased two- to threefold with hypotension. In immature fetuses, PRA basal levels were 2.42 +/- 0.86 ng.ml-1.h-1 and did not change with hypotension. No changes were observed with DW infusion in either group. Arterial blood gases were normal and remained unchanged. We conclude that in the lamb fetus, NE responses to hypotension are present before and are independent of the development of PRA responses and that before 0.72 gestation there is a functional deficit in the renin-angiotensin system.

Animals↗
PubMed1988

Differential maturation of beta-adrenoceptor-mediated responses in the lamb fetus.

To study the functional maturity of beta-receptor-mediated responses, seven chronically catheterized lamb fetuses, 93-107 days of gestation, and seven fetuses, 116-134 days of gestation, received intravenous randomly sequenced infusions of isoproterenol (ISO) 0.03, 0.06, and 0.125 micrograms.kg-1.min-1 for 10 min separated by 45-min intervals or two saline infusions followed by 0.125 micrograms.kg-1.min-1 ISO after treatment with 0.5 mg/kg propranolol (PRO). Each fetus received the two treatments 24-48 h apart. In immature fetuses, plasma renin activity (PRA) of 2.0 +/- 0.7 ng.ml-1.h-1 did not change with either protocol. In mature fetuses, PRA of 7.5 +/- 2.5 ng.ml-1.h-1 increased two- to three-fold after the infusion of the highest two doses of ISO (P less than 0.003). Propranolol blocked this response. No significant changes were observed after the infusions of the lowest dose of ISO or saline. Both groups showed significant heart rate increases with all doses of ISO. Propranolol injection decreased heart rate significantly and blocked responses to ISO. We conclude that although a cardiac beta-receptor-mediated response is present by 93 days of gestation in the lamb fetus, a renal beta-receptor-mediated response, renin secretion, is absent.

Animals↗
PubMed1988

Evidence that cortisol inhibits basal adrenocorticotropin secretion in the sheep fetus by 0.70 gestation.

To ascertain if reductions in fetal plasma cortisol cause increases in fetal plasma ACTH, we treated pregnant ewes or their fetuses with aminoglutethimide (10 mg/kg BW) and metyrapone (20 mg/kg BW) and measured the hormonal responses with RIAs. When given to fetuses (n = 9) at 0.90 +/- 0.01 gestation (term-145 days), the steroid synthesis inhibitors reduced fetal plasma cortisol from 35.1 +/- 11.9 to 18.5 +/- 6.2 ng/ml (P less than 0.01) and plasma ACTH increased from 37 +/- 7 to 189 +/- 74 pg/ml (P less than 0.02). Thus, late in gestation cortisol from the fetal adrenal suppresses basal fetal ACTH secretion. Blockade of steroid biosynthesis in pregnant ewes carrying intact fetuses at 0.76 +/- 0.02 gestation (n = 11) or adrenalectomized fetuses at 0.81 +/- 0.01 gestation (n = 6) also reduced cortisol and increased ACTH in fetal plasma. In intact fetuses cortisol declined from 9.4 +/- 2.0 to 3.6 +/- 0.9 ng/ml (P less than 0.05), and ACTH increased from 46 +/- 8 to 183 +/- 67 (P less than 0.01); cortisol declined in adrenalectomized fetuses from 2.1 +/- 0.4 to 1.1 +/- 0.3 ng/ml (P less than 0.01), and ACTH increased from 106 +/- 13 to 400 +/- 104 pg/ml (P less than 0.01). Cortisol infusions into intact and adrenalectomized fetuses prevented both the decline in steroid concentration caused by the biosynthesis inhibitors given to the ewe and the increase in fetal plasma ACTH concentration. These data indicate that reductions in plasma cortisol in adrenalectomized fetuses or intact fetuses at a time in development when the fetal adrenal produces little cortisol cause compensatory increases in fetal plasma ACTH concentration. The simplest explanation for these observations is that from approximately 0.70 gestation, basal fetal ACTH secretion is tonically inhibited by cortisol circulating in fetal plasma. This cortisol can originate from sources other than the fetal adrenal.

Adrenocorticotropic Hormone↗
PubMed1988

The effect of hypothalamic paraventricular nuclear lesions placed at 108-110 days gestational age on plasma ACTH concentrations in the fetal sheep.

Lesions that completely destroyed the paraventricular nucleus of the hypothalamus were placed in fetal sheep (n = 4) at 108-110 days of gestational age. These fetuses were then subjected to hypotension (50% of initial mean fetal arterial blood pressure), hypoxaemia (a decrease in fetal PaO2 greater than or equal to 5 torr) and bolus injection of corticotropin releasing factor (CRF-1.0 micrograms iv) in random order on successive days. The lesioned fetuses produced significantly less ACTH after hypotension (+10 min: 35.7 +/- 26.9 vs. 358.0 +/- 99.7 and +30 min: 28.2 +/- 12.2 vs. 238.0 +/- 73.0 pg.ml-1) (P less than 0.05), hypoxaemia (+40 min: 23.5 +/- 9.3 vs. 198.3 +/- 75.8 and +60 min: 32.3 +/- 18.8 vs. 295.3 +/- 99.9 pg.ml-1) (P less than 0.05) and intravenous administration of 1 microgram CRF (+15 min: 32.0 +/- 16.8 vs. 145.7 +/- 25.0 and +60 min: 33.0 +/- 23.3 vs. 161.3 +/- 43.1 pg.ml-1) (P less than 0.05). Our experiments suggest an important role for the fetal paraventricular nucleus in control of ACTH secretion. They also indicate that impairment of paraventricular nucleus function at this stage of fetal life may have a detrimental effect on the ability of the anterior pituitary to secrete ACTH in response to exogenous CRF.

Adrenocorticotropic Hormone↗
PubMed1988

Effect of cyclooxygenase inhibition on the pulmonary vasodilator response to furosemide.

Furosemide is a potent vasodilator of the systemic arterial and venous systems. The mechanism of vasodilatation, however, remains unclear. We investigated the vasodilatory effect of furosemide and its relation to endogenous prostaglandins (PGs). In the isolated canine lung lobe, furosemide significantly decreased mean pulmonary artery pressure. This effect was inhibited by indomethacin. Furosemide also attenuated the pulmonary vasoconstrictor response to the endoperoxide analog U46619 and PGF2 alpha. The pulmonary pressor response to a submaximal constrictor dose of arachidonic acid was significantly enhanced by furosemide, however, the pressor response to a maximal constrictor dose of arachidonic acid was attenuated, although not significantly. In animals pretreated with indomethacin, furosemide had no effect on the vascular response to PGF2 alpha, but the response to U46619 was significantly increased. Prostacyclin reduced pulmonary perfusion pressure and inhibited the pressor response to PGF2 alpha and U46619. Furosemide failed to alter inactivation of PGE2 on pulmonary lobe transit. We conclude that: 1) the vasodilatory activity of furosemide is mediated by increased production and not decreased metabolism of an endogenous cyclooxygenase product; 2) the effect of prostacyclin on vascular reactivity is similar to that of furosemide; and 3) local formation of prostacyclin by vascular tissue most likely mediates the vascular activity of furosemide.

Animals↗