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Biomedical subjects

P M Dix

Publications and source records attributed to P M Dix.

5 recordsLinked to original sources
PubMed1990

Electrocardiographic abnormalities during ritodrine administration.

Electrocardiographic abnormalities have been reported during ritodrine tocolysis. No previous studies, however, have included controls. The purpose of this study is to evaluate the electrocardiographic tracings of patients receiving ritodrine tocolysis and compare them with those of matched controls. Holter monitors were placed on eight patients receiving ritodrine tocolysis and eight control patients for 24 hours to make continuous electrocardiographic records. Twelve-lead electrocardiograms, serum glucose, and electrolyte concentrations were monitored serially in all patients. Four of the eight patients receiving ritodrine tocolysis demonstrated ST segment depression, while none of the control patients manifested any electrocardiographic abnormalities. The observed ST segment depression appears to be related to the degree of maternal tachycardia and the level of hypokalemia and hyperglycemia that occurs during early ritodrine tocolysis.

Adolescent↗
PubMed1985

Corticotropin-releasing factor--induced adrenocorticotropic hormone release in the sheep fetus: blockade by cortisol.

We administered intravenous injections of synthetic ovine corticotropin-releasing factor to chronically cannulated sheep fetuses and monitored fetal plasma adrenocorticotropic hormone and cortisol concentrations. The three doses of corticotropin-releasing factor used (10, 100, or 1000 ng X kg-1) increased fetal plasma adrenocorticotropic hormone; fetal plasma cortisol levels rose with the highest dose of corticotropin-releasing factor. Administration of corticotropin-releasing factor at these concentrations did not change fetal heart rate or blood pressure. Elevation of fetal plasma cortisol levels to 40 to 80 ng X ml-1 by infusions of the steroid blocked the adrenocorticotropic hormone responses to all three doses of corticotropin-releasing factor. These data indicate that corticotropin-releasing factor can increase plasma adrenocorticotropic hormone concentrations in the late-gestation fetus and that these increases can be blocked by elevations in fetal plasma cortisol levels within a physiologic range. This suggests that cortisol modulates adrenocorticotropic hormone release by the fetal pituitary gland late in gestation.

Adrenocorticotropic Hormone↗
PubMed1984

Cortisol infusion blocks adrenocorticotropic hormone but not vasopressin responses to hypotension in fetal lambs.

In eight experiments in which a paired crossover design was used, we studied the ability of physiologic levels of cortisol to block adrenocorticotropic hormone (ACTH) and vasopressin responses to hypotension in fetal lambs. On different days, each fetus received a 4-hour infusion of cortisol or ethanol-saline solution vehicle, and then hypotension was induced with nitroprusside. Mean levels of ACTH before manipulation were 20 +/- 10 pg/ml and 18 +/- pg/ml in the saline solution- and cortisol-treated animals, respectively. Mean values of ACTH increased significantly to 70, 88, and 127 pg/ml at 2.5, 5, and 10 minutes of hypotension after pretreatment with saline solution. Cortisol pretreatment abolished the fetal ACTH response to hypotension. Mean levels of vasopressin during the control period were similar in the two groups of animals (5.7 +/- 1.5 pg/ml versus 5.9 +/- 1.3 pg/ml) and rose to comparable levels (69.4 +/- 15.6 pg/ml versus 65.2 +/- 7.7 pg/ml) during hypotension. Thus, increases in plasma cortisol levels within a physiologic range can suppress hypotension-induced ACTH but not vasopressin release in the fetus.

Adrenocorticotropic Hormone↗
PubMed1978

Fasting and postprandial serum gastrin in normal human neonates.

Serum gastrin determinations were performed in 32 normal-term infants to determine the level of this hormone in normal infants at birth and its response to normal feeding. Significant differences were noted between newborn cord blood and maternal blood at birth. Further significant elevations in fasting serum gastrins were noted in these infants over the first 72 hr of life. Pre- and postprandial determinations with normal feeding failed to demonstrate a significant elevation in serum gastrin levels following ingestion of protein-containing formulas. These data suggest a relative insensitivity of the release of gastrin from the gastric antrum in response to protein, a powerful mediator of gastrin release in the adult.

Fasting↗