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Biomedical subjects

J C Rose

Publications and source records attributed to J C Rose.

At least 163 records · Page 9Linked to original sources
PubMed1979

Plasma glucocorticoid and adrenocorticotropin concentrations measured serially in growth-retarded fetal lambs.

We studied the fetal pituitrary-adrenal axis in 9 growth retarded fetal lambs by serially measuring plasma glucocorticoids and ACTH concentrations from 115 to 140 days of gestation and adrenal blood flow at 138 days of gestation. At each gestational age period studied, plasma glucocorticoid and ACTH concentrations were similar in both growth retarded and control fetuses (Figs. 1, 2). However, ACTH concentration tended to be higher in the last 20 days of gestation in the growth retarded fetuses. This resulted in a significantly lower glucocorticoid/ACTH ratio between 121 to 130 days of gestation in the growth retarded fetal lambs as compared to the control fetuses (212 +/- 111 vs. 1042 +/- 257). The glucocorticoid/ACTH ratio in the growth retarded fetuses became similar to the ratio of the control fetuses at 131 to 140 days (445 +/- 145 vs. 554 +/- 182). Adrenal blood flow was significantly increased at term in the the growth retarded fetuses (535 +/- 87 vs. 302 +/- 40 ml/min/100g). These data indicate that the pattern of maturation of the fetal adrenal gland in the growth retarded fetal lamb is similar to that of the normal sized fetus. Because of the increased adrenal blood flow observed at 138 days of gestation, there is a suggestion of a decreased sensitivity to ACTH in these animals.

Adrenal Glands↗
PubMed1978

Histological enamel indicator of childhood stress in prehistoric skeletal samples.

Although previous paleopathological studies have used disturbances in enamel formation as indicators of childhood stress, the full potential of this technique has not been realized. This paper presents a test case which demonstrates that the frequency of disturbed enamel formation (i.e., Wilson bands) is associated with other stress indicators (i.e., probability of dying and infectious lesions) in three prehistoric skeletal samples representing the Middle Woodland (10.3%), Mississippian Acculturated Late Woodland (21.4%), and the Middle Mississippian (40.0%). Additionally, the mean ages at death of individuals with at least one Wilson band are lower than those without bands. These results suggest that Wilson bands are an indicator of the relative proportion of individuals who are high susceptibles in prehistoric populations. The data also corroborate the hypothesis that the adoption of maize agriculture in the prehistoric American Midwest is associated with increased stress.

Child, Preschool↗
PubMed1978

Nycthemeral rhythm in adrenal responsiveness to ACTH.

Adrenal adenosine 3',5'-cyclic monophosphate (cAMP) and corticosterone responses to exogenous ACTH were found to be about 2.5 times greater in the evening (at lights off) than in the morning (at lights on) in rats. The rhythm in adrenal responsiveness to ACTH was found to persist in rats treated with dexamethasone 15 and 3 h before exogenous ACTH (in the presumed absence of a rhythm in endogenous ACTH). Treatment with p-chlorophenylalanine did not affect the daily rise in circulating ACTH levels but did abolish the rhythm in adrenal responsiveness to ACTH. The magnitude of the rhythm in adrenal responsiveness to ACTH is greater than the magnitude of the rhythm in ACTH. Because the rhythms are dissociable, we conclude that in vivo measurements of adrenal corticosteroid levels do not necessarily reflect ACTH levels.

Adrenal Glands↗
PubMed1978

Effect of norepinephrine on renin release and the cyclic AMP content of rat kidney slices: modification by sodium deficiency and alpha-adrenergic blockade.

The effect of L-norepinephrine (NE) on renin release by slices of kidney cortex from sodium-replete and sodium-deficient rats was studied in vitro. The rate of renin release by slices from sodium-deficient rats in the absence of added NE increased in proportion to the length of dietary sodium restriction and was significantly greater at all times than release by slices from sodium-replete animals. NE added to slices from the sodium-replete animals in concentrations ranging from 2 X 10(-9) to 2 X 10(-4)M caused a significant renin release only at a concentration of 2 X 10(-7)M. In contrast, the rate of renin release by slices from the sodium-deficient rats increased in a dose-related fashion when the NE concentration ranged from 2 X 10(-12) to 2 X 10(-7)M. NE in a concentration of 2 X 10(-5) had a lesser stimulatory effect, and 2 X 10(-4)M caused a significant inhibition of renin release. This inhibition was converted to stimulation by addition of the alpha-adrenergic blocking drug phentolamine. Phentolamine by itself was ineffective. The increases and decreases in renin release produced by NE were, in general, accompanied by increases and decreases in the cyclic AMP content of the slices. The changes in renin release were linear for 60 min, but the changes in cyclic AMP content were greater at 5 and 20 min than at 60 min. A dose-response relationship between the changes in renin release and cyclic AMP content was not observed. These data indicate that sodium deprivation enhances the sensitivity of the renin-secreting cells to catecholamine stimulation, and are consistent with the hypothesis that the increase in renin secretion produced by NE is mediated via cyclic AMP. The data also indicated that in high concentrations, NE exerts an inhibitory effect on renin release, and that this effect is mediated via stimulation of alpha-adrenergic receptors.

Animals↗
PubMed1978

Cardiovascular responses to PGI2 (prostacyclin) in the dog.

Arachidonic acid (AA) produces characteristic hemodynamic changes in the canine circulation. These responses are blocked by prostaglandin (PG) synthetase inhibitors, indicating that AA and its nonprostanoic metabolites are not vasoactive. The hemodynamic effects of the cyclic endoperoxides, thromboxanes, and PGD2, PG2, and PGF2a differ from those produced by AA. PGI2, a newly identified product of AA, is reported to relax arterial strips. However, its cardiac and systemic effects are unknown. In 12 open-chest, anesthetized dogs, PGI2 (0.25-5.0 microgram/kg) produced a dose-related decrease in systemic arterial pressure (BP) and myocardial contractile force (MCF). In five left ventricular bypass preparations, PGI2 produced only a slight decrease in MCF at all doses, whereas the BP decreases were parallel to those in the intact preparation. AA, PGD2, PGE2, and PGI2 were administered in random order by bolus intravenous injections in approximately equidepressor doses to intact dogs. BP fell with each agent (AA, 300 microgram/kg, -25 percent; PGD2, 5 microgram/kg, -26 percent; PGE2, 5 microgram/kg, -26 percent PGI2, 0.5 microgram/kg, -26 percent). The vasodepressor action of PGI2 was approximately 10 times greater than that of PGD2 and PGE2. Pulmonary arterial pressure (PAP) rose significantly with PGD2 and PGE2 (AA, -1 percent; PGD2 +66 percent; PGE2, +20 percent; PGI2, -1 percent). Only PGE2 had a significant effect on MCF (AA, +7 percent; PGD2, +5 percent, PGE2, +20 percent; PGI2, -0.3). At this dose, PGI2 resembles AA in that it has little effect on either PAP or MCF. Of all known AA metabolites the response to PGI2 most closely resembles that of exogenous AA in the dog.

Airway Resistance↗
PubMed1978

Developmental aspects of the pituitary-adrenal axis response to hemorrhagic stress in lamb fetuses in utero.

Plasma ACTH and corticosteroid concentrations were measured by radioimmunoassay in chronically catheterized fetuses of 32 pregnant sheep. Fetal plasma ACTH levels 38+/-5 pg/ml (means+/-SEM) were slightly (P < 0.05) lower than maternal 54+/-4 pg/ml levels. No general rise in fetal plasma ACTH concentration was noted before 140 days gestation; however, fetal plasma corticoid levels began to increase after about 125 days. This suggested that an increase in fetal adrenal responsiveness to endogenous ACTH occurred during gestation. Hemorrhage of 15% of estimated blood volume decreased mean arterial pressure from 54+/-3 to 36+/-3 torr and increased plasma ACTH from 30+/-5 to 130+/-30 pg/ml in fetuses older than 0.80 gestation. In fetuses younger than 0.67 gestation, 15% hemorrhage caused no change in plasma ACTH levels despite a significant fall in mean arterial pressure. This suggests that system(s) subserving the ACTH response to mild hemorrhage are either absent or nonfunctional in the younger fetuses. The hemorrhage-induced increase in plasma ACTH levels was associated with a small rise in plasma corticoids in fetuses younger than 0.94 gestation. In older fetuses, a similar increase in plasma ACTH was associated with a pronounced increase in plasma corticoid levels. This also suggests that an increase in adrenal responsiveness to endogenous ACTH occurs during gestation. No detectable changes in maternal plasma ACTH or corticoids were found in response to fetal hemorrhage, thus the fetal pituitary-adrenal axis can autonomously respond to stress.

Adrenal Cortex Hormones↗
PubMed1978

Effect of lung transit on systemic depressor responses to arachidonic acid and prostacyclin in dogs.

Arachidonic acid (AA) (100 and 200 microgram/kg) and prostacyclin (PGI2) (0.25, 0.5, 1,2 and 3 microgram/kg) were administered by bolus injection into the inferior vena cava (i.v.) and left ventricle (i.a.) in spontaneously breathing anesthesized dogs (25). PGI2 like its precursor AA, decreased arterial diastolic pressure in a dose-dependent manner. The depressor responses after i.a. administration of a given dose of either AA or PGI2 did not differ significantly when the same dose was given i.v.; the i.v./i.a. ratio was 1. In comparison, the vasodepressor response to PGE2 (1, 2 and 3 microgram/kg i.v.) was reduced 12- to 40-fold by passage through the dog lung. The vasopressor response to PGF2alpha (1, 2, 3 and 5 microgram/kg i.v.) was diminished 5- to 8-fold by lung transit. Similarly, the pressor response to norepinephrine was also reduced by pulmonary transit. These studies support the view that (1) the lung plays a minor role in the systemic depressor response to AA and PGI2 and (2) the lack of an i.v./i.a. difference for AA and PGI2 indicates that the depressor response to AA may be due to generation of PGI2 by the vessel wall.

Animals↗
PubMed1978

Antagonism of the pulmonary vasoconstrictor response to prostaglandin F2alpha by N-dimethylamino substitution of prostaglandin F2alpha.

Efforts to develop an in vivo prostaglandin (PG) antagonist have met with limited success. In this study, N-dimethylamino analogs of PGF2alpha which have proven to be effective in vitro prostaglandin antagonists, were tested for antagonism to the PGF2alpha and arachidonic acid (AA) responses in the canine lung lobe preparation. PGF2alpha (1 microgram/kg) and AA (100 microgram/kg) increased lobar arterial pressure by 54 and 83%, respectively. Infusion of analogs did not change lobar arterial pressure. N-dimethylamine PGF2alpha (0.8-3.2 microgram/ml) antagonized the PGF2alpha response by 66 to 79%. N-dimethylamide PGF2alpha (1.6-8.0 microgram/ml) produced a dose-dependent antagonism (24-75%) with an IC50 value of 3.8 microgram/ml. Neither analog significantly attenuated the pulmonary response to AA. Thus, these N-dimethylamino analogs of PGF2alpha exhibit a potency which is superior to previous in vivo prostaglandin antagonists. In addition, they have effectively differentiated the pulmonary vascular responses of AA and PGF2alpha.

Animals↗
PubMed1977

Defective enamel histology of prehistoric teeth from Illinois.

Histological enamel defects have been used as indicators of childhood morbidity and nutritional inadequacy. However, the usefulness of these defects has been hampered by a lack of clear criteria for differentiating normal and defective enamel. This report demonstrates that the criteria of abnormal prism structure can accurately differentiate defective enamel (i.e., pathological bands) from normal enamel. In addition, pathological bands can be divided into three distinct subtypes: distorted structure bands, black spot pathological bands, and structureless pathological bands. It has been assumed that the patterning of pathological bands and enamel hypoplasia is the same for all populations. Comparisons between populations show that each population has its own unique pattern. It has also been assumed that striae of Retzius, pathological bands, and enamel hypoplasias represent three grades of severity of the same phenomenon. Correlations between these three features demonstrate instead that this patterning is possibly influenced by the morphology of the teeth.

Adolescent↗
PubMed1977

Platelets and the vascular responses to arachidonic acid in dogs.

UNLABELLED: Platelets are rich in components of the prostaglandin synthetase system which converts arachidonic acid into vasoactive and platelet-active prostanoate and nonprostanoate compounds. Repeated injections of arachidonic acid in dogs cause hypotension of reproducible magnitude and lower circulating platelet counts with each injection. However, the circulatory response to injected arachidonic acid was unchanged when platelet-poor blood was exchanged in dogs. Moreover, in the hind limb preparation and the isolated lung lobe, the vasoactive responses to arachidonic acid were indistinguishable whether perfused with whole blood or an artificial perfusate. CONCLUSION: the vascular responses to arachidonic acid do not appear dependent on the presence of platelets.

Animals↗
PubMed1977

Vasoconstrictor response to arachidonic acid in the isolated hind limb of the dog.

1 Arachidonic acid(AA) (25-200 mug/kg) produced a dose-related increase in perfusion pressure in dog isolated hind limbs perfused with either blood or a platelet-free perfusate. 2 Prostaglandin E2 produced vasodilation while prostaglandin F2 alpha produced no vascular change at these administered doses. 3 Phentolamine did not alter the arachidonic acid response, eliminating possible alpha-adrenoceptor mediation. 4 Aspirin and idomethacin blocked the vasoconstrictor response to AA. 5 This study indicates that a vasoactive intermediate in prostaglandin synthesis can be elaborated in the absence of platelets.

Animals↗