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Biomedical subjects

S Otto

Publications and source records attributed to S Otto.

At least 73 records · Page 4Linked to original sources
PubMed1988

Evidence that neuropeptide Y (NPY) released into the hypophysial-portal circulation participates in priming gonadotropes to the effects of gonadotropin releasing hormone (GnRH).

NPY exhibits modulatory activity at both the adenohypophysial and the central levels of the rat hypothalamic-pituitary-gonadal axis. In the present studies, the secretion and physiological activity of endogenous irNPY was examined. We have shown that: (i) irNPY is secreted into the hypophysial-portal circulation, (ii) hypophysial-portal concentration profiles of irNPY and irGnRH are parallel throughout the rat estrous cycle, and (iii) removal of endogenous NPY via immunoneutralization inhibits the steroid-induced LH surge in ovariectomized rats. From these observations, we speculate that NPY secreted into the hypophysial-portal circulation participates in priming of gonadotropes to the actions of GnRH on the afternoon of the preovulatory surge.

Animals↗
PubMed1987

Neurotransmitter modulation of corticotropin releasing factor secretion into the hypophysial-portal circulation.

Secretion of corticotropin releasing factor (CRF) from the hypothalamic paraventricular nuclei into the hypophysial-portal circulation is modulated by a variety of neuronal afferents. Effects of intracerebroventricular acetylcholine (ACH), gamma-aminobutyric acid (GABA) and epinephrine (EPI) on immunoreactive (ir) CRF concentration in portal plasma were directly evaluated in urethanized male rats. ACH (0.1-10 nmole) administration was associated with a dose-dependent elevation of portal irCRF which was attenuated by pretreatment with either muscarinic or nicotinic receptor antagonists. GABA (0.1-10 nmole) also caused inhibition of irCRF concentration in the portal plasma which was prevented by bicuculline pretreatment. Finally, EPI (0.1-10 nmole) facilitated irCRF secretion via alpha 1- and beta-adrenergic mechanisms. These observations provide the first direct information on possible neurotransmitter actions on hypothalamic CRF secretion.

Acetylcholine↗
PubMed1986

Inhibition of immunoreactive corticotropin-releasing factor secretion into the hypophysial-portal circulation by delayed glucocorticoid feedback.

Nitroprusside-induced hypotension evokes ACTH secretion which is primarily mediated by enhanced secretion of immunoreactive corticotropin-releasing factor (irCRF) into the hypophysial-portal circulation. Portal plasma concentrations of neither arginine vasopressin nor oxytocin are significantly altered in this paradigm. Application of a delayed feedback signal, in the form of a 2-h systemic corticosterone infusion in urethane-anesthetized rats with pharmacological blockade of glucocorticoid synthesis, is without effect on the resting secretion of arginine vasopressin and oxytocin at any corticosterone feedback dose tested. Resting irCRF levels are suppressed only at the highest corticosterone infusion rate, which resulted in systemic corticosterone levels of 40 micrograms/dl. Suppression of irCRF secretion in response to nitroprusside-induced hypotension is observed and occurs at a plasma corticosterone level between 8-12 micrograms/dl. These studies provide further evidence for a strong central component of the delayed feedback process which is mediated by modulation of irCRF release.

Adrenocorticotropic Hormone↗
PubMed1985

Central modulation of immunoreactive arginine vasopressin and oxytocin secretion into the hypophysial-portal circulation by corticotropin-releasing factor.

Corticotropin-releasing factor (CRF), a potent ACTH secretagogue, has been found to exhibit many characteristics of central neurotransmitter/neuromodulatory substances. In this capacity, hypothalamic CRF might participate in postulated autoregulatory processes which regulate net secretion of adenohypophysical ACTH. We have examined the actions of centrally injected ovine CRF on the secretion of immunoreactive CRF, arginine vasopressin (AVP) and oxytocin (OT) into the hypophysial-portal circulation of urethane-anesthetized rats. Our observations do not support a short-term autoregulatory role for CRF. However, central administration of CRF was associated with a dose-dependent inhibition of hypophysial-portal concentrations of immunoreactive AVP and OT, suggesting potentially important central interactions among putative ACTH-regulatory factors.

Animals↗
PubMed1982

Evaluation of infants with acidosis using a perinatal "negative factor" score.

Using Prechtl's concept of optimal conditions as modified by Michaelis et al. [7] we analysed the case records of 50 acidotic newborn infants (umbilical artery pH of 7,250 or less) and of 34 controls. Acidotic infants had a significantly higher negative (or adverse) factor score. There was a correlation between the degree of acidosis and the negative factor score. There were, however, no relations between scores in isolated subgroups of negative factors and fetal acidosis though the same was not true for some combinations of subgroups (such as pre-eclampsia, operative delivery, fetal bradycardia in the second stage of labour).

Acidosis↗
PubMedDate not supplied

[Use and evaluation of the usefulness of synthetic materials-- Dallop, Marlex and Gore-tex in alloplasty of ventral hernia].

A trial was undertaken of the usefulness in alloplasty of abdominal hernias of three synthetic materials--Polish polyester net Dallop, polypropylene net Marlex and Gore-tex prostheses of soft tissues. In three 10-case groups of patients referred for correction of abdominal hernias Dallop, Marlex and Gore-tex were used. In the performed operations the use of synthetic materials made possible quick, simple and effective repair of tissue defect in abdominal wall. In early observations after the operations no inflammatory complications, suppuration of wound or recurrence of hernia were noted. Of the three synthetic materials used Gore-tex soft tissue prostheses were found to be most useful in alloplasty of abdominal wall defects.

Abdominal Muscles↗