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Pathology of the respiratory system --- Pathological physiology. Pathogenesis --- Biochemical markers. --- Breath tests. --- Carbon monoxide --- Lungs --- Nitric oxide --- Biological Markers --- Lung Diseases. --- Nitric Oxide --- Respiration. --- Pathophysiology. --- Diseases --- Diagnosis. --- analysis. --- Biological markers --- Breath tests --- Respiration

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Oxytocin secretion from the posterior pituitary gland is increased during parturition, stimulated by the uterine contractions that forcefully expel the fetuses. Since oxytocin stimulates further contractions of the uterus, which is exquisitely sensitive to oxytocin at the end of pregnancy, a positive feedback loop is activated. The neural pathway that drives oxytocin neurons via a brainstem relay has been partially characterised, and involves A2 noradrenergic cells in the brainstem. Until close to term the responsiveness of oxytocin neurons is restrained by neuroactive steroid metabolites of progesterone that potentiate GABA inhibitory mechanisms. As parturition approaches, and this inhibition fades as progesterone secretion collapses, a central opioid inhibitory mechanism is activated that restrains the excitation of oxytocin cells by brainstem inputs. This opioid restraint is the predominant damper of oxytocin cells before and during parturition, limiting stimulation by extraneous stimuli, and perhaps facilitating optimal spacing of births and economical use of the store of oxytocin accumulated during pregnancy. During parturition, oxytocin cells increase their basal activity, and hence oxytocin secretion increases. In addition, the oxytocin cells discharge a burst of action potentials as each fetus passes through the birth canal. Each burst causes the secretion of a pulse of oxytocin, which sharply increases uterine tone; these bursts depend upon auto-stimulation by oxytocin released from the dendrites of the magnocellular neurons in the supraoptic and paraventricular nuclei. With the exception of the opioid mechanism that emerges to restrain oxytocin cell responsiveness, the behavior of oxytocin cells and their inputs in pregnancy and parturition is explicable from the effects of hormones of pregnancy (relaxin, estrogen, progesterone) on pre-existing mechanisms, leading through relative quiescence at term inter alia to net increase in oxytocin storage, and re

Activation. --- Activity. --- Adaptation. --- Allopregnanolone. --- Behavior. --- Birth. --- Brainstem. --- C-fos expression. --- Dendrites. --- Dynorphin. --- Enkephalin. --- Estrogen receptors. --- Estrogen. --- Feedback. --- Fetuses. --- Firing. --- Gaba. --- Gamma-aminobutyric-acid. --- Gland. --- Hormone. --- Hormones. --- Hypothalamic paraventricular nucleus. --- Increase. --- Increases. --- Inhibition. --- Main olfactory-bulb. --- Mechanisms. --- Messenger-ribonucleic-acid. --- Milk-ejection reflex. --- Neurons in-vitro. --- Neurons. --- Nitric oxide synthase. --- Nitric-oxide synthase. --- Nucleus tractus solitarius. --- Opioid. --- Oxytocin mrna. --- Oxytocin. --- Parturition. --- Pattern. --- Patterns. --- Pituitary. --- Potentials. --- Pregnancy. --- Progesterone-receptor expression. --- Progesterone. --- Rat supraoptic nucleus. --- Response. --- Restraint. --- Review. --- Secretion. --- Steroid metabolites. --- Steroid. --- Stimulation. --- Stimuli. --- Supraoptic nucleus. --- System. --- Time. --- Uterus.