Subclavian artery injuries.

Thirty-two consecutive patients with subclavian artery injuries were evaluated to assess the mechanism of injury, types of repair, and results. In this series, most wounds were from firearms. Although the mortality was high (19%), most patients had the vessel repaired successfully.

Central stimulation of oxytocin release in the lactating rat by N-methyl-D-aspartate: requirement for coactivation through non-NMDA glutamate receptors or the glycine coagonist site.

Excitatory amino acid (EAA) neurotransmitters participate in the regulation of secretion of several neuropeptides, including oxytocin (OT), via actions at different receptors. In earlier studies, release of OT could be achieved reliably by injection into the supraoptic nucleus (SON) of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor agonists, but not by treatment with N-methyl-D-aspartate (NMDA) alone. This prompted further examination of the possible role of NMDA receptors in OT release following central coapplication of NMDA and AMPA-site agonists, or of NMDA and agonists active at the glycine coagonist site.

Stimulation of oxytocin release in the lactating rat by a central interaction of alpha 1-adrenergic and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-sensitive excitatory amino acid mechanisms.

These studies tested for a facilitatory interaction between noradrenergic and excitatory amino acid mechanisms controlling oxytocin (OT) release in the lactating rat. Lactating females were cannulated in the supraoptic nucleus of the hypothalamus (SON) or into the third ventricle and treated with the alpha 1-agonist phenylephrine (PHE) or the glutamate receptor agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), either alone or together. Treatment with PHE increased plasma OT dose dependently after microinjection into the SON area; strong stimulation also occurred after third ventricle injection of the drug.

Low-osmolar contrast media in the 1990s. Guidelines for urography in a cost-sensitive environment.

Objectives: The author reviews the clinical, ethical, medicolegal, and economic consequences of the routine versus limited use of low-osmolar contrast media for patients undergoing urographic and other radiologic studies.

Methods: A comprehensive review of the literature since the introduction of low-osmolar contrast media was conducted, focussing on medical decision making and the economic impact of those decisions on radiologic studies requiring the administration of water-soluble contrast agents.

Results: Compared with high-osmolar ionic contrast media, routine use of low-osmolar agents for intravascular injection during diagnostic imaging results in fewer idiosyncratic reactions in patients and potentially less renal injury in a subgroup of critically ill patients.

Central stimulation of oxytocin release in the lactating rat: interaction of neuropeptide Y with alpha-1-adrenergic mechanisms.

The possible cooperation of neuropeptide Y (NPY) and alpha-1-adrenergic mechanisms in the release of oxytocin (OT) in conscious, nonsuckled lactating rats was examined following microinjections of NPY and its analogs and/or alpha-adrenergic drugs into the supraoptic nucleus (SON) or anterior paraventricular nucleus/anterior commissural nucleus (PVN/ACN). The alpha-1-adrenergic agonist phenylephrine dose dependently increased plasma OT after injection into the SON or the PVN/ACN, and this was prevented by treatment with the specific alpha-alpha-1-adrenergic receptor antagonist prazosin, but not by the alpha-2 antagonist rauwolscine. The alpha-2-adrenergic agonist clonidine did not increase plasma OT.

Activation of central D-1 dopamine receptors stimulates oxytocin release in the lactating rat: evidence for involvement of the hypothalamic paraventricular and supraoptic nuclei.

The stimulatory effect of dopamine (DA) on the release of oxytocin (OT) in lactating rats is exerted at the D-1 DA receptor subtype. Because the neural loci mediating this effect have not been identified, the objective of the present studies was to test whether OT release in the lactating rat would be elevated after central administration of a D-1 DA receptor agonist into the third ventricle (3V) or directly into either the rostral paraventricular/anterior commissural nucleus area (PVN/ACN), the central paraventricular nucleus area, or the supraoptic nucleus (SON), all of which contain OT neurosecretory cells. Lactating rats were implanted with a stainless steel cannula directed into one of the above areas or into the arcuate-ventromedial region of the medial basal hypothalamus (MBH), or sites dorsal to the PVN/ACN or SON, which served as anatomical controls.

Neuropeptide Y modulates the binding of a gonadotropin-releasing hormone (GnRH) analog to anterior pituitary GnRH receptor sites.

Neuropeptide Y (NPY) increases LH secretion in part by enhancing the release of LH in response to GnRH. The present studies examined whether NPY influences the binding of GnRH to its receptors and also assessed whether specific binding sites for NPY exist in rat anterior pituitary membranes. In concentrations from 66-200 nM, NPY dose-dependently enhanced the binding of a 125I-labeled GnRH agonist, [D-Ala6, des-Gly10]GnRH ethylamide (GnRHa; 30 pM) to anterior pituitary membranes of chronically ovariectomized rats; higher concentrations of NPY were ineffective.

Calcitonin inhibits thyrotropin-releasing hormone-induced increases in cytosolic Ca2+ in isolated rat anterior pituitary cells.

Calcitonin (CT) and related peptides, such as CT gene-related peptide and salmon CT (sCT)-like peptide, are present in the rat nervous system and the pituitary gland, and sCT markedly inhibits basal and TRH-stimulated PRL release from anterior pituitary (AP) cells. Because TRH-induced PRL release is known to involve increases in cytosolic free Ca2+ derived from both extracellular and intracellular sources, the objective of the present study was to test whether sCT interferes with this effect. Secretogogue-induced elevations of cytosolic free Ca2+ ([Ca2+]i) in acutely dispersed AP cells were monitored using the fluorescent Ca2+ indicator Indo-1 AM and flow cytometry.