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By using immunnohistochenstry and in situ hybridization, we have demonstrated that the nitric oxide (NO)-synthesizing enzyme NO synthase is present in gonadotrophs and in folliculo-steilate cells of the anterior pituitary gland of male and female rats. A marked increase in levels of NO synthase protein and mRNA was observed after gonadectomy. In vitro studies on dispersed anterior pituitary cells suggest that NO inhibits gonadotropin-releasing-hormonestimulated luteinizing hormone release. An inhibitory effect of NO has also been shown on growth-hormone-releasinghormone-stimulated release of growth hormone [Kato, M. (1992) Endoerinology 131, 2133-2138J. Thus these findings support a dual mechanism for NO in the control of anterior pituitary hormone secretion, an autocrine mediation of luteinizing hormone release on gonadotrophs, and a paracrine effect on growth hormone secretion involving folliculo-steilate cells cloely related to somatotrophs. We speculate that NO may participate in producing the pulsatfle secretion patterns ofthese two pituitary hormones.It is now well established that nitric oxide (NO), a free radical gas, is not only an endothelium-derived relaxing factor but also an inter-and intracellular messenger in many other biological systems (1)(2)(3)(4)(5). NO is formed from L-arginine by the enzyme NO synthase (NOS). This enzyme has been purified from rat brain (6,22), and the gene for rat brain NOS has been cloned (7). Thus, by using immunohistochemistry and in situ hybridization, it has been possible to map the distribution of NOS in various tissues including the nervous system (refs. 8, 9, 23 and 24; see also ref. 10). Little is known about the cellular localization of NOS in the endocrine system, but there is information on possible functional roles for NO in hormonal regulation. For example, the cytokine interleukin 1 increases production of NO in insulin-producing cells (11,12). At the pituitary level Kato (13) has shown that NO inhibits growthhormone (GH)-releasing-hormone (GHRH)-stimulated GH secretion. With regard to localization of NOS in the pituitary gland, this enzyme has so far been demonstrated only in the posterior lobe, presumably representing nerve endings originating from the magnocellular hypothalamic neurosecretory neurons, which also contain NOS (8,10).In the present study, we have used in situ hybridization and immunohistochemistry utilizing light and electron microscopy to find evidence for NO synthesis in the anterior pituitary. In addition we have evaluated a role for NO in the release of luteinizing hormone (LH)

Background. @nbsp; Cerebrovascular complications (CVCs) have remained a major therapeutic and prognostic challenge associated with infective endocarditis, and definite risk factors have not been fully elucidated. This prospective study was designed to the evaluate the total incidence of CVC associated with infective endocarditis and major risk factors. Methods. @nbsp; During 2 study periods, from June 1998 through April 2001 and from September 2002 through January 2005, patients were prospectively enrolled in the study regardless of neurological symptoms. Study patients underwent neurological examinations and magnetic resonance imaging of the brain, and cerebrospinal fluid analyses of inflammatory and neurochemical markers of brain damage (neurofilament protein and glial fibrillary acidic protein) were performed. Results. @nbsp; Sixty patients who experienced episodes of left-sided infective endocarditis were evaluated; 35% of these patients experienced a symptomatic CVC. Silent cerebral complications were detected in another 30% of the patients, and the total CVC rate was 65% (95% confidence interval, 58%-72%). Five percent of patients experienced their first neurological symptom after the initiation of antibiotic treatment without prior surgery. No new symptomatic CVCs were detected after 10 days of antibiotic treatment. No neurological deterioration was observed after surgery in patients who were established to have a symptomatic CVC preoperatively. A larger heart valvular vegetation size was a risk factor for both symptomatic and silent CVCs; Staphylococcus aureus etiology conferred a higher risk for symptomatic cerebral complication only. Conclusions. @nbsp; The use of sensitive methods of detection indicates that the incidence of CVC associated with infective endocarditis is high, but the risk for neurological deterioration during cardiac surgery after a CVC is lower than previously assumed. The major mechanism behind cerebral complications associated with infective endocarditis is cerebral embolization, although the dominant neurological symptoms vary considerably.

Bronchial hyperresponsiveness can be demonstrated in asthmatic subjects by inhalation of adenosine, but the action of adenosine at the level of the human airway smooth muscle has received comparatively little attention. We have previously observed that bronchi isolated from one asthmatic patient contracted in response to adenosine. We have therefore, during the course of a 3-yr study, further characterized the effects of adenosine in bronchi prepared from surgical specimens of lung tissue of asthmatics and of nonasthmatics. Contraction responses were always studied in vitro the same day the tissues were obtained. Bronchi from asthmatics (19 strips from six patients) were more sensitive to adenosine than were bronchi from nonasthmatics (21 strips, seven patients). In contrast, there was no difference in sensitivity to histamine or leukotriene C4 between the two groups, nor was the maximal tissue contractility different. The contractile effect of adenosine was inhibited by the adenosine A1-antagonist 2-thio-[(1,3-dipropyl)-8-cyclopentyl]-xanthine as well as by the dual A1 and A2 antagonists 8-(p-sulfo)-phenyltheophylline and theophylline. The combination of leukotriene antagonism (receptor-antagonist ICI 198,615 or biosynthesis inhibitor MK-886) and histamine antagonism (antihistamines mepyramine and metiamide) blocked the contractile effects of adenosine, suggesting that adenosine acts indirectly by liberation of leukotrienes and histamine, possibly from mast cells. The findings of increased sensitivity to adenosine in bronchi from asthmatics to our knowledge represents the first evidence of increased bronchial reactivity in vitro in asthmatics.

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Gadolinium is a lanthanide that has in recent years become more commonly present in our society. Organic chelates of gadolinium are increasingly used as contrast agents for the imaging of body fluids. Although adverse reactions to these agents are uncommon, it is known that gadolinium salts can bring about a wide variety of changes in physiology. Gadolinium chloride is widely used experimentally as an inhibitor of stretch-activated ion channels and physiological responses of tissues to mechanical stimulation. It is also employed as a selective inhibitor of macrophages in vivo. In this review, the known biochemical actions of gadolinium are brought together with its in vivo pharmacology and toxicology.

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