@article{XuNaeveriFrerichsetal.1993,
  author    = {Xu, K. and N{\"a}veri, L. and Frerichs, K. and Hallenbeck, J. M. and Feuerstein, G. and Davis, J. N. and Sir{\´e}n, Anna-Leena},
  title     = {Extracellular catecholamine levels in rat hippocampus after a selective alpha2-adrenoceptor antagonist or a selective dopamnie uptake inhibitor: Evidence for dopamine release from local dopaminergic nerve terminals},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62997},
  year      = {1993},
  abstract  = {The effect of 6-chloro-2,3,4,5-tetrahydro-3-methyi-1-H-3-benzazepine (SKF 86466), a selectlve nonimldazoline alpha-2 adrenoceptor antagonlst, on hippocampal re1ease of norepinephrine and dopamlne in conscious rats was lnvestigated by /n vlvo mlcrodialysis and high-pressure liquid chromatography. Additionally, extracellular concentrations of hippocampal dopamine (DA) and norepinephrtne (NE), durtng Infusion of selective monoamine uptake Inhibitors, were determined in freely moving rats. The basal concentration of NE in the dialysate was 4.9 ± 0.3 pg/20 pl. lntravenous admlnistratlon of 5 or 10 mgJkg of SKF 86466 was associated wlth a transierlt inc:rease (30 min) of 2-fold (12 ± 1 pg/20 ,d; p < .05) and 8-fold (39 ± 3 pg/20 pl; p < .05), respectlvely, in dlalysate NE, whereas a 1-mgfkg dose had no effect. DA was not detected in basal dlalysates, but after the adminlstratlon of 5 or 10 mgJkg of SKF 86466, 3.9 ± 0.4 and 6.4 ± 0.6 pg/20 pl, respectlvely, was present in the dialysates. The rnaxlmum increase in dialysate DA was reached 60 to 90 min after SKF 86466. The DA was not derived from plasma because plasma NE was elevated after the 5 mgJkg dose of SKF 86466 whereas no plasma DA was detected. ln order to determlne whether DA was present in noradrenergic nerve termlnals, the dopamine ß-hydroxylase Inhibitor SKF 1 02698 was administered (50 mgJkg i.p.). The Inhibitor decreased dialysate NE but DA was stin not detected in the dialysate. When SKF 86466 (5 mgJkg t.v.) was adminlstered 4 hr after SKF 102698, DA appeared in the dialysate but there was no lncrease in dialysate NE. Administration through the dialysis probe of the DA uptake Inhibitor, GBR-12909 (0.1 and 1 pM), dose-dependently lnaeased DA Ieveis to 5.7 ± 1.2 and 9.6 ± 2.8 pg/20 pl, respectively. GBR-12909 had no effect on hippocampal NE. Desipramine (5 and 10 pM) lncreased dose-dependently dialysate NE and lncreased DA concentrations to detectable Ieveis (2.7 ± 0.5 and 3.5 ± 0.7 pg/20 ,d, respectively). These results suggest that the a/pha-2 adrenoceptors modulate both NE and DA release in the rat hlppocampus and that DA detected in the hlppocampal dialysate might be released from dopaminergic neurons.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{VonhofSirenFeuerstein1991,
  author    = {Vonhof, S. and Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Central ventilatory effects of thyrotropin-releasing hormone in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63075},
  year      = {1991},
  abstract  = {Thyrotropin-releasing hormonewas shown to exert potent ventilatory effects after centrat administration. These data, however, were derived from studies using anesthetized animal preparations. Since TRH elicits strong arousal reactions, the observed ventilatory effects of TRH under anesthesia may have been due to nonspecific reduction in the anesthetic state of the animals. In order to clarify the extent to which the reversal of anesthesia may change ventilatory parameters after TRH application, we investigated the effect of TRH on Ventilation rate, relative tidal volume, relative respiratory minute volume, CO\(_2\) production CO\(_2\) consumption, and locomotor activity in the conscious, unrestrained rat. Intracerebroventricular application of TRH induced a dose-dependent, sustained increase in ventilation rate, relative tidal volume, and relative respiratory minute volume of maximally 128\%, 890\%, and 235\%, respectively. In addition, CO\(_2\) production and O\(_2\) consumption were elevated by 4.6 and 11.7 fold, whiJe no significant changes in locomotor activity were observed. The results suggest that TRH stimulates ventilation by a mechanism independent of its analeptic properties.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenVonhofFeuerstein1991,
  author    = {Sir{\´e}n, Anna-Leena and Vonhof, S. and Feuerstein, G.},
  title     = {Hemodynamic defense response to thyrotropin-releasing hormone injected into medial preoptic nucleus in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63099},
  year      = {1991},
  abstract  = {No abstract available},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenPowellFeuerstein1986,
  author    = {Sir{\´e}n, Anna-Leena and Powell, E. and Feuerstein, G.},
  title     = {Thyrotropin releasing hormone in hypovolemia: a hemodynamic evaluation in the rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63288},
  year      = {1986},
  abstract  = {ln the present study the effects of thyrotropin releasing hormone (TRH) and its stable analogue, CG3703, on cardiac output (thermodilution, Cardiomax) and regional blood flow (BF; directional pulsed Doppler technique) were investigated in hypovolemic hypotension in the rat. In urethan-anesthetized rats TRH (0.5 or 2 mg/ kg ia) or CG3703 (0.05 or 0.5 mg/kg ia) reversed the bleeding (27\% of the blood volume)-induced decreases in mean arterial ...},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenPaakkariGoldsteinetal.1989,
  author    = {Sir{\´e}n, Anna-Leena and Paakkari, P. and Goldstein, D. S. and Feuerstein, G.},
  title     = {Mechanism of central hemodynamic and sympathetic regulation by µ-opioid receptors: Effects of dermorphin in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63123},
  year      = {1989},
  abstract  = {The effects of i.c.v. administered dermorphin, a highly selective \(\mu\)-opioid agonist, on cardiac function and renal, mesenteric and hindquarter blood ftow were studied in conscious rats. Core temperature, blood gases, arterial plasma levels of norepinephrine, epinephrine, dopamine, 3,4-dihydroxyphenylalanine and dihydroxyphenylacetic acid (DOPAC) also were examined. Cardiac output was rneasured using a thermodilution technique and regional blood ftows using directional pulsed Doppler velocimetry. Dermorphin, at doses of 0.1-100 nmol/kg, increased blood pressure and hindquarter blood flow, renal and mesenteric resistance, and core temperature. Higher doses (1-5 \(\mu\)mol/kg) caused respiratory depression, acidosis, and shock despite profaund sympatho-adrenomedullary stimulation. Circulating Ieveis of catecholamines were significantly increased at the dermorphin doses of 0.1-1 00 nmol/kg. At the 100 nmol/kg dose, plasma levels of epinephrine, norepinephrine, the dopamine metabellte dihydroxyphenylacetic acid and the catecholamine precursor 3,4,-dihydroxyphenylalanine were increased by 2-15-fold. The data indicate that mu opioid receptor Stimulation exerts potent effects on cardiorespiratory functions, activates the sympathoadrenomedullary system and produces a pattem of blood flow changes consistent with the stress-induced •detense· response (skeletal muscle vasodilation and splanchnic vasoconstriction). Excessive mu opioid receptor Stimulation Ieads to shock due to respiratory and hemodynamic collapse.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenMcCarronLiuetal.1993,
  author    = {Sir{\´e}n, Anna-Leena and McCarron, R. M. and Liu, Y. and Barone, F. and Spatz, M. and Feuerstein, G. and Hallenbeck, J. M.},
  title     = {Perivascular monocyte/macrophage interaction with endothelium as a mechanism through which stroke-risk factors operate to increase stroke likelihood. Research Initiatives in Vascular Disease; SPECIAL COMMUNICATION},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63006},
  year      = {1993},
  abstract  = {No abstract available},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenLettsFeuerstein1988,
  author    = {Sir{\´e}n, Anna-Leena and Letts, G. and Feuerstein, G.},
  title     = {N-Acetyl-leukotriene E\(_4\) is a potent constrictor of rat mesenteric vessels},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63196},
  year      = {1988},
  abstract  = {N-Acetyl-leukotriene E\(_4\) administered to conscious freely moving rats produced a dose-dependent vasoconstriction in the mesenteric vessels which led to profound reduction of blood flow to the gut. Renal and hindquarter blood flow and vascular resistance were not affected even by high doses of N-acetyl-leukotriene E\(_4\) . N-Acetyl-leukotriene E\(_4\) was 10-fold more potent than the thromboxane analog U-46619 and 1000-fold more potent than prostaglandin F\(_{2a}\) but 2-5-fold less potent than leukotriene D\(_4\)/E\(_4\) to induce mesenteric vasoconstriction. These data indicatc that N-acetylleukotriene E\(_4\) is a biologically active metabolite of peptide leukotrienes, and might play a role in cardiovascular derangements mediated by leukotrienes.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenLakeFeuerstein1988,
  author    = {Sir{\´e}n, Anna-Leena and Lake, C. R. and Feuerstein, G.},
  title     = {Hemodynamic and neural mechanisms of action of thyrotropin releasing hormone in the rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63183},
  year      = {1988},
  abstract  = {Tbe mechanisms mediating the etl'ects ofthyrotropin-releasing hormone (TRH) on the cardiovascular system were studied in the conscious rat. Intracerebroventricolar (i.c. v.) injection of TRH (8 pmol-80 nmollkg) induced dose-dependent lncreases in mean arterial pressure, heart rate, and cardiac index. Rindquarter blood Oow increased due to vasodilation, while an lncrease in renal and mesenteric vascular resistance caused a decrease in blood Oow in the respective organs. The plasma Ievels of norepinephrine a~d epinephrine were increased by TRH, while there was no change in plasma renin activity or vasopressin. Tbe cardiovascular actions of i.c. v. TRH were not in.fluenced by blockade of the renin-angiotensin system or vasopressin receptors. Tbe ganglion blocker chlorisondamine and the a 1- aod al-adrenoreceptor antagooist phentolamlne (2 mg/kg i.v.) abolished the increase in blood pressure and mesenteric vasoconstriction after i.c. v. TRH. Propranolol (2 mg/kg i. v.) blocked the TRH-ioduced increase in cardiac index, heart rate, and hindquarter blood flow. The hindquarter vasodllatlon lnduced by TRH was also blocked by the selective ß1-adrenocept9r antagonist ICI 188,551 (1 or 2 mg/kg i.v.), while tbe ,8,-adrenoceptor blocker practolol (10 mg/kg i.v.) had no eft'ect on the hindquarter vasodiJation produced by TRH but totally blocked the increase in cardiac Index. In adrenal demedullated rats, the systemic hemodynamic eft'ects ofi.c. v. TRH were dimlnished along with the decrease in renal blood flow and lncrease in renal vascular resistance; however, the iocrease in hfndquarter blood flow was attenuated only in adrenal demedullated rats pretreated with the sympathetlc blocker bretylium. The renal vasoconstriction induced by i.c. v. TRH was not abolished by renal denervation. In sinoaortic debufl'ered rats, the pressor, tachycardic, and mesenteric vasoconstrictor responses to centrally administered TRH were significantly potentiated. Taken together, these data soggest that the putative rieurotransmitter TRH may play a role in central regulation of cardiac functions and organ blood flow distribution through both tbe sympathetic nerves and the adrenal medulla. A pivotal roJe for ß1-adrenoceptors in mediation ofhindquarter vasodilation ls also demonstrated.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenHeldmanDoronetal.1992,
  author    = {Sir{\´e}n, Anna-Leena and Heldman, Eliahu and Doron, David and Yue, Tian-Li and Liu, Yong and Feuerstein, G. and Hallenbeck, JM},
  title     = {Release of proinflammatory and prothrombbtic mediators in the brain and peripheral circulation in spontaneously hypertensive and normotensive Wistar-Kyoto rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47469},
  year      = {1992},
  abstract  = {Background and Purpose: We reported previously that stroke risk factors prepared the brain stem for the development of ischemia and hemorrhage and induced the production of tumor necrosis factor following an intrathecal injection of Iipopolysaccharide, a prototypic monocyte-activating stimulus. This study evaluates whether blood or brain cells of hypertensive rats produce more proinflammatory and prothrombotic mediators than do blood or brain cells of normotensive rats. MethotJs: Levels of tumor necrosis factor, platelet-activating factor, 6-ketoprostaglandin F1a, and thromboxane B2 in the cerebrospinal fluid and blood of spontaneously hypertensive and normotensive Wistar-Kyoto rats were monitored before and after achallenge with Iipopolysaccharide. Results: Little or no activity from these media tors was found in the cerebrospinal fluid or blood of saline-injected control animals. Intravenous administration of Iipopolysaccharide (0.001, 0.1, and 1.8 mg/kg) produced dose-dependent increases in blood levels of all mediators in hypertensive rats. In normotensive rats the levels were less than in hypertensive rats and were not c1early dose-related. When Iipopolysaccharide was injected intracerebroventricularly, more tumor necrosis factor was measured in the cerebrospinal fluid than in the blood, suggesting local synthesis of this cytokine. Levels of tumor necrosis factor and platelet-activating factor in the cerebrospinal fluid were higher in hypertensive than in normotensive rats. The thromboxane A2/prostacyclin ratio was not aItered significantly between the two rat strains. Conclusions: It is suggested that the higher incidence of brain stem ischemia and hemorrhage after the intrathecal injection oflipopolysaccharide in hypertensive rats than in normotensive rats might be related to the higher levels of the two cytotoxic factors tumor necrosis factor and platelet-activating factor produced in response to such challenge.},
  subject      = {Gehirn},
  language  = {en}
}
@article{SirenFeuersteinLabrooetal.1986,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, G. and Labroo, V. M. and Coleen, L. A. and Lozovsky, D.},
  title     = {Effect of thyrotropin releasing hormone and some of its histidine analogs on the cardiovascular system and prolactin release in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63307},
  year      = {1986},
  abstract  = {The cardiovascular and endocrine activity of three analogs of thyrotropin releasing hor.mone (TRH), 4-nitro-imidazole TRH (4-nitroTRH), 2-trifluoro-methyl-imidazole TRH (2-TFM-TRH) and 4-trifluoromethyl- imidazole TRH (4-TFM-TRH), was compared to TRH in conscious rats. Injection of TRH or the three analogs (1 mg/kg or 5 mg/kg) into the arterial line induced increases in mean arterial pressure, pulse pressure and heart rate and raised plasma prolactin (PRL). None of the analogs were more potent than TRH in inducing cardiovascular changes. The 4-TFM-TRH was significantly less potent than the 2-TFM-TRH in increasing blood pressure, while the nitro-TRH was more potent than the 2-TFM-TRH in producing tachycardia. TRH induced a two-fold increase in PRL at the 5 mg/kg dose, while both the fluorinated analogs elici ted a 4 to 5 fold increase in PRL at the higher dose. The present results suggest that the receptors for TRH-elicited PRL release differ from TRH-receptors involved in its cardiovascular actions.},
  subject      = {Neurobiologie},
  language  = {en}
}