@article{FeuersteinLeaderSirenetal.1987,
  author    = {Feuerstein, G. and Leader, P. and Sir{\´e}n, Anna-Leena and Braquet, P.},
  title     = {Protective effect of PAF-acether antagonist, BN 52021, in trichothecen toxicosis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63244},
  year      = {1987},
  abstract  = {Trichothecenes are mycotoxins which produce Iethai toxicosis in humans and animals, yet no adequate therapeutic regimen has been developed. This study provides evidence that the selective platelet activating factor (PAF) antagonist, BN 52021 (5-15 mg/kg i.v.) can prolong the survival of conscious rats exposed to a highly Iethai T -2 toxicosis. These data also suggest that P AF is an important mediator of this unique toxicosis.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{LabrooCohenLozovskyetal.1987,
  author    = {Labroo, V. M. and Cohen, L. A. and Lozovsky, D. and Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Dissociation of the cardiovascular and prolactin-releasing activities of TRH by histidine replacement},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63253},
  year      = {1987},
  abstract  = {No abstract available},
  subject      = {Neurobiologie},
  language  = {en}
}
@misc{FeuersteinSiren1987,
  author    = {Feuerstein, G. and Sir{\´e}n, Anna-Leena},
  title     = {Opioid peptides: A role in hypertension? [Brief Review]},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63262},
  year      = {1987},
  abstract  = {This review is an attempt to highlight evidence that may implicate the endogenaus opioid system in the pathogenesis of hypertension in humans. The evidence raised includes biochemical, physiological, pharmacological, and behavioral studies con~ucted in in vitro andin vivo systems, experimental models of hypertension, and hornans with essential hypertension. While the compelling biochemical and pharmacological evidence in experimental animals clearly shows the presence of opioid peptides and their receptors in strategic sites of cardiovascular control and potent cardiovascular response to opioid peptides, opioid antagonists show no consistent blockade or reversal of hypertension in experimental animals or humans. One possible explanation for this phenomenon could be the vast redundancy in systems regulating blood pressure (i.e., the blockade ofone system stillleaves many other systerils fully able to rapidly offset the eliminated system). Regarding the opioid system, the situation is much more complex, since some opioid receptors (\(\mu\)-type) niediate pressor responses, while other receptors (\(\kappa\)type) mediate depressor responses. Therefore, nonselective opioid receptor antagonists (e.g., naloxone), which block both types ofreceptors, can be devoid ofany cardiovascular activity, while a selective \(\mu\)-receptor antagonist or a selective arid potent \(\kappa\)-receptor agonist may produce the desired antihypertensive elfect. A combination of both actions (i.e., a drug that is both \(\mu\)antagonist and a \(\kappa\)antagonist) might be even more advantageous. Until such compounds are developed, this hypothesis will be hard to prove.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{PaakkariNurminenSiren1986,
  author    = {Paakkari, I. and Nurminen, M-L. and Sir{\´e}n, Anna-Leena},
  title     = {Cardioventilatory effects of TRH in anesthetized rats: role of the brainstem},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63277},
  year      = {1986},
  abstract  = {Cardioventilator responses were studied in anaesthetized rats after injections of TRH into either the lateral (i.c.v. lat) or the fourth (i.c.v. IV) cerebral ventricles. TRH induced a morerapid hypertensive effect i.c.v. IV than i.c.v. lat. Blocking of the cerebral aqueduct abolished the hypertensive and tachypnoeic effects of TRH i.c.v. lat but not those of TRH i.c.v. IV. It is concluded that TRH increased blood pressure and ventilation rate via brain stem structures close to the fourtli ventricle.},
  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{SirenFeuerstein1986,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Effect of T-2 toxin on regional blood flow and vascular resistance in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63293},
  year      = {1986},
  abstract  = {The acute effect ofT-2 toxemia on local blood flow and vascular resistance in hindquarter. mesenteric. and renal vascular beds was continuously measured by the directional pulsed Doppler technique in conscious, male Sprague-Dawley rats. Intravenous injection ofT-2 toxin (I mg/kg) in the conscious rat reduced blood flow and increased vascular resistance in all blood vessels studied but had no significant effect on mean arterial pressure or heart rate. The blood flow in hindquarters gradually decreased to a minimum of -77 ± 9\% (mean ±SE) 6 hr after the toxin injection. The hindquarter vascular resistance concomitantly increased to a maximum value of + 323 ± 69\% above thc resistance before toxin administration. Mesenteric and renal blood flow initially increased (slightly) and then gradually decreased. The maximum drop of blood flow, -90 ± 13\% and -76 ± 13\% for the mesenteric and renal vascular beds, respectively, was achieved 4 hr after T-2 toxin injection and the blood flow values remained low for up to 6 hr. Simultaneously with the impairment of},
  subject      = {Neurobiologie},
  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}
}
@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{SirenEimerlFeuerstein1989,
  author    = {Sir{\´e}n, Anna-Leena and Eimerl, J. and Feuerstein, G.},
  title     = {L-649,923 : An antagonist of cardiac and vascular leukotriene D\(_4\) receptors},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63134},
  year      = {1989},
  abstract  = {The capacity of L-649,923-sodium ( ßS, -yR * )-4-(3-( 4-acetyl-3-hydroxy-2-propylphenoxy)propylthio)-- y-hydroxy-ß-methylbenzene butanoate-to block vascular receptors of leukotriene D\(_4\) ( L TD\(_4\)) was examined in the conscious rat. Hindquarter (HQ), renal, and mesenteric blood flow and vascular resistance were evaluated in the conscious rat chronically equipped with miniaturized Doppler probes for organ blood flow measurement by directional pulsed Doppler technique. In addition, cardiac outpul was measured by thermodilution technique in conscious rats equipped with minithermistors in the ascending aorta. Systemic hemodynamic variables. mean arterial pressure, and heart rate were monitored through femoral catheters. L TD\(_4\) (I or 10 \(\mu\)g/kg) produced a marked dose dependent increase in the mesenteric vascular resistance associated with a marked decrease in blood flow whereas no consistent effects were demonstrated in the renal circulation. L TD\(_4\) • at I \(\mu\)g/kg. increased the HQ blood flow whereas the higher dose of LTD\(_4\) produced a biphasic response: an early increase followed by a decrease in blood flow. Infusion of L TD\(_4\) • 3 \(\mu\)g/kg per min over 10 min decreased cardiac output and increased total peripheral resistance. L-649,923 (10 or 30 mg/kg, i.v.) effectively blocked the L TD4-induced mesenteric constriction and the second I phase of HQ vasoconstriction but did not modify the , LTD\(_4\) induced HQ vasodilation. L-649,923 also effectively attenuated the cardiac effects of LTD\(_4\) infusion. I These studies suggest that L-649,923 could preserve cardiac and vascular functions in pathologic states mediated by cysteinylleukotrienes, such as traumatic or endotoxin shock. Key Words: Leukotriene D4 -Cardiovascular system- Leukotriene antagonist- Mesenteric blood tlow-Renal blood flow-Hindquarter blood flowAnaphylaxis.},
  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{PaakkariPaakkariFeuersteinetal.1992,
  author    = {Paakkari, P. and Paakkari, I. and Feuerstein, G. and Sir{\´e}n, Anna-Leena},
  title     = {Evidence for differential opioid µ\(_1\)- and µ\(_2\)-receptor regulation of heart rate in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63017},
  year      = {1992},
  abstract  = {The possibility that \(\mu\)Opioid-induced tachycardia and bradycardia could be mediated by different subtypes of the \(\mu\)·receptor was studied in conscious Sprague-Dawley rats. The selective \(\mu\)·receptor agonist dermorphin and its analog, TAPS (Tyr-o-Arg-Phe-sarcosine), a putative \(\mu _1\)-receptor agonist, were given centrally. Tyr-o-Arg-Phe-sarcosine increased the heart rate, the response being inversely correlated to the dose (an increase of 71 ± 22, 49 ± 14 and 30 ± 17 beats/min at doses of 0.3, 3 and 30 pmol, respectively). Dermorphin induced less clear changes in heart rate (maximum increase of 39 ± 14 beats/min at the dose of 1 pmol). Aftertreatment with the Jl 1-selective antagonist naloxonazine (NAZ), TAPS 30 pmol and dennorphin I pmol decreased heart rate by -22 ± 10 and -24 ± 7 bpm, respectively. The bradycardic effect oflarger doses of dennorphin was potentiated by NAZ (from -25 ± 8 to -97 ± 22 bpm) but abolished by the non-selective antagonist naloxone. These data suggest that the high affinity \(\mu _1\)-opioid receptors mediate tachycardic responses and \(\mu _2\)-receptors mediate bradycardic responses.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{AdeyemoSiren1992,
  author    = {Adeyemo, M. and Sir{\´e}n, Anna-Leena},
  title     = {Cardio-respiratory changes and mortality in the conscious rat induced by (+)- and (±)- anatoxin-a},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63027},
  year      = {1992},
  abstract  = {0. M. ADEYEMO and A.-L. SIREN. Cardio-respiratory changes and mortality in the conscious rat induced by ( + )- and ( ± )-anatoxin-a. Toxicon 30, 899-905, 1992.-Anatoxin-a (AnTx-a) isapotent nicotinic cholinergic receptor agonist. The relative potencies of the ( + )-AnTx-a and the racemic mixture ( ± )-AnTxa were investigated in the conscious rat by comparing their effects on mean arterial blood pressure (BP), heart rate (HR), blood oxygen and carbon dioxide pressures (p02 and pC02, respective1y), acid-base balance (pH) and mortality. The present experiments show that while both forms of AnTx-a produce dose-dependent increases in BP and decreases in HR, ( + )-AnTx-a is about IO-fo1d morepotent than the optically inactive isomer. ( + )-AnTx-a was also 6-fo1d more potent than ( ± )-AnTx-a in produclog severe hypoxemia, and more than 4-fold as potent as the (±}-AnTx-a in producing significant hypercapnia accompanied with severe acidosis. The approximate median Iethai dose (Ln so) of ( + )-AnTx-a was about 5-fold less than that of ( ± )-AnTx-a. We conclude that ( + )-AnTx-a is more potent than the ( ± )-AnTx-a racemic mixture in causing detrimental cardio-respiratory changes and therefore increased mortality in the rat.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenFeuerstein1992,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {The Opioid System in circulatory control},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63045},
  year      = {1992},
  abstract  = {Opioid peptidesandmultiple opioid receptors are found in brain cardiovascular nuclei, autonomic ganglia, the heart, and blood vessels, and opioids induce potent cardiovascular changes. The role of endogenaus opioids in normal cardiovascular homeostasis is unclear; however, current data suggest opioid involvement in stress.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{DoronMcCarronHeldmanetal.1992,
  author    = {Doron, D. A. and McCarron, D. M. and Heldman, E. and Sir{\´e}n, Anna-Leena and Spatz, M. and Feuerstein, G. and Pollard, H. B. and Hallenbeck, J. M.},
  title     = {Comparison of stimulated tissue factor expression by brain microvascular endothelial cells from normotensive (WKY) and hypertensive (SHR) rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63032},
  year      = {1992},
  abstract  = {The amounts of tissue factor (TF) expressed by brain microvascular endothelial cells (BMECs) from normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were compared after stimulating the cells with different doses of lipopolysaccharide (LPS), thrombin, phorbol myristic acid (PMA), Ca\(^{2+}\)·ionophore (A23187), or tumor necrosis factor (TNF) and interleukin·l (IL.l). Treatment ofcultured BMECs fron. WKY and SHR with all of these factors dose·dependently increased their total amount of TF; no substantive differences in the Ieveis of enhanced TF expression were observed between WKY and SHR BMECs. We conclude that stimulated endothelium from rats with hypertension, a major stroke risk factor, is not hyperresponsive with respect to TF expression when compared to normotensive controls.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{FeuersteinZerbeSiren1991,
  author    = {Feuerstein, G. and Zerbe, R. L. and Sir{\´e}n, Anna-Leena},
  title     = {Supraoptic nuclei in vasopressin and hemodynamic responses to hemorrhage in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63057},
  year      = {1991},
  abstract  = {CARDIOVASCULAR and vasopressin (A VP) responses to hcmorrhagc wcrc studicd in rats with lesions of the hypothalamic supraoptic nuclei (SONL). Bleeding caused hypotension and increase in heart rate (HR) and A VP. SONL rats failed to fully recover from bleeding as compared to normal rats. Plasma A VP in SONL rats was in the normal in basal conditions, but failed to increase to levels attained in normal rats throughout the post-hemorrhage period. These data suggcst that the supraoptic nuclei are the primary regulatory sitcs for A VP release in rcsponse to hemorrhage and that lack of adequate A VP release significantly retards blood pressure recovery after bleeding.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{SirenFeuerstein1991,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Hypothalamic opioid µ-receptors regulate discrete hemodynamic functions in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63069},
  year      = {1991},
  abstract  = {The effect of the selective \(\mu\)-opioid agonist o-Ala\(^2\)-Me-Phe\(^4\)-Gly-ol'-enkephalin (DAGO), injected into the medial preoptic nucleus of hypothalamus, on cardiac output and regional blood flow was studied in the conscious rat and the effect of DAGO on renal sympathetic nerve activity and renal blood flow was studied in anesthetized rats. In conscious rats, injections of DAGO (1 or 10 nmol) into the preoptic nucleus increased the blood pressure in a dose-related manner. The maximum rises of mean arterial pressure and pulse pressure after the larger dose were +23 ± 5 mmHg (mean ±SEM, P < 0.01) and + 17 ± 3 mmHg(P < 0.01), respectively. A small dose (0.1 nmol) increased heart rate ( +47 ± 13 bpm, P < 0.05); thc 1 nmol dosc produced bradycardia (- 39 ± 11 bpm, P < 0.05), while the 10 nmol dose initially decreased heart rate ( -68 ± 15 bpm (P < 0.01) and then gradually increased heart rate to a maximum of + 74 ± 13 bpm, (P < 0.0 1). A long-lasting increase in cardiac output was also elicited by DAGO, with maximum changes after 1 and 10 nmol of + 14 ± 6\% and +22 ± 7\% (P < 0.01), respectively. B1ood flow in the hindquarters increascd after DAGO but the mesenteric and renal blood ftow decreased in a dose-related manner. Significant responscs in hindquarter and mesenteric blood fl.ow after DAGO were independent of systemic hemodynamic responses at the dose ofO.l nmol. The vascular resistance in the hindquarters significantly decreased after a small dose of DAGO while the larger doses dose-dependently increased mesenteric and renal vascular resistance. A crucial role of the sympathetic nervous system in the hemodynamic effects of DAGO was demonstrated: (1) by the profound activation of renal sympathetic nerve activity after injections of DAGO (I nmol/100 nl) into the preoptic nucleus, (2) by blockade of the pressor, tachycardic and regional hemodynamic effects of DAGO (I nmol) by the ganglion blocker ch1orisondamine (5 mg/kg i.v.). The results suggest that the pressor effect of DAGO in preoptic nucleus is due primarily to an increase in cardiac output. The differential changes in blood ftow in organs further suggest that the opioid \(\mu\)-receptors in the preoptic nucleus might be involved in the integration of peripheral blood ftow in the hypothalamus during affective behavior.},
  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{AdeyemoShapiraTombaccinietal.1991,
  author    = {Adeyemo, O. M. and Shapira, S. and Tombaccini, D. and Pollard, H. and Feuerstein, G. and Sir{\´e}n, Anna-Leena},
  title     = {A goldfish model for evaluation of the neurotoxicit of \(\omega\)-conotoxin GVIA and screening of monoclonal antibodies},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63087},
  year      = {1991},
  abstract  = {A Goldfish Model for Evaluation of the Neurotaxicity of \(\omega\)-Conotoxin GVI A and Screening of Monoclonal Antibodies. ADEYEMO, 0. M .. SHAPIRA, S., TOMBACCINI, D., POLLARD, H. 8 .• FEUERSTEIN, G .. AND SIREN, A-L. ( 1991 ). Toxicol. App/. Pharmaco/. 108, 489-496. The neurotoxicity of \(\omega\)-conotoxin (\(\omega\)-CgTx), a potent neuronal voltage-sensitive calcium channel blocker, was measured using a new bioassay. \(\omega\)-CgTx was administered intraperitoneally (ip) to goldfish weighing approximately 1.6 g, and dose-related changes were observed over a 2-hr period. \(\omega\)CgTx induced time- and dose-dependent abnormal swimming behavior (ASB) and mortality. The antitoxin activity of the antiborlies was investigated in vivo by either ( l) preincubation of the antibody with w-CgTx at 4°C overnight, or (2) pretreatment with antibody, 30 min before \(\omega\)CgTx injection in a 10:1 antibody/\(\omega\)-CgTx molar ratio. The LD50 dose of \(\omega\)-CgTx in goldfish was 5 nmol/kg ip, and preincubation of monoclonal antibody (50 nmol/kg ip) with \(\omega\)-CgTx (5 nmol/kg ip) significantly (p < 0.05) reduced mortality. ASB, and toxicity time. The antitoxin activity of the monoclonal antiborlies evidenced in the goldfish bioassay was further tested in the conscious rat. In the rat, the increases in mean arterial pressure and heart rate induced by \(\omega\)-CgTx (0.03 nmol/rat icv) were significantly (p < 0.02 and p < 0.0 l, respectively) attenuated by preincubation of the toxin with the antibody (0.3 nmol/rat). We conclude that the goldfish bioassay provides a simple. accurate, and inexpensive in vivo model for the study of the toxicity of \(\omega\)CgTx},
  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{SirenFeuerstein1990,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Cardiovascular effects of anatoxin-a in the conscious rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63103},
  year      = {1990},
  abstract  = {Cardiovascular Effects of Anatoxin-A in the Conscious Rat. SJREN, A.-L., AND FEUERSTEIN, G. (1990). Toxicol. Appl. Pharmacol. 102,91-100. The effects ofanatoxin-A on mean arterial pressure (MAP), heart rate, cardiac index (CI), and blood flow (BF) in hindquarter (HQ), renal (R). and mesenteric (M) vascular beds were studied after intravenous (iv) and intracerebroventricular (icv) administration in the conscious rat. The pharmacological profile of anatoxin-A was further compared to nicotine administered iv and icv. MAP and heart rate were measured from femoral artery, CI by thermodilution method, and blood flow by Doppler velocimetry. Anatoxin-A and nicotine (30, 100 and 300 1-!g/kg iv) produced an increase in MAP with concomitant bradycardia. The highest doses increased Cl. MBF and RBF decreased due to a vasoconstriction in M and R vasculature. These effects were attenuated by the ganglion blocker chlorisondamine (5 mg/kg, iv). Anatoxin-A ( 100 1-!g/k~ iv) increased plasma epinephrine Ievels by 2- fold with virtually no effect on norepinephrine whereas nicotine ( 100 ~oLg/kg, iv) increased plasma epinephrine and norepinephrine by 20- to 30-fold. Central administration of anatoxin-A and nicotine (30-100 ,ug/kg icv) increased MAP with no effect on heart rate and produced M and R vasoconstriction. In summary, the present study demonstrates that anatoxin-A acts as a nicotinic cholinergic agonist in the c.onscious rat after both systemic and centrat administration. Anatoxin-A and nicotine produced pressor and reno-splanchnic vasoconstrictor responses and at high doses increased cardiac output. These effects were mediated by activation ofthe nicotinic receptors in the adrenal medulla and sympathetic ganglia. However, marked differences were found in the potency ofanatoxin-A versus nicotine to stimulate the sympathoadrenomedullary axis.},
  subject      = {Neurobiologie},
  language  = {en}
}