@article{SirenKarppanen1980,
  author    = {Sir{\´e}n, Anna-Leena and Karppanen, H.},
  title     = {Influence of analgesic antipyretics on the central cardiovascular effects of clonidine in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-48640},
  year      = {1980},
  abstract  = {No abstract available},
  subject      = {Prostaglandine},
  language  = {en}
}
@article{Siren1982,
  author    = {Sir{\´e}n, Anna-Leena},
  title     = {Central cardiovascular and thermal effects of prostaglandin D2 in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-48658},
  year      = {1982},
  abstract  = {Prostaglandin D2 (PGD2) is the most common prostaglandin type of tile rat brain. Recently a neurornodulator role for PGD2 has been suggested. In the present work the central cardiovascular and thermal effects of PGDz were studied in urethane-anaesthetised rats. Mlen adrndnistered at the doses of 0.001-10 ~g/rat into the lateral cerebral ventricle(i.c.v.), PGD2 slightly increased the blood pressure, heart rate and body ternpera~ ure. The highest dose caused also an initial hypotensive effect. Upon lntravenous injections PGD2 (0.1-10 ~g/rat) initially decreased and then weakly increased the blood pressure but had only negligible effects on heart rate and body temperature. Central pretreatment with sodium meclofenamate or indomethacin (1 mg/rat i.c.v.) antagonised effectively all the recorded central effects of PGD2. The central cardiovascular and thermal effects of PGD2 were much weaker than those obtained earlier with other prostaglandins, such as PGF2alpha and PGE2.. Therefore, in spite of its abundance in the brain PGD2 may not be very important for the central cardiovascular and thermal regulation in the rat.},
  subject      = {Medizin},
  language  = {en}
}
@article{Siren1981,
  author    = {Sir{\´e}n, Anna-Leena},
  title     = {Central cardiovascular and thermal effects of prostacyclin in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47943},
  year      = {1981},
  abstract  = {Prostacyclin (PGI2) induced a dose-dependent decrease in blood pressure with slight increases in heart rate and body temperature, when administered at the doses of 0.1-100 ~g into the lateral cerebral ventricle (i.c.v.) of the urethane-anaesthetised rat. When the same doses were administered intravenously, both the blood pressure and heart rate decreased. Central pretreatment wib~ sodiurn meclofenamate (1 mg/rat i.c.v.) antagonised the central hypotensive effect of PGI2 but i.c.v. pretreatrnent of the rats with indomethacin (1 mg/rat) failed to affect the PGI 2-induced hypotension. Central pretreatment with two histamine H2-receptor antagonists, cimetidine (500 ~g/rat i.c.v.) or metiamide (488 ~g/rat i.c.v.), antagonised the blood pressure lowering effect of 0.1 ~g dose of PGI2 but failed to affect the hypotension induced by higher PGI2 doses. Therefore the main central hypotensive effect of PGI2 seems not to be associated with the stimulation of histamine H2 -receptors in the brain. The hypotensive effect of i.c.v. administered PGI2 appears to be due to an action upon the central nervous system rather than to a leakage into the peripheral circulation. This assurnption is supported by the fact that sodiurn meclofenamate i.c.v. antagonised the effect of PGI 2. In addition, the chronotropic response to i.c.v. PGI2 was opposite to that induced by intravenous administration. The results also suggest that there may be differences in the mode of action between sodiurn meclofenamate and indomethacin.},
  subject      = {Prostaglandine},
  language  = {en}
}
@article{KarppanenSirenEskeliKaivosoja1979,
  author    = {Karppanen, H. and Sir{\´e}n, Anna-Leena and Eskeli-Kaivosoja, Alice},
  title     = {Central cardiovascular and thermal effects of Prostaglandin F2α in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47955},
  year      = {1979},
  abstract  = {Administration of PGF 2IX (0.2-6.4 J.lg) into the lateral cerebral ventricle (i.c.v.) induced dosedependent increases in blood pressure , heart rate and body temperature in urethane-anaesthetised rats, but had no effect on these parameters when the same dose range was administered intravenously. Peripheral pretreatment with sodium meclofenamate (50 mg/kg s.c.) sltifted all the dose-response curves for PGF 2IX (i.c.v.) to the left, but indomethacin (50 mg/kg s.c.) did not significantly affect those changes. Central pretreatment with sodiurn meclofenamate or indomethacin (1.25 mg per rat i.c.v.) failed to modify significantly the effects of centrally administered PGF 2IX' The results support previous suggestions that PGF 2IX may participate in the central control of the cardiovascular and thermoregulatory systems, and also suggest that there may be differences in the sites and/or modes of action between sodiurn meclofenamate and indomethacin.},
  subject      = {Prostaglandine},
  language  = {en}
}
@article{Siren1982,
  author    = {Sir{\´e}n, Anna-Leena},
  title     = {Central cardiovascular and thermal effects of Prostaglandin E2 in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47960},
  year      = {1982},
  abstract  = {Prostaglandin E2 (PGE2) increased the blood pressure, heart rate and body temperature, when administered at the doses ofO.OOI-IO,ug into the lateral cerebral ventricle (i.c.v.) of the urethane-anesthetised rat. The highest dose of 10 ,ug/rat induced a strong initial hypotensive effect. lntravenously (i.v.), PGE2 at the doses of 0.01-10 ,ug/rat caused a biphasic blood pressure response with dose-related initial decreases followed by slight increases in blood pressure. The heart rate and body temperature were slightly increased by i.v. administrations of PGE2 . The highest i.v. dose of 10 ,ug/rat initially decreased also the heart rate. Central pretreatment with indomethacin ( I mg/rat i.c.v.) partly antagonised all of the recorded central effects of PGE2 , while sodium meclofenamate (I mg/rat i.c. v.) abolished the hypertensive response to i.c. v. administered PGE2 but failed to significantly affect the PGE2-induced rises of heart rate and body temperature. The results support the previous suggestions that PGE2 may participate in the central cardiovascular and thermoregulatory contro!. The results also suggest that indomethacin and sodium meclofenamate antagonize the effects of exogenous prostaglandins. Since sodium meclofenamate, unlike indomethacin, affected preferentially the hypertensive response to centrally administered PGE2 , there may be differences in the sites and/or modes of action between these drugs.},
  subject      = {Physiologie},
  language  = {en}
}
@article{SirenPaakkari1984,
  author    = {Sir{\´e}n, Anna-Leena and Paakkari, I.},
  title     = {Cardiovascular effects of TRH i.c.v. in conscious rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49071},
  year      = {1984},
  abstract  = {In addition to the endocrine effects, the thyrotropin releasing hormone (TRH) is known to induce dose-dependent increases in blood pressure and heart rate after intracerebroventricular (i.c.v.) administration in urethane-anaesthetised rats (1, 2). The a~ of the present study was to investigate whether TRH has similar effects in conscious rats of various strains i.e. spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY) and Wistar (NR) rats.},
  subject      = {Medizin},
  language  = {en}
}
@article{SirenSvarstroemFraserPaakkari1985,
  author    = {Sir{\´e}n, Anna-Leena and Svarstr{\"o}m-Fraser, M. and Paakkari, I.},
  title     = {Central cardiovascular effects of the endoperoxide analogue U-46619 i.c.v. in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49064},
  year      = {1985},
  abstract  = {Thromboxanes are abundantly present in the rat brain but their possible physiological functions in the brain are not known. The prostaglandin endoperoxide analogue U-46619 is a selective agonist of TxA2 receptors in many peripheral tissues. In the present study the ·central cardiovascular and ventilatory effects of U-46619 were investigated in rats. In conscious spontaneously hypertensive rats (SHR) U-46619 (1-100 nmol/kg i.c.v.) induced a strong dose-related increase in blood pressure but had no significant effect on heart rate. In conscious normotensive rats (NR) neither blood pressure nor heart rate was significantly affected. Furthermore, U-46619 (0.1-100 nmol/kg i.c.v.) had no significant effect on blood pressure, heart rate or ventilation in urethane-anaesthetised NR . The results demonstrate an increased sensitivity of SHR to TxA2.},
  subject      = {Medizin},
  language  = {en}
}
@article{FeuersteinSiren1986,
  author    = {Feuerstein, G. and Sir{\´e}n, Anna-Leena},
  title     = {Effect of naloxone and morphine on survival of conscious rats after hemorrhage},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-48669},
  year      = {1986},
  abstract  = {The endogenous opioid system has been reported to depress the cardiovascular system during shock states, since naloxone, a potent opiate antagonist, enhances recovery of hemodynamic variables in various shock states. However, the effect of naloxone on long-term survival of experimental animals exposed to hypovolemic hypotension is not clear. The present studies tested the capacity of various doses of naloxone to protect conscious rats from mortality following various bleeding paradigms. In addition, the effect of morphine on survival of rats exposed to hemorrhage was also examined. In the six different experimental protocols tested, naloxone treatments failed to improve short- or long-term survival; in fact, naloxone treatment reduced short-term survival in two of the experimental protocols. Morphine injection, however, enhanced the mortality of rats exposed to hemorrhage in a dose-dependent manner. It is concluded that while opiates administered exogenously decrease survival after acute bleeding, naloxone has no protective action in such states and, like morphine, it may decrease survival in some situations.},
  subject      = {Medizin},
  language  = {en}
}
@article{SirenFeuerstein1987,
  author    = {Sir{\´e}n, Anna-Leena and Feuerstein, Giera},
  title     = {Central autonomic pharmacology of thyrotropin releasing hormone},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49051},
  year      = {1987},
  abstract  = {Thyrotropin releasing hormone (TRH, I-pyroglutamyl-l-histidyl-l-prolinamide) was the fIrst hypothalamic releasing SUbstance to be isolated, chemically characterized and synthetized /1/. The studies to date have revealed that the thyrotropin release from the pituitary gland is only one of the numerous actions of TRH. In addition to its endocrine actions (TSH and prolactin release) this tripeptide has central nervous system actions totally unrelated to its effects on the hypothalamo-pituitary axis. This review aims to summarize the studies on the central nervous system' actions of TRH with special emphasis on the autonomic pharmacology of this peptide.},
  subject      = {Medizin},
  language  = {en}
}
@article{FeuersteinSiren1987,
  author    = {Feuerstein, G. and Sir{\´e}n, Anna-Leena},
  title     = {Cardiovascular effects of enkephalins},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49048},
  year      = {1987},
  abstract  = {Enkephalins and their receptors are found in neurons and nerve terminals known to be involved in central cardiovascular control as well as the peripheral sympathetic and parasympathetic systems. Enkephalins and opioid receptors were also iden tified in the heart, kidneys, and blood vessels. The enkephalins interact with several specific receptors, of which p, 0, and K have been best characterized. Enkephalins administered to humans or animals produce cardiovascular effects which depend on the spedes, route of administration, anesthesia, and the selectivity for receptor subtype. While little information exists on the role of enkephalins in normal cardiovascular control, current data suggest that enkephalins might have a role in cardiovascular stress responses such os in shock and trauma.},
  subject      = {Medizin},
  language  = {en}
}
@article{FeuersteinSiren1987,
  author    = {Feuerstein, Giora and Sir{\´e}n, Anna-Leena},
  title     = {The Opioid System in cardiac and vascular regulation of normal and hypertensive states},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47418},
  year      = {1987},
  abstract  = {The endogenous opioid system includes three major families of peptides: dynorphins (derived from pre-proenkephalin B), endorphins (derived from pre-proopiomelanocortin), and enkephalins (derived from pre-proenkephalin A). Multiple species of opioid peptides are derived from these major precursors and many of them possess potent cardiovascular properties. Opioid peptides and opioid receptors, of which multiple forms have been defined, are present in the central nervous system and peripheral neural elements. In the central nervous system, opioid peptides and receptors are found in forebrain and hindbrain nuclei involved in baroregulation, sympathoadrenal activation, and several other vital autonomic functions. In the periphery, opioid peptides are found in autonomic ganglia, adrenal gland, heart, and other organs; multiple opioid receptors are also found in vascular tissue, heart, and kidneys. Although little is known to date on the regulatory mechanisms of the opioid system in normal cardiovascular states, it became clear that cardiovascular stress situations substantially modify the activity of the endogenous opioid system. The purpose of this review is to clarify the sites of interaction of the opioid system with all major components of the cardiovascular system and indicate the potential role of this system in the ontogenesis of cardiac malfunction, vascular diseases, and hypertension.},
  subject      = {Medizin},
  language  = {en}
}
@article{HallenbeckDutkaKochaneketal.1988,
  author    = {Hallenbeck, JM and Dutka, AJ and Kochanek, PM and Sir{\´e}n, Anna-Leena and Pezeskpour, GH and Feuerstein, G.},
  title     = {Stroke risk factors prepare rat brainstem tissues for a modified localized Shwartzman reaction},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47971},
  year      = {1988},
  abstract  = {Stroke risk factors such as hypertension, diabetes, advanced age, and genetic predisposition to stroke were demonstrated to prepare rat brainstem tissues for a modified local Shwartzman reaction. A single intracisternal injection of endotoxin provoked the reaction, and affected rats manifested neurologie deficits accompanied by pathologie lesions. Brainstem infarcts developed in only a small proportion of rats without recognized risk factors after intracisternal injection of endotoxin. Thus, stroke risk factors, whieh are ordinarily regarded as operating through acceleration of atherosclerosis, may predispose to brain ischemia by local effects on brain mierocirculation such as those thought to underlie preparation of a tissue for the local Shwartzman reaction.},
  subject      = {Gehirn},
  language  = {en}
}
@article{FeuersteinSirenGoldsteinetal.1989,
  author    = {Feuerstein, G. and Sir{\´e}n, Anna-Leena and Goldstein, DS and Johnson, AK and Zerbe, RL},
  title     = {The effect of morphine on the hemodynamic and neuroendocrine responses to hemorrhagic shock in conscious rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49033},
  year      = {1989},
  abstract  = {We have previously reported that analgesic doses of morphine accelerate mortality of rats exposed to hemorrhage (Feuerstein and Siren: Circ Shock 19:293-300, 1986). To study the potential mechanisms involved in this phenomenon, rats were chronically implanted with catheters in the femoral vessels and morphine (1.5 or 5 mg/kg) was administered 30 min or 24 hr after bleeding (8.5 mll300 g over 5 min) while arterial blood pressure and heart rate were continuously monitored. Furthermore, the effect of morphine (5 mg/kg) on cardiac output (CO) response to hemorrhage was studied in rats chronically equipped with a mini thermistor for CO monitoring by a thermodilution technique. In addition, plasma catecholamines (HPLC), plasma renin activity (PRA, RIA), vasopressin (RIA), pH, and blood gases were also determined. Morphine administration 30 min after hemorrhage produced a pressor response and tachycardia which were in marked contrast to its depressor effect in intact rats. Morphine elevated PRA and epinephrine but not vasopressin, while blood pH and gases showed no consistent change as compared to salinetreated hemorrhaged rats. Morphine given after the bleeding resulted in enhanced cardiac depression in response to a second bleed of 2 m1l300 g. Our data suggest that activation of pressor mechanisms by morphine during hypovolemic hypotension might enhance vasoconstriction in essential organs, depress cardiac function, and further reduce effective tissue perfusion.},
  subject      = {Medizin},
  language  = {en}
}
@article{ShuaibXuCrainetal.1990,
  author    = {Shuaib, A. and Xu, K. and Crain, B. and Sir{\´e}n, Anna-Leena and Feuerstein, Giora and Hallenbeck, J. and Davis, JN},
  title     = {Assessment of damage from implantation of microdialysis probes in the rat hippocampus with silver degeneration staining},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47433},
  year      = {1990},
  abstract  = {We used a sensitive silver degeneration staining method to study the effects of insertion of microdialysis probes in rat dorsal hippocampus and neocortex. Nine animals were sacrificed 24 h, 3 days or 7 days after implantation of dialysis tubing. Although mild neuronal cell death and small petechial hemorrhages were seen in elose proximity to the implantation site, the striking finding was the presence of degenerating axons both adjacent to the implantation site and in remote sites such as the corpus callosum and contralateral hippocampus. The observed changes could alter brain function near or remote from the implantation site and should be considered in analysis of dialysis experiments.},
  subject      = {Neurophysiologie},
  language  = {en}
}
@article{VonhofSirenFeuerstein1990,
  author    = {Vonhof, S. and Sir{\´e}n, Anna-Leena and Feuerstein, Giora},
  title     = {Volume-dependent spatial distribution of microinjected thyrotropin-releasing hormone (TRH) into the medial preoptic nucleus of the rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47421},
  year      = {1990},
  abstract  = {The present study was performed to qua ntify the distribution of a peptide neurotransmitter after microinjection into the medial preoptic area (POM), using a technique suitable for conscious animal preparations. The results indicate that only 50-ni volumes of injected tracer were sufficiently localized with 77 ± 9\% recovery in the POM. Injections of higher volumes resulted in an increasing spread of tracer into distant anatomical regions and structures, including the needle tract and cerebral ventricles. The amount of tracer localized in the POM decreased to 38±4\% (200 nl) (P < 0.05) and 41 ±8\% (500 nl) (P <0.05), respectively. The data suggest that the volume of injection is critical for intraparenchymal injections into structures of a diameter of I mm or less, such as the POM and should not exceed 50 nl in conscious animal preparations.},
  subject      = {Neurophysiologie},
  language  = {en}
}
@article{VonhofSiren1991,
  author    = {Vonhof, S. and Sir{\´e}n, Anna-Leena},
  title     = {Reversal of µ-opioid-mediated respiratory depression by α2-adrenoceptor antagonism},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47454},
  year      = {1991},
  abstract  = {The present study was performed in order to evaluate the effects of the selective 02- adrenoceptor antagonist 6-chloro-2,3,4,5-tetrahydro-3-methyl-1H-3-benzazepine (SK\&F 86466) on dermorphin-induced analgesia, respiratory depression and inhibition of locomotor activity in the conscious rat. Intracerebroventricular (icv) administration of dermorphin (3 nmol/rat) decreased respiration rate and relative ventilatory minute volume maximally by 38 \% and 50 \% of baseline respectively. SK\&F 86466 dose-dependently reversed the dermorphin-induced depression of ventilatory parameters, while SK\&F 86466 exerted no effect on dermorphin-induced analgesia or depression of locomotor activity due to catalepsia. It appears, therefore, that a 2-adrenoceptors selectively interact with Jl2-opioid-receptor mediated effects, such as respiratory depression, but are not involved in the modulation of Jl,-opioid-related effects, such as supraspinal analgesia and depression of locomotor activity.},
  subject      = {Biowissenschaften},
  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}
}