Universiẗat, Diss., 1999--Regensburg. / Erscheinungsjahr an der Haupttitelstelle: 1998.

Objective: Dosing intervals of 12 and 24 hours for atenolol have been recommended, but an evidentiary basis is lacking. To test the hypothesis that repeated, once-daily oral administration of atenolol attenuates the heart rate response to isoproterenol for 24 hours, we performed a double-blind, randomized, placebo-controlled cross-over experiment. Animals: Twenty healthy dogs Procedures: Dogs were randomly assigned to receive either placebo (P) and then atenolol (A), [1 mg/kg PO q24h] or vice versa. Treatment periods were 5-7 days; time between periods was 7 days. Heart rates (bpm) at rest (HRr) and during constant rate [0.2 μg/kg/min] infusion of isoproterenol (HRi) were electrocardiographically obtained 0, 0.25, 3, 6, 12, 18, and 24 hours after final administration of drug or placebo. A mixed model ANOVA was used to evaluate the effects of treatment (Tr), time after drug or placebo administration (t), interaction of treatment and time (Tr*t) as well as period and sequence on HRr and HRi. Results: Sequence or period effects were not detected. There was a significant effect of Tr (p <0.0001) and Tr*t (p <0.0001) on HRi. Atenolol significantly attenuated HRi for 24 hours but did so maximally at 3 hours (least squares means ± SE, A: 146±5 bpm, P: 208±5 bpm); the effect at 24 hours was small (A: 193±5, P: 206±5). Atenolol had a small but significant effect (p <0.0001) on HRr. Conclusions and Clinical Relevance: The results of this study support a dosing interval that is less than 24 hours. / MS / This thesis was designed to test the effects of the drug atenolol on heart rate in dogs. Atenolol is used to reduce the heart rate of dogs with cardiovascular disease. The study used 20 dogs that were given oral capsules in both a placebo (no drug) and atenolol phase of the experiment. The study was designed to control for other causes of slower heart rate and make sure that the investigator did not know which treatment was given to a dog. Placebo dogs had a high heart rate response to the drug isoproterenol whereas atenolol treated dogs had a statistically significant lower heart rate response compared to placebo over a 24 hours period of time. The difference between treatments was small after 24 hours and further work is needed to determine the best time interval between doses of medication.

To evaluate whether cervical spinal neurons can influence cardiac indices and myocyte viability in the acutely ischemic heart, the hearts of anesthetized rabbits subjected to 30. min of LAD coronary arterial occlusion (CAO) were studied 3. h after reperfusion. Control animals were compared to those exposed to pre-emptive high cervical cord stimulation (SCS; the dorsal aspect of the C1-C2 spinal cord was stimulated electrically at 50. Hz; 0.2. ms; 90% of motor threshold, starting 15. min prior to and continuing throughout CAO). Four groups of animals were so tested: 1) neuroaxis intact; 2) prior cervical vagotomy; 3) prior transection of the dorsal spinal columns at C6; and 4) following pharmacological treatment [muscarinic (atropine) or adrenergic (atenolol, prazosin or yohimbine) receptor blockade]. Infarct size (IS) was measured by tetrazolium, expressed as percentage of risk zone. C1-C2 SCS reduced acute ischemia induced IS by 43%, without changing the incidence of sudden cardiac death (SCD). While SCS-induced reduction in IS was unaffected by vagotomy, it was no longer evident following transection of C6 dorsal columns or atropinization. Beta-adrenoceptor blockade eliminated ischemia induced SCD, while alpha-receptor blockade doubled its incidence. During SCS, myocardial ischemia induced SCD was eliminated following vagotomy while remaining unaffected by atropinization. These data indicate that, in contrast to thoracic spinal neurons, i) cranial cervical spinal neurons affect both adrenergic and cholinergic motor outflows to the heart such that ii) their activation modifies ventricular infarct size and lethal arrhythmogenesis.

No description available.

No description available.

Es wurde gezeigt, dass durch die Vorpositionierung von Quantenpunkten, diese mit einem gezielten Abstand im Bereich von einigen 100 nm zueinander und daher mit einer definierten Dichte in Speicherbauelemente eingebracht werden können. Es wurde bei tiefen Temperaturen wohldefinierte Coulombblockade demonstriert. Durch die Analyse der Coulomb-Rauten war es möglich, auf die Größe und Ladeenergie von Quantenpunkten im Kanal zu schliessen. Es wurde gezeigt, dass vorpositionierte Quantenpunkte sehr gut als Floating Gate eingesetzt werden können. Die Speichereigenschaften dieser Quantenpunkte wurden im Hinblick auf die Hysteresebreite DeltaVth in Abhängigkeit der Kanalbreite, der Drainspannung und der Temperatur untersucht und diskutiert. Hierbei konnte eine deutliche Abhängigkeit der Thresholdspannung von der Kanalbreite der Struktur ermittelt werden. Für Strukturen mit einem breiten Kanal wurde festgestellt, dass der Stromfluss bereits bei negativen Gatespannungen einsetzt, während für schmale Strukturen positive Gatespannungen nötig sind, um einen Ladungstransport hervorzurufen. Zur Bestimmung der Temperaturstabilität der Ladezustände wurde sowohl die Thresholdspannung als auch die Hysteresebreite als Funktion der Probentemperatur im Bereich von 4.2K bis Raumtemperatur bei verschiedenen Drainspannungen bestimmt. Hierbei wurde festgestellt, dass die Hysteresebreite bis zu einer kritischen Temperatur stufenförmig abnimmt und danach wieder leicht ansteigt. Bei der Untersuchung der Threshold- Spannung wurde ein Unterschied Vth,zu und Vth,auf festgestellt. Erstmals konnte ein lateral und vertikal positionierter InAs Quantenpunkt als Speicher für den Betrieb bei Raumtemperatur demonstriert werden. Ferner wurde die Wirkung eines Gate-Leckstromes auf den gemessenen Drain- Strom eines monolithischen Drei-Kontakt-Struktur untersucht und diskutiert. Die untersuchten Proben basieren auf einem neuen Parallel-Design, in welchem das Gate nicht wie üblich zwischen Source und Drain positioniert wurde, sondern in serieller Verbindung mit dem Drain- oder Sourcekontakt, d.h. mit einem zentralen Drain zwischen Source und Gate, gesetzt wurde. Hierdurch konnte eine merkliche Reduzierung des Probeninnenwiderstandes erreicht werde. Zu Beginn wurden zur Charakterisierung der Probe Transportmessungen bei Raumtemperatur durchführt. Hierbei konnte verglichen mit herkömmlichen Quantendrahttranistoren realisiert auf demselbenWafer, zum einen eine deutlich höhere Transconductance durch das parallele Design erreicht werden. Zum anderen zeigte die ermittelte Transconductance nicht den erwarteten linearen Verlauf in Abhängigkeit der Drainspannung, sondern einen quadratischen. Die Messungen zeigten außerdem einen Abfall des Drain-Stromes ab einer kritischen Größe des Gate-Leckstromwertes, welcher auf ein dynamisches Gate, hervorgerufen durch die Ladungsträger aus dem Gate, zurückgeführt wird. Diese zusätzliche virtuelle Kapazität addiert sich in paralleler Anordnung zum geometrischen Gate-Kondensator und verbessert die Transistoreigenschaften. Zum Abschluss der Arbeit wurden Hochfrequenzmessungen zur Ermittlung einer Leistungsverstärkung von Drei-Kontakt-Strukturen bei Raumtemperatur für unterschiedliche Gate- und Drainspannungen durchgeführt. Um die Hochfrequenzeigenschaften der untersuchten Probe zu erhöhen, wurde hierfür ein Design gewählt, in welchem die Goldkontakte zur Kontaktierung sehr nahe an die aktive Region heranragen. Für diese Spannungskombination konnte für eine Frequenz im Gigaherz-Bereich eine positive Spannungsverstärkung > 1 dB gemessen werden. Höhere Spannungen führen zu einem Sättigungswert in der Leistungsverstärkung. Dies wird zurückgeführt auf den maximal zur Verfügung stehenden Strom in der aktiven Region zwischen den nahen Goldkontakten. Zudem wurde eine Lösung vorgestellt, um das fundamentale Problem der Impedanzfehlanpassung für Hochfrequenzmessungen von nanoelektronischen Bauelementen mit einem hohen Innerwiderstand zu lösen. Eine Anpassung der unterschiedlichen Impedanzen zwischen Bauelement und Messapparatur ist unbedingt notwendig, um Reflexionen bei der Übertragung zu vermeiden und somit die Gewinnoptimierung zu erhöhen. Zur Behebung der Fehlanpassung wurde im Rahmen dieser Arbeit ein Impedanz-Anpassungs-Netzwerk auf einer PCB-Platine realisiert, welches mit der Probe verbunden wurde. Die Anpassung wurde durch eingebaute Strichleitungen in das Layout des Anpassungsboards vorgenommen. Durchgeführte Simulationen der Probe in Verbindung mit dem Anpassungs-Netzwerk bestätigten die experimentellen Ergebnisse. Durch die Anpassung konnte der simulierte Reflexionskoeffizient deutlich reduziert werden, bei gleichzeitiger Erhöhung des Transmissionskoeffizienten. Ebenfalls zeigten die Messungen an einer Drei-Kontakt-Struktur mit Anpassungs-Board eine signifikante Verbesserung der Leistungsverstärkung. / Dynamical Charging and Discharging of laterally aligned quantum dot structures We can demonstrate that the direct positioning enables us to embed quantum dots with given periods to each other of only a few 100 nm and therefore with a defined density into the memory-structures. For low temperatures, well defined Coulombblockade can be observed. The analysis of the measured diamond patterns allows the determination of the dimension and the charging energy of the embedded quantum dots in the channel. The memory properties of these quantum dots were analyzed and discussed in terms of the hysteresis width DeltaVth which depends on the channel width, the applied drain voltage and the device temperature. The measurements reveal a dependence of the threshold voltage on the channel width of the structure. For devices with a wide channel the current transport sets in with negative applied gate voltages, in contrast to structures with narrow channels, requiring positive gate voltages to cause a current flow through the channel. To explain these results we assume that in large channels a higher negative voltage is necessary to deplete the charges out of the channel due to the higher charge density. To analyze the temperature stability of the charge states the threshold voltage as well as the hysteresis width is detected as a function of the temperature for different drain voltages in the range of 4.2K up to room temperature. It is determined that the hysteresis width decreases to a critical temperature before it rises again. For the investigation of the threshold voltage a difference between Vth,up and Vth,down is demonstrated. We assume that this difference is caused by the different charging behavior for increasing charge energies. In this work, lateral and vertical positioned InAs quantum dots could be demonstrated as a memory device operated at room temperature for the first time. Improved transistor functionality caused by gate leakage currents in nanoscaled Three Terminal Structures Further we investigate the role of gate leakage on the drain current in a monolithic, unipolar GaAs/AlGaAs heterostructure based on three leaky coupled contacts. Two in-plane barriers, defined by rows of etched holes in a two-dimensional electron gas, separate the leaky gate from the central drain and the drain from the source. Because of this the internal resistance of the structure can be appreciably decreased. It should be noted that the observed differential voltage amplification in the gate leakage regime of the studied structure is by far larger compared to the voltage amplification of any in-plane wire transistor fabricated from the same wafer, which were controlled by two non-leaking in-plane gates. The calculated transconductance increases quadratically and not in a non-linear manner, as expected. A pronounced reduction of the drain current sets in when the gate starts to leak, pointing at a large parallel gate capacitor. We associate the gate-leakage current induced gating with a virtual floating gate induced by the space charge injected from the gate. The space charge can hereby be described by a parallel gate capacitor that can control a low dimensional channel lying nearby. High frequency measurements on Three Terminal Structures High frequency measurements for determination of the power gain in Three Terminal Structures are carried out at room temperature. To improve the high frequency properties of the investigated structures a special design was chosen, where the gold contacts for contacting the sample approach very closely the active switching region. The measurements show that negative gate voltages are much more efficient to the power gain than positive ones. For these voltage combinations a power gain > 1 dB for frequencies in the GHz range is detected, whereas the power gain saturates for higher voltages. This is interpreted in terms of the maximum number of charges in the active region between the gold contacts. Furthermore an answer to the fundamental obstacle of the impedance mismatch for high frequency measurements on nanoelectronic structures with high internal resistance is given. Such a matching between the device and the measurement setup is necessary to reduce signal reflections and therefore increase the gain. To match the impedances, an impedancematching- network on a PCB-plate (printed circuit board) via integrated stubs was realized. Simulation data of the sample in connection with the matching-network is in very good agreement with the experimental data. Using the network reduces the simulated reflection coefficient and simultaneously raises the transmission coefficient. The measurements also show a significant improvement of the power gain behaviour.

Die Multiple Sklerose (MS) ist eine schwere, momentan noch unheilbare Autoimmunerkrankung des Zentralnervensystems, die weltweit ca. 1 Mio. Menschen betrifft. Da die zur Zeit verfügbaren, anti-inflammatorischen und immunsuppressiven Therapieformen lediglich krankheitsverzögernd wirken, ist es Gegenstand intensiver Forschungsbemühungen, Möglichkeiten zur spezifischen Interferenz mit bei der MS ablaufenden Pathomechanismen zu ergründen und im Tiermodell zu testen. Das von uns für diese Arbeit verwendete Mausmodell einer CD8+ T-Zell vermittelten Experimentellen Autoimmunen Enzephalomyelitis (EAE) trägt dabei neuen Erkenntnissen Rechnung, die zeigen, dass zytotoxische T-Lymphozyten bei der Pathogenese der humanen MS von entscheidender Bedeutung sind. Es handelt sich um doppelt transgene Nachkommen von Mäusen, die das Modell-Antigen Ovalbumin (OVA) unter der Kontrolle eines Oligodendrozyten (ODC-)-spezifischen MBP-Promotors im ZNS exprimieren, und Mäusen, die Ovalbumin-spezifische CD8+ T-Zellen besitzen (OT-I Zellen). Es kommt in diesem Modell zur Autoantigenerkennung durch die CD8+ T-Zellen mit konsekutiver Ausbildung einer fulminanten, letal verlaufenden EAE. Ziel der vorliegenden Arbeit war es nun, die therapeutische Potenz des monoklonalen Antikörpers 25-D1.16 zu evaluieren, der gegen das Autoantigen Ovalbumin in Kombination mit einem MHC-I-Molekül gerichtet ist. Mit Hilfe von FACS-Analysen und Fluoreszenz-Mikroskopie konnten wir zunächst bestätigen, dass 25-D1.16 spezifisch den Komplex aus dem Peptid SIINFEKL (antigenes Epitop von Ovalbumin) gebunden an ein MHC-I-Molekül (H-2Kb) erkennt. In nachfolgenden in vitro Versuchen wurde der Einfluss des Antikörpers auf Aktivierung und Proliferation von durch SIINFEKL:MHC-I-Komplex stimulierten OT-I Zellen untersucht. Es wurden hierfür Zellproliferation (Proliferations-Assays), Expression des Oberflächenmoleküls CD69 (FACS-Analysen) sowie IFN-γ-Sekretion (ELISA) gemessen. In Gegenwart von 25-D1.16 zeigte sich durchweg eine hochsignifikante Reduktion der jeweiligen Proliferations-/Aktivierungsmarker. Wir konnten somit in vitro zeigen, dass der gegen das Autoantigen Ovalbumin/H-2Kb gerichtete, monoklonale Antikörper 25-D1.16 kompetitiv die Aktivierung und Proliferation entsprechender T-Lymphozyten inhibieren kann. Um diese Daten in vivo zu validieren und die pathogenetische Relevanz zu überprüfen, haben wir ODC-OVA/OT-I doppelt transgenen Mäusen verschiedene Dosen von 25-D1.16 vor Auftreten erster EAE-Symptome einmalig intraperitoneal verabreicht. Anschließend wurde der Krankheitsverlauf klinisch beurteilt. Im EAE-Stadium 4 ohne Besserungstendenz oder bei Versuchsende wurden außerdem histologische Schnitte des Zentralnervensystems angefertigt, gefärbt (H.E., CD3, Mac-3, Luxol Fast Blue/PAS) und mit unbehandelten Tieren verglichen. Ein Teil der ODC-OVA/OT-I doppelt transgenen Tiere blieb nach Applikation des Antikörpers völlig gesund, während bei einem anderen Teil der Ausbruch der EAE zwar nicht vollständig verhindert, ihr Schweregrad aber deutlich gemildert wurde. Der Effekt der Antikörpertherapie war jedoch nicht nur klinisch, sondern auch histopathologisch überzeugend. So zeigte das Zentralnervensystem erfolgreich therapierter Mäuse eine weitgehend bis vollständig intakte Gewebsarchitektur (H.E.-Färbung) mit im Vergleich zu unbehandelten Mäusen drastisch reduzierter OT-I Zell- und Makrophagen/Mikroglia-Infiltration (Immunhistochemie CD3 und Mac-3). In der Luxol Fast Blue/PAS-Färbung fanden sich keinerlei Entmarkungsherde sondern durchgängig myelinisierte Axone. Es gelang uns somit durch hohe Antikörperdosen (500 μg pro ODC-OVA/OT-I doppelt transgener Maus) bei 83 % der behandelten Versuchstiere den Ausbruch der EAE ganz zu verhindern bzw. deren Verlauf deutlich abzumildern. Zusammenfassend beschreiben wir hier erstmals die antigen-spezifische Therapie einer CD8+ T-Zell mediierten EAE mittels eines gegen Peptid:MHC-I-Komplex gerichteten, monoklonalen Antikörpers. Durch Interferenz mit der Erkennung des Autoantigens durch die CD8+ T-Zellen waren wir in vivo in der Lage, den Pathomechanismus der EAE zu inhibieren. Hieraus ergibt sich ein vielversprechendes Behandlungskonzept für die Therapie der Multiplen Sklerose am Menschen. / Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system (CNS) of presumed autoimmune origin, which affects around 1 million people worldwide. To date, anti-inflammatory and immunomodulatory therapies in clinical use can slow disease progression but are not curative and have considerable adverse effects. For this reason, researchers have begun to focus on developing antigen-specific treatment options, thereby avoiding generalized immunosuppression. Recently, the importance of CD8+ T cells in the pathogenesis of multiple sclerosis has begun to emerge. Here we employ a mouse model of CD8+ T cell mediated experimental autoimmune encephalomyelitis (EAE), in which the neo-self antigen ovalbumin (OVA) expressed by oligodendrocytes (ODC) is targeted by CD8+ T cells with transgenic T cell receptors (OT-I cells). In this animal model of ODC-OVA/OT-I double transgenic mice, recognition of the autoantigen by CD8+ T cells leads to fulminant, lethal EAE. A possible strategy to block organ-specific CD8+ T cell mediated inflammation is the interference with antigen recognition by a monoclonal antibody (mAb) specific for the complex composed of the immunodominant peptide and an MHC class I molecule. We therefore tested the therapeutic potency of the mAb 25-D1.16 which binds to the the OVA-8/MHC I complex, in our ODC-OVA/OT-I mouse model. Using flow cytometry and fluorescence microscopy, we confirmed that 25-D1.16 specifically recognizes the peptide SIINFEKL (antigenic epitope of ovalbumin) presented by H-2Kb, the murine homologue of the human MHC class I molecule. With in vitro experiments we addressed the ability of 25-D1.16 to inhibit activation and proliferation of OT-I cells stimulated by SIINFEKL:MHC I complexes. Cell proliferation (radioactive proliferation assays), expression of the early activation marker CD69 on the cell surface (flow cytometry) and IFN-γ secretion (ELISA) were measured. In the presence of 25-D1.16 we saw a highly significant reduction of the respective markers of activation/proliferation. We were thus able to show that the mAb 25-D1.16 recognizing OVA-8/H-2Kb is able to competitively inhibit the response of CD8+ T cells specific for the same peptide/MHC class I complex. To validate these findings in vivo and to study their pathogenic relevance, ODC-OVA/OT-I double transgenic mice were treated with different doses of 25-D1.16. For each mouse, a single dose was injected into the peritoneum prior to EAE onset. On a daily basis, mice were then scored for clinical symptoms of disease (scale 0 – 5). At the end of the experiment, histological and immunohistochemical analysis was performed on sections of brain and spinal cord and was compared to untreated animals. We observed a dose-dependent reduction of EAE severity after injection of 25-D1.16. At low doses (100 μg per mouse), the disease course was indistinguishable from that of untreated ODC-OVA/OT-1 double transgenic mice, whereas at 500 μg 10/12 animals survived. About half of them either showed no or only mild symptoms, while the others experienced full recovery after transient exacerbation. An intermediate phenotype was observed at 200 μg per mouse. Corresponding to the clinical results, the antibody’s effect on the extent of CNS damage was also convincing. Histopathological comparison of mice that recovered under 25-D1.16 therapy showed a virtually intact tissue architecture with only mild residual vacuolization (HE staining), less influx of T cells, as well as reduced microglia/macrophage activation (CD3 and Mac-3 immune histology). Luxol Fast Blue/PAS stained CNS sections showed remyelinated axons while extensive inflammation and myelin destruction is seen in double transgenic mice without 25-D1.16 therapy. In summary, treatment with high doses of 25-D1.16 (500 μg per mouse) saved 83% of the tested animals from lethal EAE, either preventing the development of or attenuating disease symptoms. For the first time, we here describe an antigen specific therapy of CD8+ T cell mediated EAE using a monoclonal antibody binding to peptide/MHC I complexes. By interference with recognition of the autoantigen by CD8+ T cells we were able to inhibit the onset of disease in vivo. Although there are anticipated problems in translating the present results into treatment of MS patients, they might offer a promising concept for future selective immunotherapy in human multiple sclerosis.

Submitted by Sandro Camargo (sandro.camargo@unipampa.edu.br) on 2015-03-08T23:21:51Z No. of bitstreams: 1 126110007.pdf: 716833 bytes, checksum: 33bfba912d22ee0b7d63e9af78d59c5a (MD5) / Made available in DSpace on 2015-03-08T23:21:51Z (GMT). No. of bitstreams: 1 126110007.pdf: 716833 bytes, checksum: 33bfba912d22ee0b7d63e9af78d59c5a (MD5) Previous issue date: 2014-05-21 / O presente estudo objetivou avaliar o potencial anestésico local do tramadol a 5%, por meio do bloqueio loco-regional no nervo infraorbitário equino. Avaliou-se 9 equinos mestiços (350±60Kg) que, após tranquilização e bloqueio, foram submetidos a estímulos álgicos (EA). Os animais receberam acepromazina 1% (0,05mg/kg-IV) e procedeu-se a tricotomia e aplicação de pomada anestésica, na região sobre o Forâme Infraorbitário. Após 20 minutos, procedeu-se a infiltração local com tramadol 5% (dose 5mL), no Forâme Infraorbitário Esquerdo (FIE). A partir desde momento (T0), a cada 10 minutos, durante 150 minutos foram aferidos: a frequência respiratória (f), a frequência cardíaca (FC), a temperatura retal (TR) e a pressão arterial não invasiva (PANI). Os EA foram realizados, durante um período de 30” (trinta segundos), sendo eles: inserção manual de agulha no sulco gengival (dentes cantos superiores); pregueamento da pele (na região da bochecha) e pinçamento do lábio superior, com pinça hemostática Kelly, no mesmo lado do bloqueio. Foram registrados o período de latência (PL), com EA realizados a cada minuto após T0, e a duração do bloqueio (DB) após término do PL, com EA sendo feitos a cada 10 minutos, até que a sensibilidade normal retornasse. Também coletou-se amostras sanguineas para dosagem da glicemia. O controle negativo foi realizado com a infiltração de solução fisiológica 0,9% (dose 5mL), no Forâme Infraorbitário Direito (FID) no mesmo animal, recebendo os referidos EA, até o animal evidenciar desconforto. Os dados referentes à FC, f, PANI, TR e glicose foram avaliados pelo teste de ANOVA seguido pelo pós-teste de Tukey. Para os escores em relação aos EA, foi utilizado o teste de Kruskall-Wallis, seguido pelo teste de Dunn. Houve bloqueio local com tramadol 5%, e as variáveis pesquisadas obtiveram oscilações, porém dentro dos parâmetros fisiológicos da espécie. O índice de maior variação foi a PANI, mas deveu-se a tranquilização prévia ao bloqueio. Todos os animais apresentaram ptose palpebral (achado clínico) no mesmo lado do bloqueio, porém em diferentes intensidades. O PL obteve duração média de 5 minutos e o DB teve tempo máximo de 140 minutos. Conclui-se que o tramadol 5%, na técnica e dose utilizadas, promoveu bloqueio perineural e proporcionou anestesia local com eficiência; sendo necessário mais estudos para verificar o potencial toxicológico local, a relação dose/área anestesiada e o mecanismo de ação local do fármaco. / The present study aimed to evaluate the potential local anesthetic tramadol 5% through the locoregional anesthesia in the infraorbital nerve horse. Reviewed by 9 crossbred horses (350 ± 60 kg) that after sedation and lock, underwent painful stimulations (PS). The animals received 1% acepromazine (0.05 mg / kg IV) and proceeded to shaving and applying anesthetic ointment, in the region of the foramen infraorbital. After 20 minutes, we proceeded to the local infiltration with tramadol 5% (5mL dose), the left infraorbital foramen (LIF). From long time (T0), every 10 minutes for 150 minutes were measured: respiratory rate (RR), heart rate (HR), rectal temperature (RT) and non-invasive blood pressure (NIBP). The PS were performed over a period of 30 "(thirty seconds), namely: manual needling in the gingival sulcus (teeth upper corner); wrinkling of the skin (in the cheek region) and narrowing of the upper lip, with hemostat Kelly, on the same side of the block. The latency period (LP) were recorded with PS performed each minute after T0, and the duration of block (DB) after end of the LP, with PS being made every 10 minutes until normal sensation returned. Was also collected blood samples to measure blood glucose. The negative control was performed with the infiltration of saline solution 0.9% (5mL dose), the right infraorbital foramen (RIF) in the same animal, getting the PS said, until the animal show discomfort. The data relating to HR, RR, NIBP, TR and glicemia were evaluated by ANOVA followed by Tukey post-test. For scores in relation to PS, the Kruskal-Wallis test followed by Dunn's test was used. There was local anesthesia with tramadol 5%, and the studied variables obtained oscillations, although within the physiological parameters of the species. The index was greater variation NIBP, but was due to the blockade prior reassurance. All animals showed ptosis (clinical finding) on the same side of the block, but at different intensities. The LP had an average duration of 5 minutes and the DB had maximum time of 140 minutes. It is concluded that tramadol 5%, the technique and the dose used, promoted perineural local anesthetic blockade and provided efficiently; Further studies are needed to verify the location toxicological potential, the dose / anesthetized area and local drug action mechanism.

This dissertation is a study of Leningrad during World War II and the period of postwar restoration (1941-1950). Leningrad was besieged by the Germans for nearly nine-hundred days. As hundreds of thousands of people died from bombings, shelling, cold, and starvation, local authorities surprisingly instituted measures to ensure that the city’s historic monuments be safeguarded from destruction. When Leningrad was liberated in January 1944, a concerted effort was put into place to breath life into these damaged and destroyed monuments and to heal the wounds inflicted on the city. Instead of using the damage to modernize the city, Leningrad and Soviet authorities opted to privilege the country’s tsarist heritage. In the postwar period, municipal authorities proclaimed that restored monuments commemorate the determination and heroism shown by the people of Leningrad during the war. The memory of the blockade, it was argued, was a “red thread” that must run through and be inscribed in all restoration works. Although this dissertation is a local study of war and postwar restoration, it speaks to broader trends within the Soviet Union before, during, and after World War II. I argue that the care shown for Leningrad’s imperial monuments was the result of an ideological shift that began in the mid-1930s away from iconoclasm toward rehabilitating and respecting certain events and characters from the past. With international tensions rising in the 1930s, this turn to the past acted as a unifying force that had a tremendous influence on the patriotism shown during the war with the Nazis. In the postwar period, as the Soviet state began to redefine its image based on the myth of war and the country’s tsarist heritage, this patriotism was further promoted, resulting in a flurry of work throughout the Soviet Union to restore the vessels of the country’s past. Like many other modernizing states, the Soviet Union looked to its past to create a united and patriotic citizenry.

This dissertation is a study of Leningrad during World War II and the period of postwar restoration (1941-1950). Leningrad was besieged by the Germans for nearly nine-hundred days. As hundreds of thousands of people died from bombings, shelling, cold, and starvation, local authorities surprisingly instituted measures to ensure that the city’s historic monuments be safeguarded from destruction. When Leningrad was liberated in January 1944, a concerted effort was put into place to breath life into these damaged and destroyed monuments and to heal the wounds inflicted on the city. Instead of using the damage to modernize the city, Leningrad and Soviet authorities opted to privilege the country’s tsarist heritage. In the postwar period, municipal authorities proclaimed that restored monuments commemorate the determination and heroism shown by the people of Leningrad during the war. The memory of the blockade, it was argued, was a “red thread” that must run through and be inscribed in all restoration works. Although this dissertation is a local study of war and postwar restoration, it speaks to broader trends within the Soviet Union before, during, and after World War II. I argue that the care shown for Leningrad’s imperial monuments was the result of an ideological shift that began in the mid-1930s away from iconoclasm toward rehabilitating and respecting certain events and characters from the past. With international tensions rising in the 1930s, this turn to the past acted as a unifying force that had a tremendous influence on the patriotism shown during the war with the Nazis. In the postwar period, as the Soviet state began to redefine its image based on the myth of war and the country’s tsarist heritage, this patriotism was further promoted, resulting in a flurry of work throughout the Soviet Union to restore the vessels of the country’s past. Like many other modernizing states, the Soviet Union looked to its past to create a united and patriotic citizenry.