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The ovary undergoes cyclic changes in follicular growth and luteogenesis due to the action of gonadotropins and steroids. The ovary and especially the corpus luteum has an exteremely high blood flow. There is a gap in our knowledge about the physiological role of the high blood flow of the corpus luteum. The production of lactate, progesterone and cyclic AMP of follicles and corpora lutea incubated in vitro was analyzed and related to the tissue content of ATP to elucidate possible connections between oxygen and substrate levels and energy consumption, steroid output and LH responsiveness in vitro. It was also considered of interest to investigate if the oxygen tensions needed for ATP and progesterone production of the follicle and the corpus luteum differed. A corpus luteum model using adult pseudopregnant rats was developed and characterized according to criteria for identification of corpora lutea as well as levels of plasma steroids and gonadotropins. In vitro progesterone production was compared to plasma progesterone levels. The absolute blood flow of corpora lutea of different ages and the response to injection of hCG, noradrenaline and antidiuretic hormone was investigated with the microsphere technique. Relative blood flow changes of follicles and corpora lutea during follicular growth and luteogenesis in vivo were studied by injecting radiolabelled microspheres to anaesthetized immature rats at different time periods after injection of an ovulatory dose of pregnant mare serum gonadotropin. This approach was chosen to investigate the possible relation between follicular/luteal blood flow, steroid output and morphology in relation to the endogenous gonadotropin surge, ovulation and luteogenesis. Hormonal stimulation by injection of hCG and noradrenaline increased total ovarian blood flow but no evidence was found for a parallelism between luteotropism and blood flow. The increasing effect of hCG on ovarian blood flow was partly due to a shunting of blood from the uterus towards the ovary. The antidiuretic hormone potently decreased ovarian and uterine blood flow by 80-90% while blood flow of some other organs (e.g. kidney and spleen) were hardly affected. The corpus luteum of pseudopregnancy was found to produce 15“ 20 times more progesterone in vitro as compared to the preovulatory follicle. The steroidogenesis and energy production of corpora lutea was found to be more sensitive to decreases in oxygen tension in terms of tissue ATP levels and LH responsiveness of progesterone production while the follicle could compensate by increasing glycolysis. A parallelism between follicular/luteal blood flow and progesterone production in vivo was found. It was shown that the formation, growth and progesterone production of the corpus luteum was accompanied by an increase in blood flow as well as vascularization as seen under the light microscope. The endogenous gonadotropin surge did not change follicular blood flow due to the development of a follicular oedema. We hypothesize that the corpus luteum function in vivo and in vitro is dependent on higher energy levels than the preovulatory follicle and that the transformation of the follicle to a corpus luteum is supported by a high nutritive blood flow possibly to support a high demand for energy-rich substrates. / <p>Diss. (sammanfattning) Umeå : Umeå universitet, 1987, härtill 7 uppsatser.</p> / digitalisering@umu

Brainstem derived noradrenaline (NA) in the spinal cord functions both to increase motoneuron excitability, by facilitating calcium-mediated persistent inward currents (Ca PICs), and to inhibit sensory afferent transmission to motoneurons (excitatory postsynaptic potentials; EPSPs). Spinal cord injury (SCI) results in a reduction of NA, causing a loss of Ca PICs in motoneurons below the lesion and exaggerated EPSPs to emerge. With time motoneuron Ca PICs gradually recover and are readily triggered by the exaggerated EPSPs, resulting in the development of muscle spasms. The role of the NA in the recovery of Ca PICs and muscle spasms after chronic SCI is examined in this thesis using a rat model of spasticity incorporating both the awake rat (in vivo) and the isolated rat spinal cord (in vitro). Specific activation of the adrenergic 1 receptor with agonists facilitated Ca PIC and spasms, whereas activation of the adrenergic 2 receptor with agonists decreased the EPSPs that trigger spasms. Both receptors were endogenously activated by a ligand in vivo, though the 1 receptor additionally exhibits constitutive activity (activity in the absence of NA), predominantly in vitro. The adrenergic 2 receptor was not found to be endogenously active in vitro. Use of amphetamine in rats, which causes a forced efflux of endogenous NA, confirmed the identity of the endogenous ligand as NA and demonstrated that a residual source of NA capable of facilitating the Ca PIC and spasms persists below a chronic transection. Immunohistochemical labelling for an enzyme involved in the synthesis of NA (dopamine--hydroxylase) revealed that NA is not synthesized in the spinal cord below a chronic transection, indicating that the endogenous NA is not intrinsic to the spinal cord. Peripheral injections of NA were used to demonstrate that the residual NA instead originates in the periphery (blood) and is both passively and actively transported across a compromised blood-brain barrier (BBB) after chronic injury. The peripherally derived NA activates central adrenergic receptors to modulate motoneuron excitability, sensory synaptic transmission and muscle spasms after chronic SCI. This novel finding highlights the importance of understanding the adaptations of neurotransmitter systems after injury when developing effective treatment strategies for spasticity.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 114-134).

Thesis (Ph. D.)--University of Missouri--Columbia, 1997. / "December 1997." Typescript. Vita. Includes bibliographical references (l. 167-186). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri--Columbia, 1997. / Typescript. Vita. Includes bibliographical references (leaves: 167-186). Also available on the Internet.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1990. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 107-128).

Existem crescentes evidências sobre a contribuição da liberação de noradrenalina (NA) central na consolidação das memórias. Teoricamente, o Núcleo do Trato Solitário (NTS) recebe informações e diversos estímulos periféricos, que são então projetados ao Núcleo Paragigantocelular (PGi). Este, por sua vez, utiliza neurotransmissores, predominantemente excitatórios, para influenciar a ativação do Locus Coeruleus (LC). Então, o LC envia projeções noradrenérgicas ao hipocampo e à amígdala, influenciando os processos mnemônicos. Aqui nós demonstramos que a inibição pelo muscimol do NTS, PGi ou LC até 3 horas após o treino na tarefa de reconhecimento de objetos (RO) impede a consolidação da memória medida 24 h após o treino. Adicionalmente, a infusão de timolol, um antagonista de receptores β-adrenérgicos, na região CA1 do hipocampo também impede a consolidação deste tipo de memória. A infusão de NA na região CA1 do hipocampo não altera a retenção da memória, mas, reverte o prejuízo causado pela inibição do NTS, PGi ou LC. A infusão de NMDA no LC após a inibição do NTS ou PGi também reverte essa amnésia. Concomitantemente, verificamos que a inibição NTS, PGi ou LC bloqueia o aumento da expressão do fator neurotrófico derivado do cérebro (BDNF, do inglês brain-derived neurotrophic factor) que ocorre 120 min após o treino na tarefa de reconhecimento de objetos na região CA1 do hipocampo. Também a infusão de NA na região CA1 do hipocampo após a inibição do NTS, PGi ou LC ou de NMDA no LC após a inibição do NTS ou PGi promovem novamente o aumento do BDNF120 min após o treino no RO. Com isso conclui-se que a ativação da via NTS-PGi-LC-Hipocampo é necessária para que ocorra consolidação da memória de RO, na qual desempenha um papel o BDNF hipocampal. / There is evidence of the contribution of brain noradrenaline release (NA) to memory consolidation. The Nucleus of the Solitary Tract (NTS) receives information originated by peripheral stimuli and projects to the Paragigantocellularis Nucleus (PGi), which influences the Locus Coeruleus (LC) through excitatory neurotransmitters. The LC sends noradrenergic projections to the hippocampus and amygdala, influencing the memory processes. Here we show that inhibition by muscimol of NTS, PGi or LC up to 3 h after object recognition training impairs the consolidation of the memory measured 24 h later. Additionally, the infusion of timolol in the CA1 region of hippocampus also inhibits consolidation of this type of memory. The infusion of NA into the CA1 region of hippocampus does not alter memory consolidation of this task, but reverts the deleterious effect of NTS, PGi or LC inhibition. The infusion of NMDA in LC after inhibition of NTS or PGi also reverts the amnesia. Concomitantly, the inhibition of NTS, PGi or LC blocks the increase of brain-derived neurotrophic factor (BDNF) expression in CA1 that occurs 120 min after training in the object recognition task. Further, the infusion of NA in CA1 after inhibition of NTS, PGi or LC; or of NMDA in LC after inhibition of NTS or PGi promotes the BDNF increase seen 120 min after object recognition training. Thus, it is concluded that the activation of NTSPGi- LC-Hippocampus pathway is necessary for consolidation of the object recognition memory, and hippocampal BDNF is involved in this process.

Objetivos: Este trabalho teve como objetivos avaliar in vivo os efeitos microcirculatórios e a sobrevida de animais submetidos ao choque hemorrágico tratados com vasopressina e noradrenalina associadas à reposição volêmica com solução de NaCl 0,9% . Desenho do estudo: Estudo prospectivo, randomizado, controlado, intervencionista em modelo animal. Materiais e métodos: Utilizou-se hamsters machos do tipo sírio dourado, com idade entre 6 e 8 semanas e massa corporal entre 60 e 80 gramas. Os animais foram anestesiados para colocação de uma câmara dorsal. Após 5 a 7 dias, foram re-anestesiados para implante de cânulas na carótida e na veia jugular. No dia seguinte realizou-se o experimento. Os animais sofreram choque hemorrágico por meio da retirada de 40% da volemia, definida como 7% do peso corporal, e mantidos em choque por uma hora. Após, os animais foram aleatoriamente divididos em três grupos : Grupo SF0,9% (N = 6) - recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado; Grupo VP recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado, associado à infusão contínua durante uma hora de vasopresssina (0,0001 UI/kg/min por uma hora); e Grupo Nora. recebeu solução de NaCl 0,9% em volume de duas vezes o volume de sangue retirado, associado à infusão contínua de solução de noradrenalina (2 g/kg/min por uma hora). Foram avaliados os diâmetros das arteriolas e vênulas e a densidade capilar funcional (DCF) no momento basal, após o choque e após o tratamento. Os parâmetros laboratoriais observados foram: pH, HCO-3, BEx, paO2, paCO2 e lactato durante as três fases do experimento. Após o término do tratamento, foi visualizado o rolamento e adesão de leucócitos , assim como a sobrevida dos animais durante setenta e duas horas. Resultados: A terapia com reposição volêmica por si ou associada à vasopressina ou à noradrenalina não alterou valores relativos à gasometria arterial ou lactato em relação ao choque. A terapia com vasopressina associada à reposição volêmica manteve a densidade capilar funcional após ressuscitação do choque hemorrágico, (97% do valor basal da mediana), enquanto tratamento com solução de NaCl 0,9% apenas, não obteve o mesmo resultado (70% do valor basal da mediana). A noradrenalina associada à reposição volêmica piorou a densidade capilar funcional após o tratamento (44% do valor basal da mediana). A sobrevivência em setenta e duas horas foi significativamente menor no grupo da noradrenalina do que no grupo da vasopressina (33% em relação ao grupo Vaso). Ao final do experimento não foi observada diferença estatisticamente significativa relativa à adesão ou rolamento de leucócitos. Conclusão: Durante o choque hemorrágico, o tratamento com infusão de solução de NaCl 0,9% associada à vasopressina mantém a DCF, enquanto que o tratamento com solução de NaCl 0,9% somente ou associada à noradrenalina pioram a DCF. O tratamento com vasopressina melhora a sobrevida dos animais, em comparação ao tratamento com noradrenalina. Embora a adesão leucocitária não esteja significativamente alterada entre os grupos, houve uma tendência em obtermos uma adesão menor no grupo da vasopressina. / Objectives: The goal of this work was to evaluate in vivo the microcirculatory effects and survival of animals subjected to hemorrhagic shock treated with vasopressin or noradrenalin associated to volume infusion associated with NaCl 0,9% Study design: Prospective, randomized, controlled, intervencionist study in animal model. Materials and methods: Golden Syrian hamsters were used, aging between 6 and 8 weeks with body mass ranging from 60 to 80 grams. Animals were anesthetized for dorsal chamber implant. After 5 to 7 days there was a new anesthesia for carotid artery and jugular vein catheter implantation. Next day the experiment took place. Animals suffered a hemorrhagic shock by withdrawal of 40% of blood volume, defined as 7% of body weight, and kept in shock condition for 1 hour. After, animals were randomly divided in three groups. SF0,9% group (N=6) received NaCl 0,9% two times the shed volume; VP group (N=6) received NaCl 0,9% two times the shed volume plus continuous infusion for one hour of vasopressin solution (0,0001UI/kg/min for one hour); Nora group received NaCl 0,9% two times the shed volume plus continuous infusion of noradrenalin solution (2mcg/kg/min for one hour). Arteriolar diameter, venular diameter and functional capillary density (FCD) were evaluated in baseline, after shock and after treatment. Laboratory parameters observed were: pH, HCO-3, BEx, paO2, paCO2 and lactate during all three phases of experiment. After end of treatment, leucocyte rolling and adhesion were visualized, as well as animal survival during seventy two hours. Results: Volume infusion by itself or associated with vasopressin or noradrenalin didnt altered blood gas analysis values or lactate related to hemorrhagic shock. Vasopressin therapy associated with volume infusion sustained functional capillary density after hemorrhagic shock resuscitation (97% of baseline median values), while treatment with NaCl 0,9% only, didnt obtained the same result (70% of baseline median values). Noradrenalin associated to volume infusion worsened the functional capillary density after treatment (44% of baseline median values). Survival in seventy two hours were significantly lower in noradrenalin group comparing to vasopressin group (33% relating to Vaso group). In the end of experiment wasnt observed any significantly statistical difference relative to leucocyte rolling or adhesion. Conclusion: During hemorrhagic shock, treatment with NaCl 0,9% infusion associated with vasopressin sustains FCD, while treatment with NaCl 0,9% only or associated to noradrenalin worsens FCD. Treatment with vasopressin solution improves survival comparing to noradrenalin infusion treatment. Although leucocyte adhesion wasnt significantly altered among groups, there was a trend in observe lesser adhesion in vasopressin group.