Thesis (doctoral)--Utrecht, 1979.

published_or_final_version / Physiology / Master / Master of Philosophy

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

Thesis (M. Phil.)--University of Hong Kong, 1995. / Includes bibliographical references (leaf 84-110).

Universiẗat, Diss., 2001--Bremen.

Thesis (Ph. D.)--University of Missouri-Columbia, 2008. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "June 2008" Includes bibliographical references.

O ATP mediando a sinalização purinérgica no bulbo ventrolateral rostral contribui para o controle do quimiorreflexo central e periférico regulando a pressão arterial e a respiração, mediante o envolvimento dos neurônios do núcleo retrotrapezóide (RTN). No entanto, as potenciais contribuições da sinalização purinérgica, no RTN, na função cardiorrespiratória em animais não anestesiados ainda não foram testadas. Mostramos que a injeção de ATP no RTN promoveu aumento cardiorrespiratório por um mecanismo dependente de receptores P2. Mostramos também que o bloqueio de receptor P2 não específico (PPADS), mas não de receptores específicos P2Y (MRS2179), reduziu a resposta ventilatória à hipercapnia (7% CO2) e hipóxia (8 % O2) em ratos não anestesiados. Além disso, a adenosina (ADO) no RTN atenuou o aumento da ventilação induzido por hipercapnia in vivo e o disparo dos neurônios in vitro. Estes resultados demonstram que a sinalização mediada por ATP contribui para o controle respiratório do quimiorreflexo central e periférico em ratos acordados e uma vez que o ATP se metaboliza rapidamente em ADO, esta teria ação no balanço da resposta quimiorreceptora no RTN. / ATP-mediated purinergic signaling at the level of the rostral ventrolateral medulla (RVLM) contributes to both central and peripheral chemoreceptor control of breathing and blood pressure within the retrotrapezoid nucleus (RTN). However, potential contributions of purinergic signaling in the RTN to cardiorespiratory function in conscious animals has not been tested. We show that in the absence of functional C1 cells, ATP into the RTN increased cardiorespiratory output by a P2-recepor dependent mechanism. We also show that a non-specific P2 receptor blocker (PPADS) reduced the ventilatory response to hypercapnia (7% CO2) and hypoxia (8% O2) in unanesthetized awake rats. Conversely, a specific P2Y1-receptor blocker (MRS2179) into the RTN had no measurable effect on respiratory responses elicited by hypercapnia or hypoxia. Moreover, adenosine (ADO) into the RTN could attenuate the hypercapnia-induced increase in ventilation in vivo and firing rate in RTN neurons in vitro. These results demonstrate that ATP-mediated purinergic signaling contributes to central and peripheral chemoreflex control of breathing in awake rats and ADO could provide a balance between ATP stimulation and its inhibition in RTN during hipercapnia.

O núcleo retrotrapezóide (RTN) é uma região bulbar envolvida na respiração. Estudos prévios mostraram a presença de varicosidades catecolaminérgicas na região do RTN. O objetivo deste estudo foi investigar a fonte de catecolaminas e os efeitos promovidos pela ativação dos receptores adrenérgicos no RTN. Uma densa projeção neuronal do grupamento A7 para o RTN foi revelada usando o traçador retrógrado Fluorogold. Foi registrada a atividade eletromiográfica do diafragma (DiaEMG) e do abdominal (AbdEMG) de ratos Wistar anestesiados. A injeção de noradrenalina promoveu uma inibição da DiaEMG, sem alterar a AbdEMG; este efeito foi atenuado pela injeção prévia de ioimbina e não foi afetado pela injeção de prazosina e propranolol no RTN. A injeção de fenilefrina no RTN aumentou a DiaEMG e gerou AbdEMG; estes efeitos foram bloqueados por injeções prévias de prazosina no RTN. Os resultados deste estudo suportam a ideia de que o RTN recebe projeções adrenérgicas da ponte que modula a atividade dos neurônios do RTN por meio da ativação dos receptores adrenérgicos α -1 e α- 2. / The retrotrapezoid nucleus (RTN) is a medulla region involved in breathing. Previous studies showed the presence of catecholaminergic varicosities in the RTN region. The aim of this study was to investigate the source of cathecolamines and the effects produced by the activation of adrenergic receptors in the RTN. A dense neuronal projection from A7 to RTN was revealed using retrograde tracer FluorGold. In anaesthetized male Wistar rats, diaphragm (DiaEMG) and abdominal (AbdEMG) muscle activities were recorded. Injection of noradrenaline produced an inhibition of DiaEMG, but did not change AbdEMG; These effects was attenuated by pre-injection of yohimbine and were not affect by injection of prazosin and propranolol into the RTN. Injection of phenilephrine into the RTN increased DiaEMG and was also able to generate AbdEMG; these responses were eliminated by pre-injections of into the RTN. These results support the idea that RTN has pontine adrenergic inputs that modulate RTN neurons activity through activation of &#945 - 1 and - &#945 -2 adrenergic receptors.

by Cheung Ngai Man, Edmund. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 73-83). / Acknowledgments --- p.i / Abstract --- p.iii / List of Figures --- p.viii / List of Tables --- p.xi / Chapters / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Intramedullary nailing --- p.1 / Chapter 1.2 --- Reaming technique for intramedullary nailing --- p.3 / Chapter 1.3 --- The relationship between pulmonary fat embolism and reaming technique --- p.7 / Chapter 1.4 --- Objectives --- p.10 / Chapter 2 --- Methodology --- p.12 / Chapter 2.1 --- The measurement of the intramedullary pressure --- p.12 / Chapter 2.1.1 --- Animal model --- p.12 / Chapter 2.1.2 --- Intramedullary pressure measurement device --- p.12 / Chapter 2.1.3 --- Operative procedure --- p.14 / Chapter 2.1.4 --- Intramedullary pressure measurement --- p.16 / Chapter 2.2 --- The measurement of the plasma lipids and marrow lipids --- p.19 / Chapter 2.2.1 --- Samples collection --- p.19 / Chapter 2.2.2 --- Lipid extraction --- p.19 / Chapter 2.2.3 --- Thin layer chromatography --- p.20 / Chapter 2.2.4 --- Methylation --- p.24 / Chapter 2.2.5 --- Gas chromatographic analysis --- p.24 / Chapter 2.3 --- The measurement of the pulmonary lipids and fat emboli --- p.27 / Chapter 2.3.1 --- Pulmonary tissue collection --- p.27 / Chapter 2.3.2 --- Preparation for measurement of pulmonary lipids --- p.27 / Chapter 2.3.3 --- Fat emboli staining --- p.27 / Chapter 2.3.4 --- Image analysis --- p.28 / Chapter 2.4 --- Statistical analysis --- p.31 / Chapter 3 --- Results --- p.32 / Chapter 3.1 --- Intramedullary pressure measurement --- p.32 / Chapter 3.2 --- The analysis of bone marrow lipids --- p.34 / Chapter 3.3 --- The changes of the plasma lipids during reaming --- p.39 / Chapter 3.4 --- The measurement of the pulmonary fat emboli --- p.44 / Chapter 3.5 --- The relationship between the intramedullary pressure and plasma lipids and pulmonary fat intravasation --- p.52 / Chapter 4 --- Discuss --- p.55 / Chapter 4.1 --- The experimental design --- p.55 / Chapter 4.2 --- The change of the intramedullary pressures --- p.57 / Chapter 4.3 --- The application of the gas chromatography --- p.59 / Chapter 4.4 --- The composition of bone marrow lipids --- p.62 / Chapter 4.5 --- The changes of plasma lipids --- p.63 / Chapter 4.6 --- The pulmonary fat embolisation --- p.65 / Chapter 5 --- Conclusion --- p.69 / Chapter 6 --- Future direction on this study --- p.71 / References --- p.73 / Appendix --- p.84 / Chapter 1 --- The operation of the IM Press device --- p.84 / Chapter 2 --- The calibration of the IM Press --- p.85 / Chapter 3 --- The preparation of the internal standards for the lipid analysis --- p.89 / Chapter 4 --- The composition of the bone marrow lipids --- p.91 / Chapter 5 --- The composition of plasma lipids --- p.95 / Chapter 6 --- The composition of pulmonary lipids --- p.101 / Chapter 7 --- The measurement of the pulmonary fat emboli --- p.105

O núcleo retrotrapezóide (RTN) é uma região bulbar envolvida na respiração. Estudos prévios mostraram a presença de varicosidades catecolaminérgicas na região do RTN. O objetivo deste estudo foi investigar a fonte de catecolaminas e os efeitos promovidos pela ativação dos receptores adrenérgicos no RTN. Uma densa projeção neuronal do grupamento A7 para o RTN foi revelada usando o traçador retrógrado Fluorogold. Foi registrada a atividade eletromiográfica do diafragma (DiaEMG) e do abdominal (AbdEMG) de ratos Wistar anestesiados. A injeção de noradrenalina promoveu uma inibição da DiaEMG, sem alterar a AbdEMG; este efeito foi atenuado pela injeção prévia de ioimbina e não foi afetado pela injeção de prazosina e propranolol no RTN. A injeção de fenilefrina no RTN aumentou a DiaEMG e gerou AbdEMG; estes efeitos foram bloqueados por injeções prévias de prazosina no RTN. Os resultados deste estudo suportam a ideia de que o RTN recebe projeções adrenérgicas da ponte que modula a atividade dos neurônios do RTN por meio da ativação dos receptores adrenérgicos α -1 e α- 2. / The retrotrapezoid nucleus (RTN) is a medulla region involved in breathing. Previous studies showed the presence of catecholaminergic varicosities in the RTN region. The aim of this study was to investigate the source of cathecolamines and the effects produced by the activation of adrenergic receptors in the RTN. A dense neuronal projection from A7 to RTN was revealed using retrograde tracer FluorGold. In anaesthetized male Wistar rats, diaphragm (DiaEMG) and abdominal (AbdEMG) muscle activities were recorded. Injection of noradrenaline produced an inhibition of DiaEMG, but did not change AbdEMG; These effects was attenuated by pre-injection of yohimbine and were not affect by injection of prazosin and propranolol into the RTN. Injection of phenilephrine into the RTN increased DiaEMG and was also able to generate AbdEMG; these responses were eliminated by pre-injections of into the RTN. These results support the idea that RTN has pontine adrenergic inputs that modulate RTN neurons activity through activation of &#945 - 1 and - &#945 -2 adrenergic receptors.