Thesis (doctoral)--Lunds Universitet, 1990.

Thesis (doctoral)--Lunds Universitet, 1990.

Orientador: Heitor Moreno Junior / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-19T02:49:22Z (GMT). No. of bitstreams: 1 Pereira_DanielJose_M.pdf: 8289618 bytes, checksum: f81b30485257dfeb1919e76b99cecc7d (MD5) Previous issue date: 2011 / Resumo: Introdução: estudos experimentais de embolia pulmonar (EP) são habitualmente realizados sob ventilação mecânica. Como a maioria dos pacientes com suspeita de EP adentra os Serviços de Emergência em respiração espontânea e em ar ambiente, estudos que medissem as variáveis hemodinâmicas, gasométricas e capnográficas, nestas condições, em muito contribuiriam para compreensão mais específica das alterações cardiopulmonares e gasométricas na fase aguda da doença. Observa-se que faltam na literatura estudos experimentais que avaliem animais em tais condições. Objetivo: o objetivo do presente estudo foi submeter à EP animais sob ventilação espontânea e sem oxigênio suplementar. A EP por coágulos autólogos foi induzida em seis porcos e os registros cardiorrespiratórios e gasométricos foram realizados no pré e pós-EP. O valor da pressão média de artéria pulmonar (PMAP) "quase fatal" foi previamente determinada. Resultados: a presença de choque obstrutivo agudo pôde ser evidenciada pelo aumento da PMAP (de 17,8±3,5 para 41,7±3,3mmHg) (P<0,0001) e pela queda do débito cardíaco (de 4,9±1,0 para 2,7±1,0L/min) (P<0,003). Consequentemente, a presença de acidose metabólica pode ser constatada (de 2,4±0,6 para 5,7±1,8mmol/L) (P<0,0001). Observou-se ainda a presença de hipoxemia (de 73,5±12,7 para 40,3±4,6mmHg) (P<0,0001), porém, a PaCO2 não variou (de 44,9±4,4 para 48,2±6,0mmHg) (NS). Houve expressivos aumentos, tanto para P(a-et)CO2 (de 4,8±2,8 para 37,2±5,8mmHg) quanto para a P(A-a)O2 (de 8,2±8,9 para 37,2±10,3mmHg) (P<0,0001). Como tentativa de compensação à acidose metabólica, evidenciou-se significativo aumento do volume minuto alveolar total (de 4,0±0,9 para 10,6±2,9L/min) (P<0,0001). Conclusão: neste modelo, a PMAP quase fatal foi de 2 a 2,5 vezes a PMAP basal e as variáveis capnográficas, associadas a gasometria arterial e venosa, mostraram-se eficazes em discriminar um quadro obstrutivo agudo / Abstract: Introduction: Experimental studies on pulmonary embolism (PE) are usually performed under mechanical ventilation. Most patients with suspicion of PE enter the Emergency Services in spontaneous breathing and environmental air. Thus, under these conditions, measurements of hemodynamic, gasometric and capnographic variables contribute largely to a more specific comprehension of cardiopulmonary and gasometric alterations in the acute phase of the disease. Studies which evaluated animals under conditions are lacking. Objective: This study aimed to submit animals under spontaneous ventilation and without supplemental oxygen to PE. PE was induced in six pigs using autologous blood clots, and cardiorespiratory and gasometric records were performed before and after PE. The values of "near fatal" mean pulmonary arterial pressure (MPAP) were previously determined. Results: The presence of obstructive shock could be evidenced by increased MPAP (from 17.8±3.5 to 41.7±3.3mmHg) (p<0.0001) and decreased cardiac output (from 4.9±1.0 to 2.7±1.0L/min) (p<0.003). Consequently, metabolic acidosis occurred (Lac art)(from 2.4±0.6 to 5.7±1.8mmol/L) (p<0.0001). It was observed hypoxemia (from 73.5±12.7 to 40.3±4.6mmHg) (p<0.0001); however, PaCO2 did not vary (from 44.9±4.4 to 48.2±6.0mmHg) (NS). There were significant increases in both P(a-et)CO2 (from 4.8±2.8 to 37.2±5.8mmHg) and P(A-a)O2 (from 8.2±8.9 to 37.2±10.3mmHg) (p<0.0001). There was also a significant increase in the total alveolar minute volume (from 4.0±0.9 to 10.6±2.9L/min) (p<0.0001). Conclusion: In this model, the near fatal MPAP was from 2 to 2.5 times the basal MPAP; and the capnographic variables, associated with arterial and venous gasometry, showed effective in discriminating an acute obstructive profile / Mestrado / Farmacologia / Mestre em Farmacologia

Chronic obstructive pulmonary disease (COPD) is in up to 90 % of all cases caused by smoking. COPD often has negative effects on circulation, effects that first and foremost can be observed as respiratory insufficiency. Reduced function of the right ventricle of the heart is common in patients suffering from chronic obstructive pulmonary disease, especially if they also have hypoxemi; insufficient levels of oxygen in blood or tissue. The incidence of this cardiac complication reduces the survival time. It is possible in chronic obstructive pulmonary disease that the pressure in the pulmonary circulation gradually increases resulting in pulmonary hypertension followed by a slow adaptation of the right ventricle by hypertrophy of the myocardium. To investigate a correlation between COPD and pulmonary hypertension COPD patients were subjected to spirometry and ultrasound on heart. Of 14 examined patients 5 had developed pulmonary hypertension. A correlation between obstruction in the COPD- patients and an increase in left ventricular diameter was found. DLCO (diffusion capacity) of the lungs is directly connected to PA (pulmonary arterial pressure). The lower DLCO, the higher risk to develop pulmonary hypertension. However, we could not find a significant correlation between COPD and pulmonary hypertension in this study even if most patients had a decreased DLCO.

Septic pulmonary embolization (SPE) is a rare but serious disorder. It is a well-recognized potential problem in the settings of tricuspid valve endocarditis, septic thrombophlebitis, infected central venous catheters, and postanginal septicemia. Less well documented is the occurrence of SPE in patients with periodontal disease without suppurative thrombophlebitis of the great vessels of the neck. We report a patient with SPE in whom periodontal disease was the only identifiable nidus of infection and review the literature regarding the four other patients reported to have suffered this complication.

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Yes / Aberrant transforming growth factor-β (TGF-β) signaling activation is linked to pulmonary arterial hypertension (PAH). BMPR2 mutations perturb the balance between bone morphogenetic protein (BMP) and TGF-β pathways, leading to vascular remodeling, narrowing of the lumen of pulmonary vasculature, and clinical symptoms. This forum highlights the association of the TGF-β pathway with pathogenesis and therapeutic approaches. / Research carried out at Nasim laboratories is funded by GrowMedtech, the Royal Society, the Commonwealth Scholarship Commission (CSC) and the University of Bradford (UoB). N.S. is funded by the CSC and C.C.N. is partly funded by the UoB.