[Prevention of hospital infections in various hospital units. Prevention of hospital infections at an emergency care center].
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Biomedical subjects
Publications and source records attributed to S Okubo.
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Most patients with primary pulmonary hypertension (PPH) die within two to four years of the onsets of their symptoms. However, several reports have described patients with PPH who have lived more than 10 years including a case with regression. We studied prognoses and the various determinants in 21 patients (7 men and 14 women; 18 deceased and three living) with PPH to elucidate its pathophysiology. Age at the onset of the disease varied from 12 to 73 years, with a mean of 29 years. All causes of death were of right heart failure, except for two cases of non-cardiac deaths. The prognoses were as follows: less than one year, two cases; 1-2 years, seven (one living); 2-3 years, five; 3-4 years, two; 4-5 years, one; more than six years, four (two living), with a mean of three years and five months. Pulmonary artery pressure decreased 10 years later (mean pressure, from 54 to 41 mmHg) in one patient, who lived for 13 years, followed by a non-cardiac death. Various clinical and pathological factors, including age at the onset of disease, sex, relationship to pregnancy, immunological abnormalities (4, positive; 17, negative), patent foramen ovale (five, patent; 16, not patent), PaO2, hemodynamic parameters, treatments, pathological subtypes (10, plexogenic pulmonary arteriopathy; two, pulmonary micro-thromboembolism; one, pulmonary veno-occlusive disease) numbers of plexiform lesion/cm2 were examined for prognostic correlations. None of the above factors were found to correlate significantly with prognoses. The only significant correlation was between the cardiac index (r = 0.981, p less than 0.001, n = 6), and total pulmonary resistance (r = -0.894, p less than 0.02, n = 6) in patients with pregnancy-related PPH. There was variability in the state of progression, namely, from rapid progression to regression. Clinically as well as pathologically, PPH may consist of several subgroups. However, whether it is due to differences in etiology or reactions of the disease is not clear. The pregnancy-related cases may comprise a homogenous subgroup within PPH.
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To investigate the possible mechanisms by which theophylline affects the control of ventilation, neuromuscular drive and ventilatory function were examined in 7 healthy men receiving an incremental intravenous aminophylline dosing schedule to achieve plasma theophylline concentrations of 5, 10, and 15 micrograms/ml. As compared with the baseline (predose) values, the 3 incremental aminophylline doses significantly (p less than 0.05 to 0.01) increased occlusion pressure (P0.1) and maximum inspiratory pressure static (MIPS) at functional residual capacity (FRC). This was not observed for ventilatory flow (V), tidal volume (VT), inspiratory time to total breathing cycle time ratio (Ti/Ttot) VT/Ti, and effective impedance [P0.1/VT/Ti)]. When maximum electrical activity of diaphragm (Edimax) and transdiaphragmatic pressure (Pdimax) were examined in 3 of the 7 subjects, Pdi/Edi tended to increase with increasing theophylline concentrations, while Edimax did not. Our results suggest that the increase in P0.1 during the increase in aminophylline dose is caused by an improvement in respiratory muscle contractility, rather than by a central effect or by an increase in neural drive.
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To determine whether technetium-99m-pyrophosphate (Tc-99m-PYP) scanning or two-dimensional echocardiography can detect amyloid heart disease in an earlier stage of familial amyloid polyneuropathy, 15 patients were examined. Although 10 of the 15 patients had no clinical evidence of congestive heart failure, as well as normal ventricular wall thickness and normal values for left ventricular systolic function, five (50%) of them showed mild or moderate myocardial uptake. On the other hand, none had characteristic highly refractile myocardial echoes on the two-dimensional echocardiographic images (p less than 0.01), and values for diastolic function were reduced in four of the five and normal in the remaining one. In 85 control subjects, diffuse positive pyrophosphate scans of the heart were found in four (5%) of them (three with dilated cardiomyopathy and one with sarcoidosis), and highly refractile granular sparkling echoes were observed in nine (11%) (five with hypertrophic cardiomyopathy, three with aortic stenosis, and one with hypereosinophilic syndrome). We conclude that Tc-99m-PYP scanning is a more sensitive and specific method and may have the potential ability to detect amyloid heart disease in the earlier stage of familial amyloid polyneuropathy than two-dimensional echocardiography.
The effect of increasing arterial partial pressure of CO2 (PaCO2) on respiratory mechanics was investigated in six anesthetized, paralyzed cats ventilated by constant-flow inflation. Respiratory mechanics were studied after end-inspiratory occlusions. Zero frequency resistance (Rmax), infinite frequency resistance (Rmin), and static elastance (Est) were calculated for the respiratory system, lung, and chest wall. Alveolar ventilation was manipulated by the addition of dead space to achieve a range of PaCO2 values of 29.3-87.3 mmHg. Cats did not become hypoxic during the experiment. Under control conditions marked frequency dependence in Rmax, Rmin, and Est of the respiratory system, lungs, and chest wall was demonstrated. The chest wall contributed 50% of the total resistance of the respiratory system. With increasing PaCO2 the only resistance observed to increase was Rmax of the lung (P less than 0.01). There were also no changes in the static elastic properties of either the lungs or the chest wall. These results suggest that hypercapnia increases resistance by changes in the lung periphery and not in the conducting airways.
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