Effects of hemoglobin on pulmonary arterial pressure and pulmonary vascular resistance in patients with chronic emphysema.

BACKGROUND: The increase in viscosity caused by secondary polycythemia is thought to be one of the major causes of pulmonary hypertension secondary to chronic emphysema. However, very few clinical studies considered the relation between pulmonary hypertension and polycythemia in the case of chronic obstructive pulmonary disease. OBJECTIVE: The purpose of this study is to elucidate the relative contribution of an increase in hemoglobin level (Hb) to mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR). METHODS: We retrospectively investigated 41 patients with chronic emphysema who had undergone a right heart catheterization. Multiple-regression analysis and F test were performed to investigate both direct effects of Hb and PaO(2) as independent variables on mPAP and PVR as dependent variables. RESULTS: Significant correlations were found between PaO(2) and mPAP (or PVR), or Hb and mPAP (or PVR), indicating that both Hb and PaO(2) are contributory to mPAP and PVR. The F test demonstrated that Hb and PaO(2) could directly affect the level of either mPAP or PVR. CONCLUSIONS: It was concluded that Hb had a direct effect on mPAP and PVR, independently of hypoxia in patients with chronic emphysema.

Characterization of chitinases excreted by Bacillus cereus CH.

Bacillus cereus CH was shown to excrete chitinases into the culture supernatant when cultivated in a medium containing 0.2% colloidal chitin, whereas the removal of colloidal chitin resulted in a low activity. After concentration of the culture supernatant by precipitation with ammonium sulfate, the induced chitinases were purified by sequential chromatography. Four different chitinases, A, B1, B2, and B3 with molecular masses of 35, 47, 58, and 64 kDa, respectively, were separated. All chitinases showed similarities in their kinetic parameters when observed with colloidal chitin, including an optimal pH of 5.0-7.5, and an optimal temperature between 50-60 degrees C. Chitinase A hydrolyzed glycol chitin and p-nitrophenyl-di-N-acetyl-beta-chitobioside at similar rates to that of colloidal chitin, whereas group B chitinases hydrolyzed both substrates in much lower rates. From analyses of the reaction products, it is most likely that chitinase A and all group B chitinases hydrolyze the substrates tested in an endo-fashion. However, group B chitinases were distinct from chitinase A in possessing high transglycosylation activity. From amino terminal sequencing, chitinases B1, B2, and B3 were shown to have almost identical sequences, which differed from that of chitinase A. The similarities in the reaction modes and amino terminal sequences among chitinases B1, B2, and B3 suggest that these chitinases may be derived from a presumptive precursor protein through C-terminal processing.

[Investigation of pulmonary hemodynamics and chest X-ray findings in hypercapnic patients with pulmonary tuberculosis sequelae].

We investigated pulmonary hemodynamics and chest X-ray findings to explore pathophysiological significance of chronic hypercapnia in patients with pulmonary tuberculosis sequelae. One hundred and seven patients underwent examinations of blood gases and right cardiac catheterization. The patients were divided into two groups, according to arterial carbon dioxide tension under room air breathing (PaCO2). Group I (n = 35) was defined as 45 Torr or lower of PaCO2, and Group II (n = 72) was the hypercapnic group whose PaCO2 was over 45 Torr. In addition, spirometry was done in 34 patients of Group I and 68 of Group II. First, the values of blood gases, spirometry and pulmonary hemodynamics were compared between the two groups. Secondly, between 22 of Group I and 50 of Group II, the values of pulmonary arteriolar resistance (PAR) before and after 100% oxygen breathing for 10 minutes were compared. These comparisons were made by exploratory data analysis. Lastly, we described in all cases with five items of chest X-ray findings and the extent of each finding we had defined. The items were emphysematous change; fibrosis, bronchiectasis, and/or cavity (hereafter abbreviated as "fibrosis"); lung resection and/or atelectasis; pleural thickening; and thoracoplasty. We explored the items of X-ray findings which may relate to hypercapnia by ridit (abbreviation for "relative to an identified distribution") analysis. The results were as follows. (1) Hypercapnic patients tended to have severer restrictive ventilatory impairment and hypoxemia. Under an even level of arterial oxygen tension (PaO2), tissue oxygenation was not poorer in Group II than in Group I. (2) Hypercapnic patients tended to have more unfavorable pulmonary hemodynamics. More than half of them had pulmonary hypertension defined as 20 mmHg or higher of pulmonary artery mean pressure (PAm). Under an even level of PaO2, PAm was higher in Group II. Although 34 patients of Group II showed PaO2 over 60 Torr, 23 of them had pulmonary hypertension. (3) PAR after oxygen breathing was more likely to decrease in Group II than in Group I. (4) As any mean ridit was standardized and adjusted to 0.5 in Group I, the maximum was the mean ridit of "pleural thickening" (= 0.67), next "fibrosis" (= 0.65) in Group II. The above two items of X-ray findings, in which each mean ridit was higher than in any other item, were more influential on hypercapnia. We conclude as follows. (1) Pulmonary hypertension is severer in hypercapnic patients with pulmonary tuberculosis sequelae; it may be mainly attributable to hypoxic pulmonary vasoconstriction. (2) An important cause of chronic hypercapnia may be pathological changes such as "pleural thickening" and "fibrosis" seen on the radiogram.

[Investigation of pulmonary hemodynamics and chest X-ray findings in patients with pulmonary tuberculosis sequelae and obstructive ventilatory impairment].

We investigated pulmonary hemodynamics and chest X-ray findings to explore significance of obstructive ventilatory impairment in patients with pulmonary tuberculosis sequelae. One hundred and two patients underwent examinations of blood gases, spirometry, and right cardiac catheterization. The patients were divided into two groups, according to forced expiratory volume in one second as the percentage of forced vital capacity (FVC), which was expressed as FEV1%. Group A (n = 38) had FEV1% of 55% or lower and Group B (n = 64), FEV1% above 55%. First, the values of blood gases and hemodynamics were compared between the two groups, regarding the percent predicted value of FVC as a covariate. Secondly, between 26 of Group A and 42 of Group B, the change of pulmonary arteriolar resistance (PAR) before and after 100% oxygen breathing for 10 minutes was compared. These comparisons were made by exploratory data analysis. Lastly, we described every case with five items of chest X-ray findings and the extent of each finding we had defined. The items were emphysematous change; fibrosis, bronchiectasis and/or cavity; pulmonary resection and/or atelectasis; pleural thickening; and thoracoplasty. We explored X-ray findings influenced on airway obstruction by ridit (abbreviation for "relative to an identified distribution") analysis, taking smoking status into consideration. The results were as follows. (1) The patients of Group A tended to show severer hypoxemia and tissue hypoxia than the patients of Group B. (2) The patients of Group A tended to show worse values of pulmonary hemodynamics than the patients of Group B. Under an even level of the arterial oxygen tension that was 60 Torr or lower, pulmonary artery mean pressure was higher in Group A than in Group B. (3) PAR after oxygen breathing was less likely to decrease in Group A than in Group B. (4) As any mean ridit was standardized and adjusted to 0.5 in Group B, every mean ridit of "emphysematous change" in Group A was the largest-0.63 in non-smokers, 0.74 in ex-smokers and 0.70 in current smokers. Therefore, "emphysematous change" was more influenced on airway obstruction than any other finding because of the largest mean ridit. We conclude as follows. Pulmonary hypertension is more serious in patients suffering from severe airway obstruction with pulmonary tuberculosis sequelae, and it may be attributable to reduction in capacity of anatomical pulmonary vascular bed rather than hypoxic pulmonary vasoconstriction. Pathological changes such as "emphysematous change" on the radiograph might be considered as an important cause of obstructive ventilatory impairment.

[A case of Bence-Jones protein-lambda positive multiple myeloma complicated by abnormal plasma cells in pleural effusion].

A 53-year-old woman was admitted to this institution with chest pain and dyspnea. Chest roentgenogram showed pleural effusion and multiple tumor shadows, bilaterally which represented extrapleural signs. Numerous atypical plasma cells were found in the pleural effusion. Bone marrow biopsy showed atypical plasma cells. Immunoelectrophoresis revealed monoclonal Bence-Jones protein-lambda in serum and urine. Myeloma was subsequently diagnosed and chemotherapy was started. Multiple myeloma is a plasmacytoma, and myeloma cells proliferate in the bone marrow. The incidence of myeloma associated with malignant pleural effusion is rare with only 33 cases previously reported in Japan, to the best of our knowledge.

[A case of pneumoconiosis (welder's lung) suspected to be lung cancer].

A 60-year-old man, employed as a welder for 25 years, was admitted with an abnormal shadow on chest X-ray. An ill-defined and solitary mass shadow 3 cm in diameter was subsequently detected in the left upper lung field. The mass shadow exhibited high attenuation on chest CT scan. Transbronchial lung biopsy (TBLB) revealed an organized lesion possessing a large quantity of iron. Although pneumoconiosis was suspected, the possibility of lung cancer could not be dismissed. Pneumoconiosis (welder's lung) was diagnosed after thoracotomy and examination of the resected mass. Pneumoconiosis (welder's lung) rarely presents as a solitary mass lesion.

[Allergic bronchopulmonary mycosis caused by Schizophyllum commune].

In December 1989, a 72-year-old woman was hospitalized with atelectasis in the left lower lobe. The atelectasis resolved after bronchoscopic removal of impacted mucous plugs. Histopathological examination showed pulmonary mycosis. Microscopy suggested that a species of Aspergillus was responsible, but no definite diagnosis was made. After treatment with flucytosine and nebulized amphotericin, the patient's condition improved and she was discharged. In the middle of August 1994, she visited a local hospital complaining of fatigue. Eosinophilia (22%) was detected, and a few days later she visited that hospital again due to sudden dyspnea. A chest X-ray examination showed an abnormal shadow, and she was referred to our hospital. Atelectasis was seen in the left upper lobe. This finding, together with eosinophilia, suggested recurrence of pulmonary mycosis, and therefore bronchoscopy was performed. White mucous plugs obstructing the left upper lobe were observed and were bronchoscopically removed. Microscopical examination of the mucous plugs showed marked eosinophil infiltration and hyphae. Cultures of specimens obtained during bronchoscopy showed Schizophyllum commune, and allergic bronchopulmonary mycosis due to this microorganism was diagnosed. Identification of this microorganism as a cause of deep-seated pulmonary mycosis is very rare.

[Invasive amebiasis at an institution for the mentally retarded in Shizuoka Prefecture].

Amebiasis caused by Entamoeba histolytica at an institution for mentally retarded in Shizuoka Prefecture is reported. Five of the 50 patients showed E. histolytica cysts in their stools and 4 were positive serologically. The polymerase chain reaction and restriction fragment length polymorphism revealed that the isolates were pathogenic-type E. histolytica. Epidemiological analysis revealed that the amebic infection was caused by the abnormal behavior of mentally retarded patients. Administration of diloxanide furoate and metronidazole for cyst-carriers eliminated cysts from the stool and lowered the antibody titer.

[Varicella pneumonia with multiple nodular shadows after allogeneic bone marrow transplantation in chronic myeloid leukemia].

A 30-year-female with chronic myelogenous leukemia received allogeneic bone marrow transplantation (BMT). On day 104, low-grade fever, cough, and general malaise developed, resulting in hospitalization 10 days later. Chest X ray revealed diffuse infitrates, suggesting cytomegalovirus interstitial pneumonia. Ganciclovir (DHPG) was given daily and all symptoms disappeared three days later. However, a very few vesicular lesions appeared on her trunk and her two children had chickenpox at that time. Chest CT was taken and disclosed diffuse nodular shadows. Clinical course and chest CT suggested varicella pneumonia. DHPG administration was stopped and acyclovir PO started to be given. She was discharged in excellent condition. In this report, we show a rare case of varicella pneumonia after allogeneic BMT and efficacy of DHPG for the treatment of varicella pneumonia.

[An autopsy case of lung cancer metastasizing to renal cell cancer and rectal villous adenoma].

A 67-year-old woman with bloody stool was admitted to our hospital. Chest radiograph on admission showed a tumor shadow in the right lower lung field. Lung adenocarcinoma of right S6 and villous adenoma of the rectum were detected. Although she was treated with chemotherapy and radiotherapy, she died of respiratory failure. At autopsy, moderately differentiated adenocarcinoma of the right lung, renal cell carcinoma, and villous adenoma of the rectum were confirmed. Lung adenocarcinomas were detected in the focus of the renal cell carcinoma and in the villous adenoma. Metastasis of a cancer into another coexisting tumor in the same individual is extremely rare, and a satisfactory explanation for this phenomenon has not yet been offered.

[The relationship between pulmonary hemodynamics and chest X-ray findings in patients with sequelae of pulmonary tuberculosis].

For better understanding of pathophysiological aspects of tuberculosis sequelae, we investigated the relationship between pulmonary hemodynamics and chest X-ray findings. One hundred and seven patients with sequelae of pulmonary tuberculosis were examined by the right cardiac catheterization, and pulmonary hemodynamic values were measured and calculated. Chest X-ray findings were defined and classified into the following five items. The items were emphysematous change; fibrosis, bronchiectasis and/or cavity (hereafter abbreviated as "fibrosis"); pulmonary resection and/or atelectasis; pleural thickening; and thoracoplasty. The extent of each finding was defined. We tried to describe chest X-ray findings by applying and categorizing these classifications and the extent to each case. First, we tried to estimate the grade of pulmonary hypertension by categorized X-ray findings. Further, we analyzed what kinds of findings were most influential on the increase of pulmonary artery mean pressure (PPA) and pulmonary arteriolar resistance (PAR). Secondly, we investigated whether PPA, cardiac index (CI) and PAR changed before and after oxygen administration. Thirdly, we analyzed what kind of X-ray findings most affected pulmonary hemodynamics under 100% oxygen administration for 10 minutes. The results were as follows: (1) Out of 107 cases, it was possible to predict PPA by categorized chest X-ray findings in 75 cases by Hayashi's first method of quantification, one of multivariative analyses. "Pleural thickening" was the most influential finding on the increase of PPA. "Fibrosis" was the most influential on the increase of PAR. (2) The values of PPA, CI and PAR decreased more after 100% oxygen administration than under room air breathing. Therefore, PAR was used as the index to estimate pulmonary hemodynamics under the condition of oxygen administration. (3) It was possible to measure PAR under oxygen administration (PARO2) in 72 cases. "Emphysematous change" was the most influential X-ray finding on the increase of PARO2. From these results, it was thought that pulmonary circulatory disorder in patients with tuberculosis sequelae was caused by the combination of various chest X-ray findings with the different extent. It was possible to predict pulmonary hypertension to a certain degree from categorized chest X-ray findings. It was suggested that "emphysematous change" less related to hypoxic pulmonary vasoconstriction than "fibrosis" and "pleural thickening" from the results of comparison among the partial correlation coefficients, which were associated with the increase of PAR under room air breathing and oxygen administration.(ABSTRACT TRUNCATED AT 400 WORDS)

[Computed tomographic appearances of pulmonary alveolar proteinosis].

We evaluated longitudinal changes in chest CT images in six cases (5 males and one female, age: 35-57 yr) of pulmonary alveolar proteinosis treated with bronchopulmonary lavage. Chest CT images on admission showed a mixed pattern of air-space consolidation and reticular or reticulonodular shadows in most cases and showed a peripheral clear zone in all cases. These shadows gradually diminished after bronchopulmonary lavage. Some cases revealed early improvement in the hilar zone while others had equal improvement in all lung lesions. In one case, consolidation was changed into reticular shadows by treatment. Previous reports have indicated that "interstitial shadows which disappeared with lavage" reflect edematous thickening of interlobular septa. However, our longitudinal evaluation suggests that interstitial shadows on CT images may reflect not only real interstitial infiltration but also inhomogeneous distribution of intralobular deposits.

[A case of pulmonary actinomycosis that was difficult to distinguish from pulmonary carcinoma].

A 45-year-old male was admitted with chief complaint of hemoptysis. Prior to admission, a tumor in the S3 segment of the right lung had been detected by chest radiography. Despite a detailed examination after admission, no definite diagnosis was made, and right upper lobectomy was performed. Histopathological examination of the surgically resected tissue led to the diagnosis of pulmonary actinomycosis. In Japan, 52 cases of this condition were reported between 1964 and 1991. This paper discusses the epidemiology, diagnosis and diagnostic imaging of the condition, with reference to the literature.

[Clinical efficacy of ceftriaxone when administered once daily for respiratory tract infections in patients with advanced ages].

Ceftriaxone (CTRX), a new third generation cephalosporin, was investigated upon once daily administration for its clinical efficacy and safety on respiratory tract infections in patients with advanced ages. The results are summarized as follows: 1. Clinical responses to CTRX of 48 cases of advanced age patients with respiratory tract infections were good with an efficacy rate of 89.6%. 2. Adverse reactions to CTRX were mainly exanthema in 7 cases (14.6%). 3. Serum levels of CTRX were determined in 4 cases after intravenous drip infusion of 2 g CTRX. Serum levels were analyzed by one-compartment model. There was no evidence of accumulation of CTRX in the patients with advanced ages.

Evidence for hypoxic depression of CO2-ventilation response in carotid body-resected humans.

Steady-state CO2-ventilation response curves with hyperoxia (end-tidal PO2 greater than 200 Torr) and mild hypoxia (end-tidal PO2 approximately equal to 60 Torr) were compared in five carotid body-resected (BR) patients and five control patients. The data were analyzed by fitting a linear equation, V = S(PETCO2-B), where V is minute ventilation S is the response curve slope. PETCO2 is end-tidal PCO2, and B is the response curve threshold. S slightly increased from hyperoxia to hypoxia in both BR and control groups. On the other hand, B moderately increased with hypoxia in BR patients, whereas it slightly decreased in controls. These changes were all not significant. However, in accordance with the change in B, the response curve to hypoxia at V of 10 1/min was significantly shifted in opposite directions in the two groups, i.e., rightward and leftward shift in BR and control groups, respectively. Thus the average magnitude of V calculated at PETCO2 of 40 Torr in hypoxia was significantly lower in BR patients than in controls (P less than 0.01). We conclude that this hypoxic depression of the CO2-ventilation response found in BR patients may have resulted, at least in part, from modulation of the brain stem neural mechanisms that were elicited by loss of afferent discharges from the carotid body.

[A case of Pryce's type I intralobar pulmonary sequestration diagnosed by noninvasive techniques].

The patient was a female who came to our hospital with a chief complaint of hemoptysis. Radiography of the chest demonstrated a funicular shadow, and CT of the chest also revealed a similar shadow in contact with the thoracic aorta enhanced by the contrast material. Pulmonary arteriography and aortography showed that the left S8, S9 and S10 areas were supplied by abnormal blood vessels bifurcating from the thoracic aorta, rather than the pulmonary artery. This finding was supported by scintigraphy of the pulmonary blood flow and pulmonary RI angiography. Since bronchography revealed no obvious abnormality in the bronchial system, the diagnosis of Pryce's type I intralobar pulmonary sequestration was established, and left lower lobectomy was carried out. While the evidence of abnormal blood vessels is important for the definitive diagnosis of pulmonary sequestration, concurrent image processing of the results of scintigraphy of the pulmonary blood flow and pulmonary RI angiography permits noninvasive demonstration of the fact that the sequestral pulmonary tissue is regulated by the systemic circulatory system, rather than the pulmonary circulatory system and thus is a useful technique.

[Open loop gain of the CO2-ventilation feedback control system in chronic obstructive pulmonary disease].

To evaluate the stability of the CO2-ventilation feedback system, we measured its open loop gain (G) in 12 patients with chronic obstructive pulmonary disease (COPD) and 15 control subjects. Then, we compared G to the conventional slope of the CO2-ventilation response line (S) and that of the metabolic hyperbola (SL). G was determined as the ratio of S to SL by applying external dead space of 250 and 500 ml. G, S and 1/SL in the control and the COPD were +17.1 +/- 7.2 (Mean +/- SD), 1.70 +/- 0.75 L.min-1.Torr-1 and -10.4 +/- 2.0 L-1.min.Torr, and -7.2 +/- 3.3, 0.48 +/- 0.27 L.min-1.Torr-1 and -16.1 +/- 6.4 L-1.min.Torr, respectively. G was significantly correlated with S in both groups, but that was not the case in 1/SL. The magnitude of G and S in COPD was about 42% and 28% of the control, indicating that G was maintained more stable than S. These data suggest that the decreased G in the COPD resulted from insufficient compensation of ventilatory drive, whereas 1/SL increased higher than the control. We conclude that G can be used to indicate the stability of the CO2-ventilation feedback system better than S.

Bilateral carotid body resection in man enhances hypoxic tachycardia.

In three groups of subjects we studied heart rate (HR) and ventilatory responses to progressive eucapnic hypoxia, steady-state hypercapnia with and without hypoxia, and hyperoxic and hypoxic breathholding (BH). Groups were six subjects about 25 years after bilateral carotid body resection (BR), eight subjects of an equally long period after unilateral resection (UR), and three control subjects similar to the study groups in age and pulmonary function (C). During progressive hypoxia, HR increased more in BR than in UR and C subjects. Ventilatory response was lowest in BR subjects (as expected). Steady-state hypoxic hypercapnia (end-tidal PO2, 60 Torr) depressed HR significantly more in C than in BR and UR subjects. Again, ventilatory response was lower in BR than in C subjects. HR progressively increased during BH initiated in hyperoxia (end-tidal PO2, 200 Torr) and hypoxia (end-tidal PO2, 70 Torr). In the BR group, the HR increment during hypoxia was significantly larger than that during hyperoxia. No such difference was apparent in UR and C groups. Thus, hypoxia with or without hypercapnia tends to accelerate HR in BR subjects whereas either less tachycardia or slowing is seen in UR and C subjects.