Astrup Method Research Articles

CLINICAL AND FUNCTIONAL CHARACTERISTICS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE IN CONDITIONS OF EXPOSURE TO INDUSTRIAL AEROSOLS

The aim is to study the clinical and functional characteristics and indicators of blood gas composition in workers with chronic obstructive pulmonary disease (COPD) exposed to the effects of industrial aerosols (IA). Material and Methods. The study included 132 patients with a diagnosis of COPD, stage I, category C; 68 were working in conditions of exposure to IA toxico-chemical action, and 64 people had COPD (comparison group which never worked in conditions of exposure to IA). Patients in both groups were divided into 2 subgroups: subgroup 1 — the duration of exposure to IA did not exceed 10 years, 2 — more than 10 years. Spirography was carried out on the device Care Fusion UK 232 Ltd. carbon monoxide (CO) content in exhaled air was determined using gas analyzer CareFusion Smoke check. Determination of blood oxygen saturation was carried out using pulse oximetry method. The content of the partial pressure of carbon dioxide (pCO2 ) and oxygen (pO2 ) in the venous blood were studied by Astrup method. Results. Most smokers were identified in the group exposed to long-term IA. The lowest values of forced expiratory volume in one second, vital capacity and Tiffeneau index were observed among persons exposed to IA differed significantly (p<0.05) from the control group. The highest values of CO and pCO2 , and pO2 were lowest in the group of patients with COPD in the combination of IA and in smokers. Conclusion. The high frequency and long duration of smoking was found out among the workers exposed to IA. Florid violations of wheeze were detected in individuals exposed to IA. As duration of the production contact with IA increasing, more serious violations of gas exchange are formed in patients with COPD. Keywords: chronic obstructive pulmonary disease, pollutants, industrial enterprise, function of external respiration, dyspnea><0.05) from the control group. The highest values of CO and pCO2 , and pO2 were lowest in the group of patients with COPD in the combination of IA and in smokers. Conclusion. The high frequency and long duration of smoking was found out among the workers exposed to IA. Florid violations of wheeze were detected in individuals exposed to IA. As duration of the production contact with IA increasing, more serious violations of gas exchange are formed in patients with COPD.

Demonstration of increasing standard pH value of lacrimal fluid with increase of flow rate.

To test the hypothesis that pH value of human tears is affected by flow rate. After stimulation with a drop of 70% alcohol into the ipsilateral nasal cavity tears from the left eyes of 30 healthy volunteers were collected with glass capillaries while flow rate of tear secretion was registered. The pCO(2), actual and standard pH were determined in the collected samples with the Astrup method: Standard pH is defined as the pH of the sample that has been equilibrated at 37 degrees C with a gas mixture having pCO(2)=40 mmHg. The flow rate correlated positively and significantly with both the standard pH value (r=0.503, p<0.01) and the pCO(2) (r=0.517, p<0.01) while there was no correlation between the actual pH and the flow rate. Loss of CO(2) from the sample is a cause of serious uncertainty in tear pH determination. A positive flow rate-pH relationship was found for human tears when the uncertainty was removed by determination of the standard pH.

The pH/Log PCO2 Buffer Curve of Horse Blood

Samples of jugular venous blood from six horses were equilibrated with six oxygen and carbon dioxide gas mixtures of PCO 2 between 28 and 54 mm Hg. In all six samples the correlations between the pH and the log PCO 2 values were linear and highly significant, with r in all six samples greater than 0.985. It was concluded that the Astrup method for the determination of the acid-base status of the blood of horses is valid.

Tissue coagulating system and fibrinolytic activities in brain tumors (author's transl)

The relation between tissue coagulating, fibrinolytic system and cyst-formation of brain tumors was studied. Twenty-nine cases of brain tumor, which contained 1 1 cases with cystic tumor and 18 cases with solid tumor, were examined. Four pieces of normal brain which were obtained by operation were examined as control. The levels of fibrinolytic activities of contents of cystic tumors were measured by plasmin activity, SK-activated plasmin activity using fibrin plate (Kowa Co., Japan) and FDP values using FDP Kit (Wellcome, England). Plasmin activity was found in 7 cases of cystic tumor. SK-activated plasmin activity was also found in 9 cases of cystic brain tumor. The FDP values measured in 7 cases of cystic tumor were 40-800 ug/ml. In only 2 cases with cystic brain tumors, the activities of plasmin and SK-activated plasmin were not found. In one of these FDP value was 160 ug/ml. Thus, cystic content of most cystic brain tumor had fibrinolytic activities. The levels of tissue thromboplastin of 29 cases of brain tumor were measured by a modified Astrup's method. Coagulation time of normal brain tissues was 14.8 sec. (thromboplastin content in 100 mg. tissues: 100%), that of tumor tissues with cyst was 12.5 sec. (215%), and that of tumor tissues without cyst was 19.3 sec. (29.9%). Hence, the levels of tissue thromboplastin of cystic brain tumors were higher than those in normal brain tissues and the levels of solid brain tumors were much lower than those of normal ones. The tissue local fibrinolytic activities were measured by Permis' method, using fibrin plate, and the levels of tissue plasminogen activator were measured by a modified Astrup's method. Trypsin solution was used as control and fibrinolytic activity of normal brain tissues were 0.80±1.78 TU, those of cystic brain tumor tissues were 4.35±3.25 TU, and those of solid brain tumor tissues were 0.14±0.64 TU. These results showed that the levels of tissue fibrinolytic activity of cystic brain tumor were much higher than those of normal brains and brain tumors without cysts (p<0.05, p<0.01). However, the levels of plasminogen activator of the tissues of cystic brain tumor were almost the same compared with normal brains. The levels of tissue plasminogen activator of solid brain tumor were much lower than those of normal brains and of cystic brain tumors (p<0.01). Both local coagulating system and fibrinolytic system of brain tumor tissues might be concerned with the cyst formation of the tumor.

Etiology of chronic subdural hematoma--role of local hyperfibrinolysis (author's transl)

Local fibrinolytic activity is studied to explain the physiopathogenesis of chronic subdural hematoma. 1. Using FDP-kit (Wellcome, England), FDP levels in hematoma fluid and serum are determined in 15 cases with unilateral hematoma and a case with bilateral hematoma. The FDP values in all hematomas are higher than 20 μg/ml. Two cases show the FDP values over than 320 μg/ml. The FDP values in hematoma fluid is always higher than that in serum of the same patient. The FDP values in hematoma fluid correlate to the volume of hematoma in fluid type subdural hematomas. 2. The levels of fibrinolytic activity in hematoma fluid and plasma are determined in 12 cases with subdural hematoma by Enzo-diffusion fibrin plate (Hyland, U.S.A.). Active plasmin, available plasmin and total plasminogen in hematoma fluid are not found in all cases with subdural hematoma. The fibrinolytic activity in hematoma fluid is remarkably lower than that in plasma in all cases. Absence of plasminogen might be for consumption. 3. The amounts of tissue active plasmin in 7 cases and tissue plasminogen activator in 8 cases are measured by modified Astrup's method. Tissue active plasmin levels in dura maters, outer membranes and inner membranes are 3.7-7.2 mm (average 6.1 mm), 4.3-6.5 mm (5.5 mm) and 0-4.8 mm (1.7 mm), respectively. Tissue plasminogen activator levels in dura maters, outer membranes and inner membranes are 0-5.5 mm (average 2.7 mm), 3.3-8.1 mm (6.1 mm) and 0 mm, respectively. The tissue activator level is highest in the outer membrane. 4. Fibrinolysis autography by Todd's method demonstrates the remarkable fibrinolysis around the vessels of outer membrane. The fibrinolysis in tissue increases with time. 5. After clotting of subdural hemorrhage, capsule (grows out) from the dura mater. Then tissue plasminogen activator in outer membrane would activate fibrinolytic system in order to absorb subdural clot. If the fibrinolytic activity is adequate, the clot could be absorbed. If the fibrinolytic activity is excess, it would inhibit the coagulating system in vessels of outer membrane and so that the continual or intermittent bleeding from outer membrane would occur into subdural cavity. As the result, the FDP levels in hematoma fluid increase and the amounts of plasminogen decrease for consumption. Such fibrinolytic bleeding from outer membrane of hematoma induces gradually the enlargement of hematoma and clinical symptoms appear after a latent interval.

Isolation and Characterization of Plasminogen Activator from Pig Leucocytes

SummaryPlasminogen activator was isolated from disrupted pig leucocytes by the aid of DEAE chromatography, gel filtration on Sephadex G-100 and final purification on CM cellulose, or by preparative gel electrophoresis.Isolated plasminogen activator corresponds No. 3 band of the starting sample of leucocyte cells (that is composed from 10 gel electrophoretic bands).pH optimum was found to be in pH range 8.0–8.5 and the highest pH stability is between pH range 5.0–8.0.Inhibition studies of isolated plasminogen activator were performed with EACA, AMCHA, PAMBA and Trasylol, using Anson and Astrup method. By Astrup method 100% inhibition was found with EACA and Trasylol and 30% with AMCHA. PAMBA gave 60% inhibition already at concentration 10–3 M/ml. Molecular weight of plasminogen activator was determined by gel filtration on Sephadex G-100. The value obtained from 4 different samples was found to be 28000–30500.

Paediatric Fluid Therapy.

This book successfully combines basic physiology of water and electrolyte metabolism with applicable schedules of fluid therapy. It can be divided into three sections. The first 30 pages discuss principles of water, electrolyte and acid-base balance including basic differences in fluid compartment size, turnover and components in infants, children, and adults. The acid-base section includes a discussion of buffers, the use of the Astrup method, examples of classical problems and the usual indications and precautions observed when treating patients with bicarbonate or THAM buffer. Unfortunately not even simple renal physiology is included. Maintenance requirements including nutritionally complete parenteral feeding are summarized. The bulk of the text deals with treatment situations. Following definition of the problem, each section contains a brief discussion of pathophysiology, clinical and laboratory features, and treatment. Chapters that are especially informative are those considering iso-, hypo- and hypertonic dehydration and neonatal problems. Other subjects discussed

A computer program for calculating the acid-base parameters in samples of blood using a mini-computer

A computer program is presented and evaluated, which calculates all acid-base parameters from data provided by either the indirect Astrup method or the direct method using empirical formulae derived from the Siggaard-Andersen curve nomogram. The program is implemented on a PDP 8 in a multi-user FOCAL environment and can be adapted to other electronic calculators.

Effect of O 2 desaturation on the determination of blood P co 2, by the astrup method

The influence of hemoglobin deoxygenation on the P co 2 determination by the Astrup interpolation method was studied in the range of 28 to 86 mm Hg P co 2 . Blood samples drawn from subjects with different acid-base status were tonometered at known CO 2 pressures. The differences between the actual and the “uncorrected” (measured) P co 2 per g reduced hemoglobin, were studied in function of the P co 2 ; and the pH. These differences in P co 2 , which we called the “P co 2 correction factors”, were approximately half of these determined when using the Siggaard-Andersen nomogram. The study of the pH differences between partially and fully oxygenated blood showed that this discrepancy can be explained by the extra amount of CO 2 bound to hemoglobin in the carbamate form when the hemoglobin is freed of O 2.

Studies on the fibrinolytic activity of the human kidney

The localization of the fibrinolytic activity in the kidney tissue and the origin of the urokinase are not fully understood.The purpose of the present report is to study the localization of the tissue fibrinolytic activity and the changes of the fibrinolytic activity in various diseases of human kidney.Examinations were made of kidneys in 53 autopsy cases and 49 operation cases with the 2M KSCN extraction method (Astrup's method) using human fibrinogen and with fibrinolytis autographs (Todd's method) using human fibrinogen.The results were as follows.1. A larger amount of tissue activator was extracted from the medulla than from the cortex of the kidney.2. Lower activity was found in children and young adults than in adults.3. No difference of the fibrinolytic activity was found between the saline perfused kidneys and the nonperfused kidneys by the 2M KSCN extraction method.4. The fibrinolytic activity in the kidney was found in the wall of the intrarenal vessels by Todd' method. The activity seemed to be localized in the endothelium. The intensity of the activator activity of the vessels was roughly in the following order, 1) vasa recta and arcuate veins, 2) interlobular veins, venulae adjacent to glomerulus and subcapsular venulae, 3) glomerular capillaries. In addition to these vessels, fibrinolytic activity was found in the wall of arterioles, interlobular arteries, and arcuate arteries. In the glomerulus, fibrinolytic activity was found to be high in the vascular pole.Fibrinolytic activity was not found in tubular epithelium, juxtaglomerular cells or epithelium of macula densa.5. In cortical peritubular capillaries, fibrinolytic activity was not found, except for those around tubules adjacent to juxtamedullary glomeruli.6. Very little fibrinolytic activity was found in a case of ischemic renal infarction which had completely lost the renal functions.7. The relation between the degree of renal function disturbance and the degree of fibrinolytic activity was not always parallel.8. In 9 cases of renal carcinoma (so-called Grawitz's tumor), fibrinolytic activity was not found in cancer cells, but in stromal capillaries.9. Antifibrinolytic activity of the kidney tissue seemed to be higher in the cortex than in the medulla, and was considered to be the antiactivator activity.

Reliability of blood P CO 2, measurements by the CO 2-electrode, the whole-blood C CO 2/pH method and the astrup method

The reliability of three methods commonly used for blood P co 2 measurements (CO 2-electrode, whole-blood C CO 2 /pH method, Astrup method) was evaluated by analysis of human blood samples tonometered at known CO 2 pressures. P CO 2 , was in the physiological region (38–53 mm Hg); S O 2 ranged from 93% to 16%. The COa-electrode yielded the most satisfactory results (smallest scat- ter, no directional error). The whole-blood C CO 2 /pH method was likewise devoid of directional error, but its scatter was appreciably larger. The Astrup method showed, along with an intermediate scatter, a desaturation-dependent systematic error. This error could be attributed to two factors affecting the desaturation correction: 1. the presence of small but not negligible amounts of non-oxygenable Hb in the samples (COHb+metHb), and 2. an overestimation of the Haldane effect in terms of BB change.

Untersuchungen �ber die postnatale Regulation des S�ure-Basen-Stoffwechsels bei gesunden Fr�hgeborenen

In 67 healthy prematures the actual pH, the actual pCO2, the standard bicarbonate and the base excess have been examined by the Astrup method. The examinations were done at the first day of life, partly also during the following 4 days.