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  • A cell  (2)
  • Blood Pressure  (2)
  • Phagocytose  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 52 (1974), S. 544-548 
    ISSN: 1432-1440
    Keywords: Monocytes ; phagocytosis ; tuberculosis ; antituberculous therapy ; Monocyten ; Phagocytose ; Tuberkulose ; Tuberkulostatika
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird von vergleichenden Monocyten-Funktionstest bei 15 Tuberkulosekranken und 15 gesunden Normalpersonen berichtet. Die Ausbreitungs- und Haftfähigkeit der Tbc-Monocyten ist gegenüber der Norm significant gesteigert, die Phagocytose von IgG-beladenen Erythrocyten signifikant vermindert. Diese Funktionseinschränkung beruht mit Wahrscheinlichkeit auf einer Blockade des IgG-Rezeptors oder einer Verminderung seiner Dichte auf der Zellmembran. 14 der untersuchten Fälle erhielten im Rahmen einer kombinierten tuberkulostatischen Therapie Rifampicin. Eine immunsuppressive Wirkung von Rifampicin ist auch in therapeutisch üblichen Dosen belegt. Es wird diskutiert, ob die verminderte Phagocytose-Aktivität durch Rifampicin bedingt ist. Die Beeinflussung des IgG-Rezeptors des Makrophagen bietet gleichzeitig eine Erklärungsmöglichkeit für die Unterdrückung der Delayed-Hypersensitivity-Reaktionen durch Rifampicin.
    Notes: Summary Tests of several monocyte functions were performed in fifteen patients with tuberculosis under treatment and fifteen healthy normal persons in parallel. The spreading activity and the attachment rate of the tbc-monocytes on the bottom of a plastic petri dish was significantly enhanced, the phagocytosis of IgG-coated red cells significantly impaired. The reduction of this monocyte function probably depends upon a blockade or modification of the monocyte IgG-receptor. Fourteen patients received antituberculous therapy including rifampicin. The immunosuppressive effect of rifampicin is well established; thus the impairment of phagocytosis could be induced by rifampicin. The modification of the IgG-receptor in addition could be an explanation for the suppression of delayed hypersensitivity reactions by rifampicin.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 53 (1975), S. 437-440 
    ISSN: 1432-1440
    Keywords: Monocyten ; Phagocytose ; NBT-Test ; M. Hodgkin ; Lymphorsarkom ; Monocytes ; phagocytosis ; NBT test ; M. Hodgkin ; lymphosarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The monocytes of 7 patients with advanced Hodgkin disease (stages III and IV) and of two patients with generalized lymphosarcoma exhibited a highly significant impairment of the phagocytosis of IgG-coated red cells, regardless of receiving therapy or not. In contrast three patients with M. Hodgkin, stage II B, and one with lymphorsarcoma in complete remission showed a rather elevated monocyte phagocytic activity. The nitroblue tetrazolium reduction by monocytes in the mean was significantly enhanced in all patients investigated, compared with normal persons, although only in one patient a bacterial infection was apparent at the time of the test. The possible implication of the findings in the well known immunodeficiency present in M. Hodgkin and lymphosarcoma is discussed.
    Notes: Zusammenfassung Die Monocyten von 7 Patienten mit fortgeschrittenem M. Hodgkin (Stadium III und IV) und von 2 Patienten mit generalisiertem Lymphosarcom zeigten eine hoch signifikant verminderte Phagocytose von IgG-beladenen Erythrocyten, unabhängig davon, ob eine Therapie bereits durchgeführt war oder nicht. Demgegenüber war die Phagocytose-Aktivität bei 3 Patienten mit M. Hodgkin, Stadium II und einem mit Lymphosarkom in Vollremission eher gegenüber der Norm gesteigert. Die Reduktion von Nitroblau-Tetrazolium durch Monocyten war bei allen untersuchten Patienten im Vergleich zu Normalpersonen im Mittel signifikant gesteigert, obwohl nur ein Patient zum Zeitpunkt der Untersuchung einen gesicherten bakteriellen Infekt aufwies. Die mögliche Bedeutung dieser Befunde für die bei diesen Erkrankungen bestehenden Immundefekte wird diskutiert.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Glucose ; insulin ; glucagon ; glucose metabolism ; A cell ; 2-deoxyglucose ; subtotal pancreatectomy ; ducks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible action of insulin via glucose metabolism on the pancreatic A cell response to glucose, was studied in ducks. 2-Deoxyglucose, a non metabolizable analogue of glucose was used. In normal ducks, the hyperglycaemia induced by 2-deoxyglucose (IV: 0.5g/kg) resulted in hyper glucagonaemia, while the same degree of hyper glycaemia, induced by glucose infusion (IV injection 25 mg/kg, and infusion 5 mg/kg/min) immediately suppressed glucagon secretion. In diabetic ducks, two days after subtotal pancreatectomy, glucose responsiveness of the A cell was abolished, but could be restored by insulin treatment before (IM 0.2 U/kg insulin + 8 μg/kg glucagon every 6 h) and during (IV 3.6 mU/kg + infusion 0.9 mU/kg/min) the glucose test (IV: 0.5 g /kg). The normal response of the A cell to glucose was not observed in diabetic insulintreated ducks after the administration of 2-deoxyglucose (IV: 0.5 g/kg). These data suggest an inhibitory effect of the metabolism of glucose on the release of glucagon. In addition, the action of insulin on the A cell may be mediated by its effect on glucose metabolism within the A cell.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Glucose ; insulin ; glucagon ; glucose metabolism ; A cell ; 2-deoxyglucose ; subtotal pancreatectomy ; ducks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible action of insulin via glucose metabolism on the pancreatic A cell response to glucose, was studied in ducks. 2-Deoxyglucose, a non-metabolizable analogue of glucose was used. In normal ducks, the hyperglycaemia induced by 2-deoxyglucose (IV: 0.5 g/kg) resulted in hyperglucagonaemia, while the same degree of hyperglycaemia, induced by glucose infusion (IV injection 25 mg/kg, and infusion 5 mg/kg/min) immediately suppressed glucagon secretion. In diabetic ducks, two days after subtotal pancreatectomy, glucose responsiveness of the A cell was abolished, but could be restored by insulin treatment before (IM 0.2 U/kg insulin+8 μg/kg glucagon every 6 h) and during (IV 3.6 mU/kg+infusion 0.9 mU/kg/min) the glucose test (IV: 0.5 g /kg). The normal response of the A cell to glucose was not observed in diabetic insulin-treated ducks after the administration of 2-deoxyglucose (IV: 0.5 g/kg). These data suggest an inhibitory effect of the metabolism of glucose on the release of glucagon. In addition, the action of insulin on the A cell may be mediated by its effect on glucose metabolism within the A cell.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 335 (1972), S. 29-45 
    ISSN: 1432-2013
    Keywords: Blood Flow Velocity ; Renal Artery ; Blood Pressure ; Vessel Distensibility ; Autoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In three healthy conscious dogs blood pressure was measured in the abdominal aorta with an implanted miniature transducer. Flow velocity in the left renal artery was recorded by an electromagnetic flowmeter. An appropriate distance between the transducer sites compensated the time-lag introduced by the flowmeter system and allowed records with a negligable foot to foot phase shift between the flow- and the pressure pulse. Pressure-flow curves (I.-P. curves) were obtained recording flow versus pressure beat by beat on an oscilloscope. Electrical stimulation of the right cervical vagus nerve produced I.-P.-curves, which decayed in less than 3 sec down to a blood pressure of 25 mm Hg (dynamic I.-P.-curve). Static I.-P.-curves were recorded by reducing blood pressure within 1 to 2 min to the same pressure level. The following results were obtained: A unique dynamic I.-P.-curve, which follows the power functionI=a·P n exists for each level of arterial mean pressure i.e. “myogenic” vascular tone. An increase of arterial mean pressure (i.e. “myogenic” vascular tone) decreases the exponentn and increases the coefficienta of the power function. The static I. P.-curve, which runs parallel to the pressure axis above 90 mm Hg is actually composed of a family of different dynamic I.-P.-curves. The kidney resistance vessels are rather distensible. The pressure-dependent increase of “myogenic” vascular tone, which developes at perfusion pressures above 55 mm Hg, decreases the vessel distensibility. A change of mean perfusion pressure causes the kidney resistance vessels to shift from one to another dynamic I.-P.-curve without altering mean blood flow.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 327 (1971), S. 203-224 
    ISSN: 1432-2013
    Keywords: Pressoreceptors ; Cardiac Output ; Blood Pressure ; Autoregulation ; Sympatholytics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Flow velocity in the ascending aorta and aortic blood pressure were recorded continuously in healthy conscious dogs. Using implanted pneumatic cuffs the effect of bilateral carotid occlusion on heart rate, stroke volume, cardiac output, peak velocity, maximum acceleration, blood pressure, and total peripheral resistance (T.P.R.) was studied in the resting animal. Following carotid occlusion heart rate rose within 3–4 sec by 13 beats/min; during the steady state it exceeded the control by 8 beats/min. Cardiac output closely followed heart rate, since stroke volume decreased slightly (3–4%), mainly because of the elevated aortic pressure. During the first 3–4 sec cardiac output increased by 10–15% reaching a steady state level 8% above control. The initial fast increase of cardiac output caused mean aortic pressure to rise rapidly, while T.P.R. transiently decreased. Subsequently T.P.R. rose, causing a secondary slow increase of pressure. During the steady state blood pressure was elevated by 27 mm Hg (26%), T.P.R. by 12.1 mm Hg×l−1×min (20%). Maximum acceleration did not change with heart rate and was hardly affected (−1.5%) by the pressure rise. Peak velocity was little influenced by heart rate; it decreased by 7% mainly because of the elevated aortic pressure. β-blockade (0.5 mg/kg propranolol) affected T.P.R. only during control (+18%), but did not modify the time course of the reflex and its steady state changes. α-blockade (5.0 mg/kg phenoxybenzamine) decreased aortic mean pressure (5 mm Hg) and T.P.R. (7%) during control. Following carotid occlusion T.P.R. rose by the same amount, but much more slowly. Starting from the lower control the same pressure level was now obtained by a higher reflex increase of heart rate and cardiac output. It is concluded that the initial pressor response is initiated by an increase of cardiac output mediated by vagal inhibition. The secondary rise of blood pressure is predominantly caused by an increase of T.P.R. due to autoregulation in some vascular beds. The higher stroke work during the reflex is not accomplished by an increased contractility due to sympathetic activation.
    Type of Medium: Electronic Resource
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