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  • Blood Flow Velocity  (2)
  • Blood Pressure  (2)
  • 1
    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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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 327 (1971), S. 152-166 
    ISSN: 1432-2013
    Keywords: Kidney ; Renal Artery ; Blood Flow Velocity ; Isoproterenol ; β-adrenergic Receptors ; Niere ; Nierenarterie ; Nierendurchblutung ; Isoproterenol ; β-Receptoren
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An wachen Hunden wurden mit einem Miniaturdruckaufnehmer der Blutdruck in der abdominalen Aorta und mit einem elektromagnetischen Flußmesser die Strömungsgeschwindigkeit in der linken Nierenarterie gemessen. Die Reaktion der Nierenstromstärke und des Blutdrucks auf rasche (〈1 sec) Injektion von 2,5, 5,0, 10,0 und 20,0 μg Isoproterenol in die abdominale Aorta proximal der Nierenarterie wurde untersucht. Bei allen vier Dosen wurde regelmäßig eine Steigerung der Nierendurchblutung und eine Abnahme des arteriellen Blutdrucks beobachtet. Die maximale Widerstandssenkung betrug im Mittel 25–30%. Während der ersten 6 sec nach Injektion erreichte die Nierenstromstärke bei noch unverändertem arteriellen Mitteldruck einen signifikant erhöhten Wert. Ebenso fand sich eine signifikant erhöhte Stromstärke, nachdem der Blutdruck sein Ausgangsniveau wieder erreicht hatte. Nach β-Blockade mit 0,5 mg/kg Propranolol hatte Isoproterenol in den verwendeten Dosen keinen Einfluß auf die Nierenstromstärke und den arteriellen Blutdruck. Das Ausmaß der beobachteten Vasodilatation läßt sich durch Autoregulation nicht erklären. Aus den Experimenten wird geschlossen, daß Isoproterenol (2,5 bis 20,0 μg i.a.) am wachen Hund in Ruhe β-Receptoren der Nierengefäße erregt.
    Notes: Summary In unanesthetized dogs abdominal aortic pressure was measured with an implanted miniature transducer, left renal artery flow velocity by an electromagnetic flowmeter. The effect of rapid injections (〈1 sec) of 2.5, 5.0, 10.0 and 20.0 μg isoproterenol into the abdominal aorta proximal to the renal artery on kidney blood flow and arterial blood pressure was investigated. Isoproterenol in every dose used regularly caused kidney blood flow to increase and arterial blood pressure to fall. The maximum decrease of resistance to flow in the average amounted to 25–30%. During the first 6 sec after drug injection kidney blood flow was already significantly elevated while arterial blood pressure was still unchanged.A significantly augmented kidney blood flow was also found when blood pressure had returned again to its original level. After β-blockade (0,5 mg/kg propranolol) isoproterenol (2.5–20.0 μg i.a.) had no effect on kidney blood flow and arterial blood pressure. The extent of the vasodilation cannot be attributed to autoregulation. It is concluded, that isoproterenol (2.5–20.0 μg i.a.) causes a β-adrenergic vasodilation in the kidney vasculature of the resting conscious dog.
    Type of Medium: Electronic Resource
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