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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 78 (1983), S. 473-491 
    ISSN: 1435-1803
    Keywords: atrial fibrillation ; coronary circulation ; coronary vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 21 narkotisierten thorakotomierten Hunden wurde der Einfluß von Vorhofflimmern auf die Koronardurchblutung untersucht. Vorhofflimmern wurde entweder durch lokale Applikation einer 10%-Acetylcholinlösung auf das linke Herzohr oder durch elektrische Stimulation (2–7 Volt, 2 ms, 50 Hz) induziert. Unter Vorhofflimmern (n=10) kam es zu einem signifikanten Abfall des mittleren Aortendruckes und Anstieg der Herzfrequenz; die Koronardurchblutung änderte sich nicht (78±6 gegenüber 75±5 ml/min×100 g), dagegen nahmen der Koronargefäßwiderstand von 1,16±0.05 auf 0,87±0.07 (mmHg×min×100 g)/ml (RU), p〈0,0001 und die koronarvenöse Sauerstoffsättigung von 26±2% auf 22±1%, p〈0,05, ab. Nach maximaler Koronardilatation durch Carbochromen (5mg/kg in 3 min i.v.) waren Koronardurchblutung (311±48 gegenüber 205±30 ml/min×100 g, p〈0,01) und koronarvenöse Sauerstoffsättigung (65±6 gegenüber 42±6%, p〈0,01) bei Vorhofflimmern deutlich niedriger, der Koronargefäßwiderstand (0,27±0,03 gegenüber 0,37±0,04 RU, p〈0,0001) hingegen um 38±8% (p〈0,0005) größer als bei Sinusrhythmus. Während der ebenfalls durch elektrische Vorhofstimulation ausgelösten supraventrikulären Tachykardie mit identischer Herzfrequenz wie bei Vorhofflimmern (n=11) waren Koronardurchblutung (92±9 gegenüber 125±14 ml/min×100 g, p〈0,001) und koronarvenöse Sauerstoffsättigung (24±2 gegenüber 30±2%, p〈0,0025) größer, der Koronargefäßwiderstand (1,16±0,11 gegenüber 0,97±0,10 RU, p〈0,0005) niedriger als bei Vorhofflimmern; auch bei maximaler Koronardilatation waren Koronardurchblutung (168±16 gegenüber 233±24 ml/min×100 g, p〈0,0005) und koronarvenöse Sauerstoffsättigung (57±2 gegenüber 70±3%, p〈0,0005) größer, der Koronargefäßwiderstand (0,46±0,02 gegenüber 0,35±0,02 RU, p±0,0005) niedriger als bei Vorhofflimmern. Die Ergebnisse zeigen, daß bei Vorhofflimmern zwar der Koronargefäßwiderstand abnimmt, dennoch die Sauerstoffausschöpfung ansteigt. Dieser vasokonstriktorische Effekt des Vorhofflimmerns wird dann sichtbar, wenn die Herzfrequenz kontrolliert wird. Das vasokonstriktorische Effekt ist unter maximaler Koronardilatation größer als unter Ausgangsbedingungen.
    Notes: Summary The influence of atrial fibrillation on coronary circulation was studied in 21 anesthetized open-chest dogs. Atrial fibrillation was induced either by local application of acetylcholine (10% in normal saline) on the left atrial appendage or by electric stimulation (2–7 volts, 2 ms, 50 Hz). When atrial fibrillation was induced (n=10), mean aortic pressure fell and heart rate rose significantly; coronary blood flow (CBF) remained unchanged (78±6 vs. 75±5 ml/min×10 g) while coronary vascular resistance (CVR) (1.16±0.05 vs. 0.87±0.07 [mHg×min×100 gl/ml [RU], p〈0.0001) and sinus oxygen saturation (26±2 vs. 22±1%, p〈0.05) decreased. Following the application of carbochromen (5 mg/kg in 3 min i.v.) resulting in maximal coronary dilatation, atrial fibrillation resulted in a reduction in CBF (311±48 vs. 205±30 ml/min×100 g, p〈0.01) and coronary sinus oxygen saturation (65±6 vs. 42±6%, p〈0.01), while CVR (0.27±0.03 vs. 0.37±0.04 RU, p〈0.0001) was 38±8% (p〈0.0005) higher during atrial fibrillation than at sinus rhythm. When hearts were paced to a rate which was identical to the average heart rate at atrial fibrillation (n=11), CBF (92±9 vs. 125±14 ml/min×100 g, p〈0.001) and sinus oxygen saturation (24±2 vs. 30±2%, p〈0.0025) were higher and CVR (1.16±0.11 vs. 0.97±0.10 RU, p〈0.0005) lower than during atrial fibrillation; during maximal coronary dilatation by carbochromen, pacing also resulted in a higher CBF (233±24 vs. 168±16 ml/min×100 g, p〈0.0005) and sinus oxygen saturation (70±3 vs. 57±2%, p〈0.0005), while CVR (0.35±0.02 vs. 0.46±0.02 RU, p〈0.0005) was lower than during atrial fibrillation. Thus atrial fibrillation results in a decrease in coronary vascular resistance but an increase in coronary oxygen extraction. When heart rate is controlled, the vasoconstrictor effect of atrial fibrillation becomes unmasked. Coronary vasoconstriction during atrial fibrillation appears to be greater during maximal coronary dilatation than during control.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 81 (1986), S. 29-39 
    ISSN: 1435-1803
    Keywords: atrial fibrillation ; coronary blood flow ; alpha-adrenoceptor ; coronary constriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of coronary vasoconstriction induced by atrial fibrillation during maximal coronary dilatation was studied in 19 chloralose-urethane anesthetized dogs. Maximal coronary dilatation was achieved by carbochromene (5 mg/kg i.v.) or dipyridamole (0.2 mg/kg i.v.) Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Atrial fibrillation was compared with rhythmic atrial pacing at similar heart rates (207±12 vs. 204±12 beats/min). During maximal coronary dilatation, coronary resistance was 0.38±0.05 mm Hgxminx100 g/ml (RU) at sinus rhythm, 0.41±0.06 RU at atrial pacing, and 0.52±0.07 RU at atrial fibrillation, that was significantly (p〈0.005) higher than during sinus rhythm and atrial pacing. Accordingly, coronary oxygen extraction was 14±1% at sinus rhythm, 17±1% at atrial pacing (p〈0.005 vs. sinus rhythm) and 27±2% at atrial fibrillation (p〈0.001 vs sinus rhythm and atrial pacing). Beta-adrenoceptor blockade with propranolol (1 mg/kg i.v.) did not prevent this coronary vasoconstrictive effect. Following alpha-blockade with phenoxybenzamine (10 mg/kg i.v.), however, coronary resistance was 0.52±0.08 RU during sinus rhythm, 0.54±0.10 RU during atrial pacing and 0.57±0.09 RU during atrial fibrillation. The data suggest coronary vasoconstriction induced by atrial fibrillation mediated by an alpha-adrenoceptor mechanism.
    Type of Medium: Electronic Resource
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