Spontaneous oscillation of systemic arterial pressure during cardiopulmonary bypass in the dog

1989 ◽  
Vol 84 (2) ◽  
pp. 160-164 ◽  
Author(s):  
V. Vainionpää ◽  
J. Timisjärvi ◽  
M. Tarkka
Keyword(s):  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Spontaneous Oscillation

Vasomotor waves of arterial blood pressure after cessation of cardiopulmonary bypass in man

Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi
Keyword(s):  
Blood Pressure ◽  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Heart Patients ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Epicardial Pacing

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.

Function of human intrinsic cardiac neurons in situ

2001 ◽  
Vol 280 (6) ◽  
pp. R1736-R1740 ◽  
Author(s):  
Rakesh Christopher Arora ◽  
Gregory Matthew Hirsch ◽  
Kristine Johnson Hirsch ◽  
Camille Hancock Friesen ◽  
John Andrew Armour
Keyword(s):  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Artery Bypass ◽  
Systemic Arterial Pressure ◽  
Right Atrial ◽  
Pharmacological Agents ◽  
Cardiac Dynamics ◽  
Extracellular Activity

We sought to determine the behavior of intrinsic cardiac neurons in human subjects undergoing cardiac surgery and to correlate their activity with hemodynamics status. A lead II electrocardiogram, pulmonary artery pressure, and systemic arterial pressure were recorded along with extracellular activity generated by right atrial neurons in 10 patients undergoing coronary artery bypass surgery. Identified neurons generated spontaneously activity that was, for the most part, unrelated to the cardiac cycle. Most neurons were activated by gentle mechanical distortion of ventricular epicardial loci. The activity generated by neurons in each patient increased when arterial pressure increased and decreased when arterial pressure fell. Intrinsic cardiac neurons continued to generate activity during cardioplegia and cardiopulmonary bypass, but at reduced levels. Normal neuronal activity was restored postbypass. It is concluded that human intrinsic cardiac neurons generate spontaneous activity and that many receive inputs from ventricular mechanosensory neurites. The latter may account for the fact that their behavior depends, in part, on cardiac dynamics. They are also sensitive to intravenously administered pharmacological agents. These data also indicate that cardiopulmonary bypass and cardioplegia do not induce residual depression of their function.

Inhibitory actions of serotonin on glutamate release in dorsal medulla suppress systemic arterial pressure of cats

2004 ◽  
Vol 355 (1-2) ◽  
pp. 73-76 ◽  
Author(s):  
Chi-Li Gong ◽  
Yung-Tsung Chiu ◽  
Nai-Nu Lin ◽  
Shinn-Zong Lin ◽  
Fu-Chou Cheng ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Glutamate Release ◽  
Systemic Arterial Pressure ◽  
Dorsal Medulla

Nocturnal headache: systemic arterial pressure and heart rate during sleep

Cephalalgia ◽  
1983 ◽  
Vol 3 (1_suppl) ◽  
pp. 54-57 ◽  
Author(s):  
Fabio Cirignotta ◽  
Giorgio Coccagna ◽  
Tommaso Sacquegna ◽  
Emiliana Sforza ◽  
Giuseppe Lamontanara ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rem Sleep ◽  
Continuous Monitoring ◽  
Systemic Arterial Pressure ◽  
Fréquence Cardiaque ◽  
The Awakening ◽  
Sono Stati ◽  
Autonomic Instability ◽  
Polygraphic Recording

In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N–REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks. On a étudié avec des méthodes polygrafiques trois sujets (1 homme et deux femmes) souffrant d'hémicranie chronique avec des crises nocturnes. Chez deux malades les crises étaient précédées d'augmentation et d'irrégularité de la tension artérielle. Ces modifications commençaient pendant le sommeil N-REM et contineaient pendant le sommeil REM qui précédait le réveil avec hémicranie. La fréquence cardiaque n'a pas subi de modification avant les crises. Les résultats obtenus ne confirment l'hypothèse selon laquelle le facteur causant les crises est l'instabilité anticronique à la fase REM. Sono stati studiati con metodiche poligrafiche 3 soggetti (1 maschio e 2 femmine) affetti da emicrania cronica con attacchi notturni. In 2 di essi gli attacchi erano preceduti da incrementi ed irregolarità della pressione arteriosa. Tali modificazioni iniziavano durante il sonno N-REM e perduravano nel corso del sonno REM che precedeva il risveglio con cefalea. La frequenza cardiaca non si modificava prima dell'attacco. I risultati ottenuti non confermano l'ipotesi che il fattore precipitante gli attacchi emicranici sia l'instabilità anticronica della fase REM.

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