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.

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.

Baroreceptor-mediated compensation for hemodynamic effects of positive end-expiratory pressure

1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Baroreceptor Reflex ◽  
Right Atrial ◽  
Positive End Expiratory Pressure ◽  
Carotid Baroreceptor ◽  
The Right

The roles of the carotid arterial baroreceptor reflex and of vagally mediated mechanisms during positive end-expiratory pressure (PEEP) were determined in pentobarbital-anesthetized dogs with isolated carotid sinuses. Spontaneously breathing dogs were placed on PEEP (5–10 cmH2O) with the carotid sinus pressure set to the systemic arterial pressure (with feedback) or to a constant pressure (no feedback). Right atrial volume was measured with a conductance catheter. With carotid baroreceptor feedback before bilateral cervical vagotomy, total peripheral resistance increased ( P < 0.01) and mean arterial pressure decreased (−9.8 ± 4.3 mmHg) in response to PEEP. With no feedback after vagotomy, mean arterial pressure decreased to a greater extent (−45 ± 6 mmHg, P < 0.01), and total peripheral resistance decreased ( P < 0.05) in response to PEEP. In contrast, cardiac index decreased similarly during PEEP ( P < 0.01) for all baroreceptor and vagal inputs. This response comprised a decrease in the passive phase of right ventricular filling ( P< 0.01) that was not matched by the estimated increase in active right atrial output. Although the carotid baroreceptor reflex and vagally mediated mechanisms elicit vasoconstriction to compensate for the effects of PEEP on the arterial pressure, these processes fail to defend cardiac output because of the profound effect of PEEP on the passive filling of the right ventricle.

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

Effect of increased afterload on right ventricular function in newborn pigs

1989 ◽  
Vol 66 (2) ◽  
pp. 863-869 ◽  
Author(s):  
J. Belik ◽  
R. B. Light
Keyword(s):  
Arterial Pressure ◽  
Right Ventricular ◽  
Ductus Arteriosus ◽  
Progressive Increase ◽  
Systemic Arterial Pressure ◽  
Right Atrial ◽  
Stroke Work ◽  
Mean Pulmonary Arterial Pressure ◽  
Group I ◽  
Group Ii

The effect of a progressive increase in right ventricular (RV) afterload was studied in pigs less than 24 h (group I) and 3–5 days old (group III). RV load was applied to increase mean pulmonary arterial pressure (Ppa) until right to left shunt was observed. Initially, pigs in group I had a significantly lower systemic arterial pressure (Psa = 63 +/- 2 vs. 82 +/- 5 mmHg) and higher Ppa (30 +/- 1 vs. 23 +/- 2 mmHg) even though the RV stroke work (RVSW) was similar (54.3 +/- 10.8 vs. 32.4 +/- 2.1 mmHg/ml) to group II. After a progressive rise in afterload, pigs in group I could maintain a higher RV stroke volume than those in group II (1.3 +/- 0.3 vs. 0.4 +/- 0.1 ml; P less than 0.05). At shunt condition, the RVSW was increased by 21 +/- 14% of the initial value in group I vs. a 32 +/- 8% decrease in group II (P less than 0.05). The ductus arteriosus was constricted and right-to-left shunt was observed in all animals at the foramen ovale level even though Ppa exceeded Psa before the rise in the right atrial pressure in group I. Thus, as RV afterload is increased in the pig, the older animals' right ventricle is progressively less capable of maintaining pulmonary blood flow than animals within 24 h of birth.

Effects of intraphrenic injection of potassium on diaphragm activation

1993 ◽  
Vol 74 (3) ◽  
pp. 1186-1194 ◽  
Author(s):  
G. S. Supinski ◽  
T. Dick ◽  
D. Stofan ◽  
A. F. DiMarco
Keyword(s):  
Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Diaphragm Muscle ◽  
Emg Activity ◽  
Inferior Phrenic Artery ◽  
Excitatory Response ◽  
Integrated Emg ◽  
Phrenic Artery ◽  
Sustained Increase

The purpose of the present study was to determine whether potassium, injected into the arterial supply of the diaphragm, would reflexly alter efferent diaphragmatic motor outflow and systemic arterial pressure. Studies were performed using in situ canine diaphragm muscle strips in which the inferior phrenic artery and vein were cannulated and all other sources of strip blood flow were ligated. Injection of potassium (0.1 meq) into the inferior phrenic artery elicited a small transient (1–2 breaths) decrease in the peak strip tension developed during spontaneous muscle contractions, in peak integrated strip electromyographic (EMG) activity, and in the peak integrated EMG activity of the contralateral hemidiaphragm. This was followed by a more pronounced and more sustained increase in each of these parameters as well as an increase in systemic arterial pressure. This latter excitatory response was qualitatively similar to that induced by the injection of capsaicin (5 and 25 micrograms) into the phrenic artery. Section of the left phrenic nerve abolished the effects of intra-arterial potassium and capsaicin on systemic arterial pressure and right hemidiaphragm EMG activity. These data support the existence of a potent excitatory phrenic-to-phrenic reflex that can be activated by potassium injection into the diaphragm. Activation of this pathway increases diaphragm motor activation and augments systemic arterial pressure.

Deep Pericardial Stitch Enables Hemodynamically Stable Exposure of Beating Heart

2003 ◽  
Vol 11 (3) ◽  
pp. 203-207 ◽  
Author(s):  
Bartlomiej Perek ◽  
Marek Jemielity ◽  
Jadwiga Tomczyk ◽  
Estilita Camacho ◽  
Wojciech Dyszkiewicz
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Artery Bypass ◽  
Systolic Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Stroke Index ◽  
Circumflex Artery ◽  
Off Pump ◽  
Before And After ◽  
Pump Coronary Artery Bypass

The use of a deep pericardial stitch to obtain optimal exposure for precise distal anastomoses was assessed in 51 patients (mean age, 56.5 ± 9.1 years) undergoing off-pump coronary artery bypass grafting. Hemodynamic data were recorded after sternotomy, before, and after each of the 120 distal anastomosis. Most hemodynamic parameters did not change throughout the procedures. During exposure of the circumflex artery, there were significant decreases in systolic arterial pressure from 106.0 ± 15.5 to 87.7 ± 13.6 mm Hg, mean systemic arterial pressure from 83.9 ± 11.7 to 68.5 ± 17.0 mm Hg, stroke volume from 68.5 ± 23.3 to 50.5 ± 18.3 mL, and stroke index from 34.4 ± 11.5 to 24.3 ± 8.7 mL·m−2. Cardiac function was not affected when other coronary arteries were bypassed. On completion of all anastomoses, hemodynamics returned to baseline status. It was concluded that the deep pericardial stitch enabled stable and safe exposure of the heart for off-pump coronary artery grafting.

A model of embolic chronic pulmonary hypertension in the dog

1984 ◽  
Vol 56 (3) ◽  
pp. 810-815 ◽  
Author(s):  
I. Shelub ◽  
A. van Grondelle ◽  
R. McCullough ◽  
S. Hofmeister ◽  
J. T. Reeves
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Histological Study ◽  
Systemic Arterial Pressure ◽  
Right Atrial ◽  
Pulmonary Vasodilation ◽  
Reliable Model ◽  
Chronic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Despite numerous efforts, a reliable model of chronic embolic pulmonary hypertension has not been established. To develop such a model five conscious mongrel dogs were embolized repeatedly over 16–30 wk with Sephadex microspheres 286 +/- 70 micron in diameter. Hemodynamic and respiratory measurements were obtained just prior to each embolization. Chronic pulmonary hypertension developed in all dogs. Pulmonary hypertension was not accounted for by increased cardiac output, wedge pressure, right atrial pressure, or systemic arterial pressure. Gas exchange was little altered. Lung histological study revealed microspheres clustered within vessels. In three dogs increased pulmonary arterial pressure was sustained despite cessation of embolization for up to 5 mo. Reembolization in one of these caused further pulmonary hypertension. In two dogs acute pulmonary vasodilation by O2 breathing and administration of prostaglandin E1 reduced, but did not abolish, the increased pulmonary vascular resistance, suggesting some vascular tone was present. An embolic model of chronic pulmonary hypertension in awake dogs allows further investigation into the evolution of pulmonary hypertension.

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