Transmural metabolic gradients in the normal dog left ventricle: effect of right atrial pacing

1977 ◽  
Vol 233 (2) ◽  
pp. H217-H221 ◽  
Author(s):  
T. B. Allison ◽  
J. W. Holsinger
Keyword(s):  
Right Atrial ◽  
Control Group ◽  
Base Line ◽  
Atrial Pacing ◽  
Stroke Work ◽  
Ischemic Insult ◽  
Circumflex Artery ◽  
Heart Work ◽  
Anesthetized Dogs ◽  
The Right

The effects of atrial pacing on tissue metabolite levels known to be sensitive to ischemia were examined. Anesthetized dogs were thoracotomized and a pacing electrode was sutured to the right atrium. Pacing at rates of 200 or 250 beats/min (10 animals per group) was performed for 15 min after base-line hemodynamic data had been obtained. At the end of the pacing period, a transmural biopsy was taken, frozen in liquid nitrogen, and sectioned into subepicardial, midmyocardial, and subendocardial layers. ATP, phosphocreatine, lactate, and glycogen were extracted and analyzed. Significant (P less than 0.001) transmural gradients of each of these metabolites existed in the control group. Pacing had no significant (P greater than 0.2) effect on any metabolite from layer to layer at 200 or 250 beats/min. However, indices of heart work (i.e., contractility (dP/dt), stroke work, and stroke volume) demonstrated significant reductions (P less than 0.01) due to pacing, while circumflex artery blood flow increased more than twofold (P less than 0.001) at the highest rate. These data suggest that physiologic autoregulation occurred during pacing and protected the subendocardium from stress-induced ischemic insult.

Influence of the right ventricle on canine left ventricular function with PEEP

1982 ◽  
Vol 52 (1) ◽  
pp. 254-259 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Arterial Occlusion ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Stroke Work ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
The Right ◽  
Extracorporeal Bypass

In anesthetized dogs we evaluated the influence of increased right ventricular (RV) pressures on left ventricular (LV) function by comparing the hemodynamic effects of increases in RV afterload (pulmonary arterial pressure) produced by positive end-expiratory pressure (PEEP) with those due to pulmonary arterial occlusion (PAO). Left atrial (Pla) and right atrial (Pra) pressures increased with PEEP and PAO [for Pla: 3.1 +/- 0.7 Torr (PEEP), 2.4 +/- 0.9 Torr (PAO); for Pra: 2.9 +/- 0.4 Torr (PEEP), 3.1 +/- 1.2 Torr (PAO)]. RV septal-free wall dimension (RVD) increased, and LV septal-posterolateral dimension (L2) decreased with both conditions [increases in RVD: 1.9 +/- 0.3 mm (PEEP), 2.2 +/- 0.5 mm (PAO); decrease in L2: 1.1 +/- 0.4 mm (PEEP), 0.9 +/- 0.3 mm (PAO)]. Extracorporeal bypass of the great veins did not alter these findings. LV function curves showed less stroke work at any Pla during PEEP, this being unaffected by vagotomy. When the RV was bypassed, there were no PEEP or PAO related changes in Pla or LV function. Thus diminished LV function with PEEP is probably due to the influence on the LV of a stressed RV in this situation.

Control of breathing in anesthetized dogs by a left-heart baroreflex

1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Vagal Afferents ◽  
Low Flow ◽  
Base Line ◽  
Left Heart ◽  
Breathing Frequency ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Vagal Cooling

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.

scholarly journals Prolonged Sinus Pauses upon Termination of Paroxysmal Atrial Fibrillation: Abnormal Right Atrial Electrophysiologic and Electroanatomic Findings

2017 ◽  
Vol 44 (2) ◽  
pp. 107-114 ◽  
Author(s):  
Zhengyu Bao ◽  
Hongwu Chen ◽  
Bing Yang ◽  
Michael Shehata ◽  
Weizhu Ju ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Node ◽  
P Wave ◽  
Right Atrial ◽  
Control Group ◽  
Paroxysmal Supraventricular Tachycardia ◽  
Group A ◽  
Group B ◽  
Activation Times ◽  
The Right

The efficacy of pulmonary vein antral isolation for patients with prolonged sinus pauses (PSP) on termination of atrial fibrillation has been reported. We studied the right atrial (RA) electrophysiologic and electroanatomic characteristics in such patients. Forty patients underwent electroanatomic mapping of the RA: 13 had PSP (group A), 13 had no PSP (group B), and 14 had paroxysmal supraventricular tachycardia (control group C). Group A had longer P-wave durations in lead II than did groups B and C (115.5 ± 15.4 vs 99.5 ± 10.9 vs 96.5 ± 10.4 ms; P=0.001), and RA activation times (106.8 ± 13.8 vs 99 ± 8.7 vs 94.5 ± 9.1 s; P=0.02). Group A's PP intervals were longer during adenosine triphosphate testing before ablation (4.6 ± 2.3 vs 1.7 ± 0.6 vs 1.5 ± 1 s; P <0.001) and after ablation (4.7 ± 2.5 vs 2.2 ± 1.4 vs 1.6 ± 0.8 s; P <0.001), and group A had more complex electrograms (11.4% ± 5.4% vs 9.3% ± 1.6% vs 5.8% ± 1.6%; P <0.001). Compared with group C, group A had significantly longer corrected sinus node recovery times at a 400-ms pacing cycle length after ablation, larger RA volumes (100.1 ± 23.1 vs 83 ± 22.1 mL; P=0.04), and lower conduction velocities in the high posterior (0.87 ± 0.13 vs 1.02 ± 0.21 mm/ms; P=0.02) and high lateral RA (0.89 ± 0.2 vs 1.1 ± 0.35 mm/ms; P=0.04). We found that patients with PSP upon termination of atrial fibrillation have RA electrophysiologic and electroanatomic abnormalities that warrant post-ablation monitoring.

"Closing volume" changes in alloxan-induced pulmonary edema in anesthetized dogs

1975 ◽  
Vol 39 (2) ◽  
pp. 235-241 ◽  
Author(s):  
R. Lemen ◽  
J. G. Jones ◽  
P. D. Graf ◽  
G. Cowan
Keyword(s):  
Pulmonary Edema ◽  
Control Group ◽  
Closing Volume ◽  
Base Line ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Period 2 ◽  
System Pressure ◽  
Before And After ◽  
Anesthetized Dogs

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.

Optimal matching between canine left ventricle and afterload

1988 ◽  
Vol 254 (6) ◽  
pp. H1051-H1058
Author(s):  
E. S. Myhre ◽  
A. Johansen ◽  
H. Piene
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Stroke Work ◽  
External Work ◽  
Volume Load ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Volume Relationship ◽  
Optimal Values

A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external stroke work, optimum values of stroke volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure, RAP) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10–1.20 (RAP 5–15 mmHg); Emax/mEmax 1.21–1.41; and Rp/mRp 0.84–0.69. After LV depression, SV/mSV was 0.80–0.83, Emax/mEmax was 0.78–0.71, and Rp/mRp was 1.56–1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

Effect of cervical vagal stimulation on chicken heart rate and atrioventricular conduction

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw
Keyword(s):  
Heart Rate ◽  
Vagal Stimulation ◽  
Atrioventricular Conduction ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Chicken Heart ◽  
Av Conduction ◽  
Supramaximal Stimulation ◽  
The Right ◽  
Stimulation Of

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.

Effect of pacing on oxygen supply-to-consumption ratio in ischemic myocardium

1985 ◽  
Vol 249 (2) ◽  
pp. H249-H254
Author(s):  
G. J. Grover ◽  
H. R. Weiss
Keyword(s):  
Base Line ◽  
Atrial Pacing ◽  
Blood Flows ◽  
Consumption Ratio ◽  
Ischemic Region ◽  
Line Flow ◽  
Before And After ◽  
Anesthetized Dogs ◽  
O2 Supply ◽  
Partially Occluded

This study was performed to determine if the partially occluded myocardium could maintain its O2 supply-to-consumption ratio during atrial pacing. In 14 open-chest anesthetized dogs, the left anterior descending coronary artery was occluded to 50% of base-line flow, and in half of the dogs the hearts were paced to 50% above base-line heart rate. Blood flows were determined by use of microspheres before and after occlusion, and O2 supply-consumption variables were determined by use of microspectrophotometry. After occlusion in control and paced groups, blood flow was depressed in the ischemic region compared with the nonischemic region. In paced animals, blood flows in all regions were significantly higher compared with their respective values in nonpaced animals. After pacing, mean O2 consumption was 34% higher (53% in the occluded region) compared with control animals. The O2 supply-to-consumption ratio was similar in the occluded region of paced animals compared with the same region in controls. This ratio was lower in ischemic regions of both groups compared with their respective nonischemic regions. This indicates that, despite a reduced O2 supply-to-consumption ratio in the ischemic area, an unutilized reserve of flow exists.

Effect of autonomic neurotransmitters on excitable gap composition in canine atrial flutter

2001 ◽  
Vol 79 (1) ◽  
pp. 13-17
Author(s):  
Marc M Rahme ◽  
Elise Jalil ◽  
Martin Laflamme ◽  
Teresa Kus
Keyword(s):  
Atrial Flutter ◽  
Recovery Period ◽  
Safety Margin ◽  
Right Atrial ◽  
Constant Infusion ◽  
Anesthetized Dogs ◽  
Gap Characteristics ◽  
Excitable Gap ◽  
Right Atrial Appendage ◽  
The Right

Atrial arrhythmias are believed to be influenced by autonomic nervous system tone. We evaluated the effects of sympathetic and parasympathetic activation on atrial flutter (AFl) by determining the effects of norepinephrine (NE) and acetylcholine (ACh) on the composition of the excitable gap. A model of reentry around the tricuspid valve was produced in 17 chloralose anesthetized dogs using a Y-shaped lesion in the intercaval area that extended to the right atrial appendage. Excitable gap characteristics were determined during AFl by scanning diastole with a single premature extrastimulus at progressively shorter coupling intervals to define the reset-response curve. Measurements were made during a constant infusion of NE (15 µg/min) into the right coronary artery and repeated during ACh infusion (2 µg/min) following a 15 min recovery period. The excitable gap (27 ± 1 ms) was significantly (P < 0.001) increased by NE (34 ± 1 ms) and ACh (50 ± 2 ms). The fully excitable portion (7 ± 1 ms) was also significantly (P < 0.001) increased by NE (17 ± 1 ms) and ACh (43 ± 2 ms). We conclude that both neurotransmitters increase the safety margin of full excitability ahead of the wavefront, demonstrating that parasympathetic and sympathetic activation can facilitate the persistence of this refractory atrial arrhythmia.Key words: atrial flutter, acetylcholine, norepinephrine, excitable gap.

scholarly journals Atrial function after treatment of atrial septal defects in children under 5 years

2020 ◽  
Author(s):  
Eun-Young Choi ◽  
Eun Sun Kim ◽  
Jung-Yoon Kim ◽  
Su-Jin Park ◽  
Ja-kyoung Yoon ◽  
...  
Keyword(s):  
Right Atrium ◽  
Global Longitudinal Strain ◽  
Atrial Function ◽  
Right Atrial ◽  
Control Group ◽  
Closure Device ◽  
Right Atrial Function ◽  
One Year ◽  
Asd Closure ◽  
The Right

Abstract BackgroundRecently, the patient’s age of atrial septal defect (ASD) treatment has been gradually decreasing. However, the most appropriate age and treatment method remain controversial. We hypothesized that treatment of ASDs in patients under 5 years would be able to adequately normalize bi-atrial function over one year after treatment. The purpose of this study is to confirm the normalization of hypothesized atrial function.MethodsData of fifteen patients who underwent surgical ASD closure under 5 years of age (Operation group), 15 patients who underwent percutaneous ASD closure (Device group), and 15 age- and gender-matched normal control patients (Control group) were extracted from our echocardiographic data. Conventional 2D images and 2D speckle tracking method were used to evaluate bi-atrial function.ResultsLeft atrial function, εS, εE, and εA showed no significant differences in the three groups. Indicators representing the right atrial function varied with the three groups. However, there were no significant differences in the global longitudinal strain of the right atrium between the Operation and Device groups.ConclusionsAfter ASD treatment, right atrial function recovery is less than that of the left atrium. The function of the right atrium is not normalized after more than one year of treatment for ASD in patients under 5 years. After ASD treatment, further follow-up of the bi-atrial function is necessary.

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