Breathing response to lung congestion with and without left heart distension

1988 ◽  
Vol 65 (1) ◽  
pp. 131-136 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Main Pulmonary Artery ◽  
Vagal Afferents ◽  
Left Heart ◽  
Anesthetized Dogs ◽  
Group 3 ◽  
Group 2 ◽  
Lung Vessels ◽  
Depressor Reflex ◽  
Depressor Effect

This study compared the effect of lung congestion with and without left heart (LH) distension on breathing frequency (fr) and discriminated among responses mediated by myelinated and nonmyelinated vagal afferents. Cardiopulmonary bypass perfusion of anesthetized dogs was used to isolate reflexes. The following three groups were prepared: 1) lung vessels pressurized by pumping into the main pulmonary artery (MPA); 2) lungs and fibrillating LH pressurized by pumping into MPA while draining from LH; 3) lungs congested by occluding several pulmonary veins while holding cardiac output constant. Congestion of lungs alone in groups 1 and 3 depressed fr. Congestion of lungs and distension of LH (group 2) caused transient depression of fr but a steady-state excitation. Cooling cervical vagi to 8 degrees C prevented depression of fr by congestion in all groups. In groups 1 and 2, in which MPA pressure was higher than in group 3, congestion during vagal cooling stimulated breathing. I conclude that lung congestion may stimulate fr via C-fiber afferents, but this may be overcome by a depressor effect via myelinated afferents. Simultaneous LH distension may reflexly stimulate breathing and overcome the lung depressor reflex.

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by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle.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.

Reflex effects of left heart and pulmonary vascular distension on airways of dogs

1980 ◽  
Vol 49 (4) ◽  
pp. 620-626 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Dynamic Compliance ◽  
Pulmonary Congestion ◽  
Wall Tension ◽  
Left Heart ◽  
Pulmonary Vessels ◽  
Vascular Congestion ◽  
Inspiratory Resistance ◽  
Anesthetized Dogs ◽  
Lung Vessels ◽  
Airway Tone

Two types of experiments were performed in anesthetized dogs on cardiopulmonary bypass to see if pulmonary vascular congestion and left heart distension would induce reflex bronchoconstriction. First we distended the isolated left heart and lung vessels with blood while ventilating the lungs and measuring airflow, tidal volume, and transpulmonary pressures. Congestion reduced dynamic compliance and increased inspiratory resistance. Vagotomy increased compliance and decreased resistance but did not alter the effects of congestion. Then we measured changes in tracheal wall tension while we separately distended the pulmonary vessels and left heart. Left heart distension increased tracheal tension, whereas pulmonary congestion increased tension in some dogs but decreased it in others. All effects were eliminated by vagotomy. We concluded that although left heart distension and pulmonary vascular congestion may reflexly increase airway tone, pulmonary congestion may at some times reflexly reduce tone. None of these reflex changes, however, appear to be important in the modest (approximately 20%) changes in airflow dynamics observed during combined left heart and pulmonary vascular distension.

Abstract 15733: Long-Term Follow-Up of Patients With Paroxysmal Atrial Fibrillation and Severe Left Atrial Scarring: Comparison Between Pulmonary Vein Antrum Isolation Only or PVAI Combined With Either Scar Homogenization or Trigger Ablation

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Sanghamitra Mohanty ◽  
Prasant Mohanty ◽  
Luigi Di Biase ◽  
Chintan Trivedi ◽  
Rong Bai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Paroxysmal Atrial Fibrillation ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Group 3 ◽  
Group 2

Background: Left atrial (LA) scarring, a consequence of cardiac fibrosis is a powerful predictor of procedure-outcome in atrial fibrillation (AF) patients undergoing catheter ablation. We sought to compare the long-term outcome in patients with paroxysmal AF and severe LA scarring/fibrosis identified by 3D mapping undergoing ablation of the pulmonary veins (PVAI) only or PVAI and the entire scar areas (scar homogenization) or PVAI plus ablation of the non-PV triggers. Methods: One-hundred seventy seven consecutive patients with paroxysmal atrial fibrillation and severe left atrial scarring were included in this study. LA scarring was diagnosed by 3D voltage mapping. The degree of scar was described as severe when >60% of the LA area was involved. Non-PV triggers were defined as ectopic triggers originating from sites other than pulmonary veins such as interatrial septum, superior vena cava, left atrial appendage, ligament of Marshall, crista terminalis and coronary sinus. Patients underwent ablation of the pulmonary vein antrum (PVAI) only (n=45, group 1), PVAI extended to the entire scar areas (scar homogenization [n=66, group 2]) or PVAI plus ablation of non-PV triggers (n=66, group 3). Choice of ablation strategy was determined by the operator. Patients were followed up for arrhythmia recurrence with event recorders, ECG and Holter monitoring. Results: Baseline characteristics were not different between the groups (age 63±9 vs 58±10 vs. 60±11 years, p=0.23; male 71%, vs. 72% vs. 73% p= 0.91). After a single procedure, all patients were followed-up for a minimum of two years. The long-term success rate at the end of the follow up was 19% (12 pts) in group 1, 21% (14 pts) in group 2, and 61% (40 pts) in group 3. Kaplan-Meier log-rank test indicated that the cumulative probability of AF-free survival was significantly higher in group 3 (overall log-rank p <0.001, pairwise comparison 1 vs. 3 and 2 vs. 3 was significant at p<0.01). Conclusions: In patients with paroxysmal atrial fibrillation and severe left atrial scarring, PVAI plus ablation of non-PV triggers is associated with significantly better long-term outcome than PVAI alone or when PVAI is combined with scar homogenization.

Pulmonary vascular effects of serotonin (5-OH-tryptamine) in dogs: its role in causing pulmonary edema

1959 ◽  
Vol 197 (5) ◽  
pp. 955-958 ◽  
Author(s):  
S. A. Kabins ◽  
C. Molina ◽  
L. N. Katz
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Left Heart ◽  
Vascular Effects ◽  
Left Heart Failure ◽  
Rapid Injection ◽  
Anesthetized Dogs ◽  
Group 3 ◽  
Group Ii

Rapid injection of serotonin (0.5–6.5 mg) was made into the pulmonary artery in 22 experiments in 12 open-chest anesthetized dogs. Serotonin caused pulmonary arteriolar and venous constriction in the majority of experiments, shown by an increase in the pressure gradients between the pulmonary artery and pulmonary artery wedge pressures, and between the latter and the left atrial pressure, respectively. Three groups of responses were obtained as far as the production of pulmonary edema is concerned. The first group (3 dogs) showed no pulmonary edema. The second ( group II—6 dogs) showed moderate to severe bilateral pulmonary edema without evidence of left heart failure. The third (3 dogs) also showed severe bilateral pulmonary edema but in the presence of left heart failure. In group II, the evidence suggests that an increase in capillary permeability is responsible, at least in part, for the pulmonary edema found. The similarity of results in group II to those obtained in the formation of bilateral pulmonary edema following unilateral starch embolization, suggests that serotonin could be the initiating factor in the neurohumoral mechanisms involved—or one of them.

Effect of increased left atrial pressure on breathing frequency in anesthetized dog

1990 ◽  
Vol 69 (6) ◽  
pp. 1973-1980 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Breathing Frequency ◽  
Anesthetized Dogs ◽  
The Right

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.

Radiocontrast medium-induced declines in renal function: a role for oxygen free radicals

1990 ◽  
Vol 258 (1) ◽  
pp. F115-F120 ◽  
Author(s):  
G. L. Bakris ◽  
N. Lass ◽  
A. O. Gaber ◽  
J. D. Jones ◽  
J. C. Burnett
Keyword(s):  
Filtration Rate ◽  
Oxygen Free Radicals ◽  
Oxygen Free Radical ◽  
Group 4 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Group 3 ◽  
Group 2 ◽  
Radiocontrast Medium ◽  
Group 1

Intrarenal injection of radiocontrast medium (RCM) results in transient vasoconstriction and a persistent decline in glomerular filtration rate (GFR). Adenosine modulates this vasoconstrictor response and is postulated to increase oxygen free radical (OFR) generation. We hypothesized that the persistent decline in (GFR that follows RCM administration results in an increased generation of OFR. We evaluated the effects of RCM injection on renal blood flow, inulin clearance, hypoxanthine, xanthine, and malondialdehyde concentrations in four groups of non-volume-expanded, pentobarbital sodium anesthetized dogs in the presence and absence of intravenous allopurinol, 25 mg/min (group 1), intrarenal superoxide dismutase (SOD), 400 U/min (group 2), heat-inactivated intrarenal SOD, 400 U/min (group 3), and simultaneous infusions of intrarenal SOD, 400 U/min, to one kidney and saline to the other (group 4). Both allopurinol and SOD significantly attenuated the fall in GFR after RCM administration over control. Malondialdehyde concentrations were attenuated over control in all treated groups, indicating a decrease in OFR generation. We conclude that intrarenal injection of RCM results in increased production of OFR. Inhibition of OFR production by allopurinol and increased OFR removal by SOD attenuates the effects of RCM on declines in GFR.

scholarly journals EXPRESS: Pulmonary vasodilator treatment in pulmonary hypertension due to left heart or lung disease: time for a high-definition picture?

2021 ◽  
pp. 204589402110180
Author(s):  
Lucilla Piccari ◽  
Roberto J Bernardo ◽  
Diego Rodríguez ◽  
Patrizio Vitulo ◽  
Stephen John Wort ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Randomised Controlled Trials ◽  
Controlled Trials ◽  
Left Heart ◽  
Pulmonary Vasodilators ◽  
Pulmonary Vasodilator ◽  
Vasodilator Treatment ◽  
Group 3 ◽  
Group 2 ◽  
Randomised Controlled

Dear Editor, We read with great interest the article “Outcomes of pulmonary vasodilator use in Veterans with pulmonary hypertension associated with left heart disease and lung disease” by Gillmeyer et al. The study findings of increased risk of death or organ failure in patients exposed to pulmonary vasodilators, are consistent with findings from randomised clinical trials and other cohort studies and “real-world scenarios”, as quoted by the authors. However, a very important lesson from over two decades of studies is that proper phenotyping of pulmonary vascular disease is key to assess risk of progression of disease. As we progress in the study of these phenotypes, both in Group 2 and Group 3 PH, we might understand which mechanisms produce these subtle but clear differences in response to vasodilator treatment. We fully agree with the authors of the paper that the use of pulmonary vasodilators in Group 2 and Group 3 PH should be confined to randomised-controlled trials, not only in order to gather data on the numerous safety concerns, but also in order to generate new, reliable evidence. We also think that the use of registries will help garner more information on “real-world” scenarios and confirm on retrospective cohorts the results obtained in randomised-controlled trials, provided we are careful to study disease groups and subgroups appropriately, avoiding the temptation of lumping them together in a bigger cohort which will inevitably mixed pears with apples. Furthermore, in full agreement with the recommendations for future directions in research on Group 3 PH, we call for studies that delve deeper into these heterogeneous groups of diseases. After the low-definition group photos, we believe it is time to zoom in the picture to gather a better understanding of what exactly is killing the different subgroups within Group 2 and Group 3 PH patients.

scholarly journals EXPRESS: Outcomes of pulmonary vasodilator use in Veterans with pulmonary hypertension associated with left heart disease and lung disease

2021 ◽  
pp. 204589402110017
Author(s):  
Kari Gillmeyer ◽  
Donald R. Miller ◽  
Mark E. Glickman ◽  
Shirley X. Qian ◽  
Elizabeth Klings ◽  
...  
Keyword(s):  
Primary Outcome ◽  
Case Control Study ◽  
Case Control ◽  
Left Heart ◽  
Disease Group ◽  
Pulmonary Vasodilators ◽  
Increased Risk ◽  
Group 3 ◽  
Group 2 ◽  
Control Study

Randomized trials of pulmonary vasodilators in pulmonary hypertension (PH) due to left heart disease (Group 2) and lung disease (Group 3) have demonstrated potential for harm. Yet these therapies are commonly used in practice. Little is known of the effects of treatment outside of clinical trials. We aimed to establish outcomes of vasodilator treatment for Groups 2/3 PH in real-world practice. We conducted a retrospective cohort study of 132,552 Medicare-eligible Veterans with incident Groups 2/3 PH between 2006-2016, and a secondary nested case-control study. Our primary outcome was a composite of death by any cause or selected acute organ failures. In our cohort analysis, we calculated adjusted risks of time to our outcome using Cox proportional hazards models with facility-specific random effects. In our case-control analysis, we used logistic mixed-effects models to estimate the effect of any past, recent, and cumulative exposure on our outcome. From our cohort study, 3,249 (2.5%) Veterans were exposed to pulmonary vasodilators. Exposure to vasodilators was associated with increased risk of our primary outcome, in both Group 3 (HR 1.58 [95% CI 1.37-1.82]) and Group 2 (HR 1.26 [1.12-1.41]) PH patients. The case-control study determined odds of our outcome increased by 11% per year of exposure (OR 1.11 [1.07-1.16]). Treating Groups 2/3 PH with vasodilators in clinical practice is associated with increased risk of harm. This extension of trial findings to a real-world setting offers further evidence to limit use of vasodilators in Groups 2/3 PH outside of clinical trials.

scholarly journals REMOdELLING OF THE LEFT ATRIAL AT THE PATIENTS WITH ATRIAL FIBRILLATION IN VARIOuS METHOdS OF SINuS RHYTHM RECOVERY

2017 ◽  
Vol 9 (2) ◽  
pp. 51-59
Author(s):  
T Y Gromyko ◽  
S A Sayganov
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Medical Therapy ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Tissue Doppler ◽  
Estimated Parameters ◽  
Reliable Parameter ◽  
Group 3 ◽  
Group 2

Aim. To compare features of straight and return remodeling of the left atrial (LA) at patients with atrial fibrillation (AF) at various options of sinus rhythm (SR) restoration depending of a choice of the cardioversion. Material and methods. We examined.153 patients with the nonvalvular AF lasting from24 hours to 6 months. All patients were divided in 3 groups. In group 1 (49 patients) SR was restored medically, in the group 2 (57 patients) SR was restored by means of electrical cardioversion (EC), in the group 3 (47 patients) underwent radio-frequency isolation of pulmonary veins (RFI PV). Echocardiog- raphy was performed to all patients at the time of AF, and also on 1, 3, 5, 15 days and in 6 months after recovery of SR with an assessment systolic and the diastolic function of left ventricle (LV), thickness of walls of a myocardium, the front and back size of the LA, volume of LA, and also design parameter of LA pressure (E\E’) by Tissue doppler visualization.Results. Index LA (ILA) authentically decreased at the patients, who are exposed to RFI PV, at preservation of SR compared with recurrence of AF for 6 months (р<0,05). In group of medical therapy index of volume LA (IVLA) initially it was authentically lower at patients with resistant SR for 6 months, compared with recurrence of AF (р<0,05). And also IVLA authentically decreased in group RFI PV without paroxysms of AF for 6 months (р<0,001). At the medical cardioversion LA pressure (E\E’) authentically decreased by 2 weeks (р<0,05) without paroxysms of AF and significantly didn't change by 6 months. While in the presence of paroxysms of AF for 6 months only the tendency to de- crease of this parameter was noted. And in group of RFI PV reliable dynamics of pressure in LA was recorded at patients without paroxysms of AF by 2 weeks (р<0,05) and by 6 months (р<0,05). While in the presence of paroxysms of AF this parameter significantly didn't change by 6 months. In the group of EC reliable dynamics of the estimated parameters of LA remodeling isn't detected.Conclusions. At patients with AF after cardioversion and without paroxysms of AF for 6 months LA sizes authentically decrease in group of medical therapy (IVLA, (р<0,05)) and at RFI PV (ILA, (р<0,05), IVLA (р<0,001)). LA pressure (E/E’) could be considered as a reliable parameter of the return remodeling of LA after cardioversion and without paroxysms of AF for 6 months in cases of medical therapy (р<0,05) and RFI PV (р<0,05).

Effect of jugular venous pressure on cerebral autoregulation in dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1516-H1524
Author(s):  
R. W. McPherson ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Autoregulation ◽  
Venous Pressure ◽  
Transmural Pressure ◽  
Periventricular White Matter ◽  
Jugular Venous Pressure ◽  
Cerebrovascular Resistance ◽  
Anesthetized Dogs ◽  
Group 3 ◽  
Group 2

We determined the importance of a myogenic sensor of cerebral autoregulation by assessing the effect of vascular transmural pressure on cerebral blood flow (CBF) as cerebral perfusion pressure (CPP) was decreased. Decreasing CPP by decreased arterial pressure (Pa) or increased intracranial pressure (Pcsf) decreases transmural pressure, whereas increased jugular venous pressure (Pjv) increases transmural pressure. Regional CBF was measured in barbiturate-anesthetized dogs using radiolabeled microspheres. In group 1 (n = 5), CPP was decreased by decreasing Pa; in group 2 (n = 5), CPP was decreased by increasing Pcsf (Pa = 80 mmHg); and in group 3 (n = 5) CPP was decreased by increasing Pjv (Pa = 80 mmHg). CPP was reduced from 80 to 30 mmHg in 10-mm increments in each group. In groups 1 and 2 regional CBF was maintained as CPP was decreased to 40 mmHg; however, at CPP of 30 mmHg, blood flow to cerebrum, caudate, and periventricular white matter decreased, whereas flow to cerebellum and medulla remained unchanged. In group 3 regional CBF was unchanged as CPP decreased from 80 to 50 mmHg but decreased in all regions as CPP decreased further. In all three groups, cerebrovascular resistance continuously declined as CPP was decreased. In all groups, cerebral O2 uptake was unaltered. Autoregulation fails at a higher CPP with increased Pjv than with decreased Pa or increased Pcsf, particularly in brain stem. We conclude that metabolic autoregulation predominates over the myogenic mechanism until CPP is low.

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