Comparative effects of arachidonic acid, bisenoic prostaglandins, and an endoperoxide analog on the canine pulmonary vascular bed

1977 ◽  
Vol 55 (6) ◽  
pp. 1369-1377 ◽  
Author(s):  
Philip J. Kadowitz ◽  
Ernst W. Spannhake ◽  
Stan Greenberg ◽  
Larry P. Feigen ◽  
Albert L. Hyman
Keyword(s):  
Cardiac Output ◽  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Pulmonary Arterial Pressure ◽  
Superior Vena ◽  
Vena Cava ◽  
Aortic Pressure ◽  
Pulmonary Arterial

The effects of bolus injections of the postaglandin precursor, arachidonic acid, and PGD2, PGF2α, PGE2, and the PGH2 analog ((15S)-hydroxyl-9α,11α(epoxymethano)-prosta-5Z-dienoic acid) were compared on the pulmonary circulation in the intact spontaneously breathing pentobarbital-anesthetized dog. Arachidonic acid increased pulmonary arterial pressure, decreased aortic pressure, and increased cardiac output when injected into the superior vena cava or right atrium. PGE2, like arachidonic acid, increased pulmonary arterial pressure and cardiac output and decreased aortic pressure, whereas PGF2α and PGD2 increased pulmonary arterial pressure but did not affect cardiac output or aortic pressure when injected into the superior vena cava or right atrium. The PGH2 analog increased pulmonary arterial pressure and to a lesser extent, aortic pressure, without affecting cardiac output. None of these substances changed left atrial or right atrial pressure. The cardiopulmonary effects of arachidonic acid were blocked by indomethacin whereas the rise in pulmonary arterial pressure in response to the bisenoic prostaglandins and the analog were enhanced by the cyclooxygenase inhibitor. These data suggest that the increase in pulmonary vascular resistance in response to arachidonic acid may be due to conversion of the precursor into vasoactive intermediates and products such as bisenoic prostaglandins whereas the decrease in systemic vascular resistance is probably due to the formation of PGE2 and other peripheral vasodilator substances.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

Developmental changes in oxygenation and circulatory responses to hypoxemia in lambs

1983 ◽  
Vol 245 (4) ◽  
pp. H674-H682 ◽  
Author(s):  
D. Sidi ◽  
J. R. Kuipers ◽  
D. Teitel ◽  
M. A. Heymann ◽  
A. M. Rudolph
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Regional Blood Flow ◽  
Saturation Pressure ◽  
Aortic Pressure ◽  
Pulmonary Arterial ◽  
Group 1

We studied moderate [fractional inspired O2 (FIO2) 0.09] and severe (FIO2 0.06) hypoxemia in 21 lambs (group 1, 1 wk old; group 2, 3-4 wk old; group 3, 5-7 wk). With moderate hypoxemia, all groups increased heart rate, cardiac output, and pulmonary arterial pressure and decreased systemic and pulmonary vascular resistance; cardiac output and pulmonary arterial pressure increases were less in group 1, because of higher resting values. With severe hypoxemia, heart rate increased similarly, cardiac output was unchanged, and aortic pressure fell associated with severe metabolic acidosis or arrhythmias. Regional blood flow changed similarly in all groups; heart and brain flow increased, carcass flow was unchanged, and skin, GI tract, and kidney flow fell. O2 consumption (VO2) and mixed venous PO2 decreased, though O2 saturation was higher in group 1 due to the lower O2 half-saturation pressure of hemoglobin. With a given decreased VO2 there was more metabolic acidosis in older lambs and an increased VO2 after termination of hypoxemia, suggesting greater O2 debt. As in the fetus, young lambs are better able to tolerate a decreased VO2 than older lambs.

Assessment of superior vena cava flow and cardiac output in different patterns of patent ductus arteriosus shunt

2021 ◽  
Author(s):  
Adrianne Rahde Bischoff ◽  
Regan E. Giesinger ◽  
Amy H. Stanford ◽  
Ravi Ashwath ◽  
Patrick J. McNamara
Keyword(s):  
Cardiac Output ◽  
Patent Ductus Arteriosus ◽  
Superior Vena Cava ◽  
Superior Vena ◽  
Ductus Arteriosus ◽  
Vena Cava ◽  
Patent Ductus

scholarly journals P649 Before and after: sinus venosus atrial septal defect

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I Marco Clement ◽  
R Eiros ◽  
R Dalmau ◽  
T Lopez ◽  
G Guzman ◽  
...  
Keyword(s):  
Atrial Septal Defect ◽  
Left Atrium ◽  
Atrial Flutter ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Septal Defect ◽  
Superior Vena ◽  
Pulmonary Veins ◽  
Vena Cava ◽  
The Right

Abstract Introduction The diagnosis of sinus venosus atrial septal defect (SVASD) is complex and requires special imaging. Surgery is the conventional treatment; however, transcatheter repair may become an attractive option. Case report A 60 year-old woman was admitted to the cardiology department with several episodes of paroxysmal atrial flutter, atrial fibrillation and atrioventricular nodal reentrant tachycardia. She reported a 10-year history of occasional palpitations which had not been studied. A transthoracic echocardiography revealed severe right ventricle dilatation and moderate dysfunction. Right volume overload appeared to be secondary to a superior SVASD with partial anomalous pulmonary venous drainage. A transesophageal echocardiography confirmed the diagnosis revealing a large SVASD of 16x12 mm (Figure A) with left-right shunt (Qp/Qs 2,2) and two right pulmonary veins draining into the right superior vena cava. Additionally, it demonstrated coronary sinus dilatation secondary to persistent left superior vena cava. CMR and cardiac CT showed right superior and middle pulmonary veins draining into the right superior vena cava 18 mm above the septal defect (Figures B and C). After discussion in clinical session, a percutaneous approach was planned to correct the septal defect and anomalous pulmonary drainage. For this purpose, anatomical data obtained from CMR and CT was needed to plan the procedure. During the intervention two stents graft were deployed in the right superior vena cava. The distal stent was flared at the septal defect level so as to occlude it while redirecting the anomalous pulmonary venous flow to the left atrium (Figure D). Control CT confirmed the complete occlusion of the SVASD without residual communication from pulmonary veins to the right superior vena cava or the right atrium (Figure E). Anomalous right superior and middle pulmonary veins drained into the left atrium below the stents. Transthoracic echocardiographies showed progressive reduction of right atrium and ventricle dilatation. The patient also underwent successful ablation of atrial flutter and intranodal tachycardia. She is currently asymptomatic, without dyspnea or arrhythmic recurrences. Conclusions In this case, multimodality imaging played a key role in every stage of the clinical process. First, it provided the diagnosis and enabled an accurate understanding of the patient’s anatomy, particularly of the anomalous pulmonary venous connections. Secondly, it allowed a transcatheter approach by supplying essential information to guide the procedure. Finally, it assessed the effectiveness of the intervention and the improvement in cardiac hemodynamics during follow-up. Abstract P649 Figure.

Increased cardiac output following occlusion of the descending thoracic aorta in dogs

1982 ◽  
Vol 243 (1) ◽  
pp. R152-R158 ◽  
Author(s):  
J. K. Stene ◽  
B. Burns ◽  
S. Permutt ◽  
P. Caldini ◽  
M. Shanoff
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Superior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Mean Systemic Pressure ◽  
Extracorporeal Bypass

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

TYPES OF CORRECTION OF THE SUPRACARDIAC FORM OF PARTIAL ABNORMAL DRAINAGE OF THE PULMONARY VEINS. WARDEN PROCEDURE

2021 ◽  
pp. 28-31
Author(s):  
Inkar Sagatov ◽  
Nurzhan Dosmailov
Keyword(s):  
Left Atrium ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Superior Vena ◽  
Pulmonary Veins ◽  
Vena Cava ◽  
Artificial Circulation ◽  
The Right

The article describes the types of correction of the supracardial form of abnormal drainage of the pulmonary veins. One of the methods of correcting this defect is the Warden operation, which includes: after sternotomy, connection of artificial circulation, cardioplegia, the superior vena cava is cut off, the proximal end is sutured. Next, a right atriotomy is performed, an anastomosis is formed using an autopericardial patch between the abnormal drainage and the left atrium through the ASD. Then an anastomosis is formed between the auricle of the right atrium and the distal end of the superior vena cava. As a result, blood from the abnormal pulmonary veins begins to drain into the left atrium through the ASD.

Cardiorespiratory effects of rapid saline infusion in normal man

1975 ◽  
Vol 38 (5) ◽  
pp. 786-775 ◽  
Author(s):  
A. L. Muir ◽  
D. C. Flenley ◽  
B. J. Kirby ◽  
M. F. Sudlow ◽  
A. R. Guyatt ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Control Period ◽  
Lung Compliance ◽  
Saline Infusion ◽  
Tidal Range ◽  
Closing Volume ◽  
Rapid Infusion ◽  
Pulmonary Arterial

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

Persistent left superior vena cava and its clinical correlation - A cadaveric study

2021 ◽  
Vol 12 (4) ◽  
pp. 118-121
Author(s):  
Sachendra Kumar Mittal ◽  
Rekha Parashar ◽  
Pankaj Kumar Singh ◽  
Leena Jadon
Keyword(s):  
Superior Vena Cava ◽  
Right Atrium ◽  
Superior Vena ◽  
Vena Cava ◽  
Medical Sciences ◽  
Left Superior Vena Cava ◽  
Persistent Left Superior Vena ◽  
Male Cadaver ◽  
The Right ◽  
Brachiocephalic Veins

Background: Presented is a case of persistent left superior vena cava draining into the right atrium through coronary sinus and finally opens into right atrium. Abnormalities of the vascular system are more commonly seen due to its importance in circulation. Persistent left superior vena cava is rare but important congenital vascular anomaly. It results when the left superior cardinal vein caudal to the innominate vein fails to regress.The venous anomaly of a persistent left superior vena cava (PLSVC) affects 0.3%–0.5% of the general population. Normally the superior vena cava is a single vascular structure formed by the union of right and left brachiocephalic veins which are in turn formed by the union of internal jugular and subclavian veins of corresponding side, draining the head and neck as well as the superior extremity. Aims and Objective: To evaluate the accuracy of persistent left superior vena cava and to find out the opening of PLSVC and formations of both SVC. Materials and Methods: During routine dissection of Thorax, we have opened the thoracic cage and take out the Heart. during that we found separate SVC and then we did the study on this PLSVC in the Department of Anatomy, Jaipur National University Institute for Medical Sciences and Research Centre (JNUIMSRC) Jaipur and National Institute of Medical Sciences and Research (NIMS & R). Results: We found persistent left superior vena cava in two cadavers out of 30 cadavers (6.66%) one was 64-year-old male cadaver and another 72-year-old male cadaver. Both the vena cavae were formed as of brachiocephalic veins of the corresponding side. The persistent left superior vena cava opened into the enlarged coronary sinus that drained into the right atrium between the opening of inferior vena cava and right atrio-ventricular orifice. Conclusion: It has important clinical implications in certain clinical interventions. It may complicate placementof cardiac catheters or pacemaker leads.

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