Pulmonary arterial pressure changes in human newborn infants from birth to 3 days of age

1964 ◽  
Vol 65 (3) ◽  
pp. 327-333 ◽  
Author(s):  
George C. Emmanouilides ◽  
Arthur J. Moss ◽  
Edward R. Duffie ◽  
Forrest H. Adams
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Newborn Infants ◽  
Human Newborn ◽  
Pulmonary Arterial ◽  
Pressure Changes

Modulation of vascular reactivity to serotonin in the dog lung

1991 ◽  
Vol 71 (1) ◽  
pp. 217-222 ◽  
Author(s):  
W. F. Hofman ◽  
W. F. Jackson ◽  
H. el-Kashef ◽  
I. C. Ehrhart
Keyword(s):  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Venous Occlusion ◽  
Lung Lobe ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Pressure Changes ◽  
Related Increase

Experiments were conducted to compare the effects of cyclooxygenase inhibition (COI) on vascular reactivity to serotonin (5-HT) in the isolated blood-perfused canine left lower lung lobe (LLL) and in isolated canine intrapulmonary lobar artery rings with and without a functional endothelium. LLLs (n = 6), perfused at constant blood flow, were challenged with bolus doses of 50, 100, and 250 micrograms 5-HT before COI, after COI with 45 microM meclofenamate, and after infusion of prostacyclin (PGI2) during COI. Lobar vascular resistance was segmentally partitioned by venous occlusion. Pulmonary arterial pressure increased from 13.5 +/- 1.0 to 16.3 +/- 0.8 cmH2O (P less than 0.01) after COI but declined to 13.1 +/- 1.1 cmH2O (P less than 0.01) subsequent to PGI2 infusion (91.3 +/- 14.5 ng.min-1.g LLL-1). The pulmonary arterial pressure changes were related to changes in postcapillary resistance. The dose-dependent pressor response to 5-HT was potentiated by COI (P less than 0.01) but reversibly attenuated (P less than 0.05) by PGI2 infusion. Isolated intrapulmonary artery rings (2–4 mm diam) exhibited a dose-related increase in contractile tension to 5-HT. The response to 5-HT was enhanced (P less than 0.05) in rings devoid of a functional endothelium. However, COI (10 microM indomethacin) did not alter (P greater than 0.05) the dose-related increase in contractile tension to 5-HT in rings with an intact endothelium. Our results suggest that both PGI2 and endothelium-derived relaxing factors modulate pulmonary vascular reactivity to 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial pressure changes by drugs injected into isolated pulmonary circulation in dogs

1962 ◽  
Vol 203 (5) ◽  
pp. 947-950 ◽  
Author(s):  
Koichiro Takasaki
Keyword(s):  
Arterial Pressure ◽  
General Circulation ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Cardiovascular Effects ◽  
Left Pulmonary Artery ◽  
Systemic Arterial Pressure ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Pressure Changes

In open-chested, anesthetized dogs the pulmonary venous outflow of the left lung was diverted into an external bypass so that the flow rate could be measured and blood prevented from returning immediately to the general circulation. Pulmonary arterial pressure was recorded in the left pulmonary artery; systemic arterial pressure and heart rate were also recorded. Injection of nicotine, veratrine, or Veriloid into this limited lung circulation produced a systemic depressor response and bradycardia. Both effects were abolished by vagotomy. It is concluded that these systemic cardiovascular effects are mediated through vagal chemoreceptors. There is no reason to implicate a mechanical pulmonary depressor reflex since these drugs produce no change in the pulmonary arterial pressure.

scholarly journals Effect of Renal and Left Ventricular Function on Serial Pulmonary Arterial Pressure Changes after Device Closure of Atrial Septal Defect

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Chul Shin ◽  
Young Won Yoon ◽  
In-Soo Kim ◽  
Jong-Youn Kim ◽  
Pil-Ki Min ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Arterial Pressure ◽  
Septal Defect ◽  
Pulmonary Arterial Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Device Closure ◽  
Pulmonary Arterial ◽  
One Year ◽  
Pressure Changes

Background. The age of candidates for device closure of atrial septal defect (ASD) has been increasing. Thus, concerns exist about dyspnea aggravation or atrial fibrillation development after device closure due to augmentation of left ventricular (LV) and left atrial (LA) preload. This study aimed to examine patterns and determinants of serial pulmonary arterial pressure and left ventricular filling pressure changes after device closure of ASD. Methods. Among the 86 consecutive patients who underwent percutaneous device closure of ASD, those with end-stage renal disease or those without pre- or postprocedural Doppler data were excluded. The clinical, transesophageal, and transthoracic echocardiographic findings of 78 patients were collected at baseline, one-day postprocedure, and one-year follow-up. Results. The mean age of study patients was 49.8 ± 15.0 years, and the average maximal defect diameter and device size were 20.2 ± 6.0 mm and 23.8 ± 6.4 mm. Four patients (5.6%) underwent new-onset atrial fibrillation, and five patients (6.4%) took diuretics within one-year after closure. Some patients (n = 21; 27%) exhibited paradoxically increased tricuspid regurgitant velocity (TRV) one-day postprocedure; they also were older with lower e’, glomerular filtration rate, and LV ejection fraction and a higher LA volume index. However, even in these patients, TRV deceased below baseline levels one-year later. Both E/e’ and LA volume index significantly increased immediately after device closure, but all decreased one-year later. Larger defect size and higher TRV were significantly correlated with immediate E/e’ elevation. Conclusion. In older, renal, diastolic, and systolic dysfunctional patients with larger LA and scheduled for larger device implantation, peri-interventional preload reduction therapy would be beneficial.

Acute vasodilator testing following Fontan palliation: an opportunity to guide precision care?

2020 ◽  
Vol 30 (6) ◽  
pp. 829-833
Author(s):  
Ronald W. Day
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Fontan Procedure ◽  
Pulmonary Vasodilators ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Acute Changes ◽  
Pressure Changes ◽  
Fontan Palliation

AbstractBackground:Pulmonary vasodilators improve the functional capacity of some patients with pulmonary arterial hypertension. However, pulmonary vasodilators frequently fail to improve unequivocal endpoints of efficacy in patients with lower pulmonary arterial pressures who have been palliated with a Fontan procedure.Objective:Haemodynamic measurements and the results of acute vasodilator testing in a subset of patients were reviewed to determine whether some patients acutely respond more favourably to sildenafil and might be candidates for precision care with a phosphodiesterase V inhibitor long term.Materials and Methods:Heart catheterisation was performed in 11 patients with a Fontan procedure. Haemodynamic measurements were performed before and after treatment with intravenous sildenafil (mean 0.14, range 0.05–0.20 mg/kg). Results (mean ± standard deviation) were compared by paired and unpaired t-tests to identify statistically significant changes.Results:Sildenafil was acutely associated with changes in mean pulmonary arterial pressure, transpulmonary gradient, indexed blood flow, and indexed vascular resistance. Changes in mean pulmonary arterial pressure were greater for patients with a mean pulmonary arterial pressure greater than 14 mmHg compared to patients with a lower mean pulmonary arterial pressure. Changes in transpulmonary gradient were greater for patients with a transpulmonary gradient greater than 5 mmHg compared to patients with a lower transpulmonary gradient.Conclusion:Sildenafil acutely decreases mean pulmonary arterial pressure and transpulmonary gradient and causes greater acute changes in patients with higher mean pulmonary arterial pressures and transpulmonary gradients. Haemodynamic measurements and vasodilator testing might help to guide precision care following Fontan palliation.

RESPONSE OF DUCTUS ARTERIOSUS AND PULMONARY AND SYSTEMIC ARTERIAL PRESSURE TO CHANGES IN OXYGEN ENVIRONMENT IN NEWBORN INFANTS

PEDIATRICS ◽  
1964 ◽  
Vol 33 (6) ◽  
pp. 937-944
Author(s):  
Arthur J. Moss ◽  
George C. Emmanouilides ◽  
Forrest H. Adams ◽  
Katok Chuang
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Ductus Arteriosus ◽  
Newborn Infants ◽  
Systemic Arterial Pressure ◽  
Full Term ◽  
Oxygen Environment ◽  
Term Newborn ◽  
Pulmonary Arterial ◽  
Umbilical Arteries

Hemodynamic studies were performed through the umbilical arteries in 15 normal unanesthetized full-term newborn infants breathing air, 13% oxygen in nitrogen, and 100% oxygen. The investigation was aimed at studying the effect of changes in oxygen environment on shunts through the ductus arteriosus and on pressures in the pulmonic and systemic circuits. Left-to-right shunts disappeared with administration of 100% oxygen and recurred with 13% oxygen. This response was most pronounced during the first 3 hours but diminished noticeably or disappeared completely thereafter. During the first few hours there was a tendency for the ductus to reopen spontaneously after closure was effected with 100% oxygen. Hypoxia consistently caused a rise in pulmonary arterial pressure whereas inhalation of 100% oxygen caused a fall. The data support the concept that oxygen environment of the ductus arteriosus may be one of the factors which determines its closure.

scholarly journals Effect of Renal and Left Ventricular Function on Serial Pulmonary Arterial Pressure Changes After Device Closure of Atrial Septal Defect

2020 ◽  
Author(s):  
Chul Shin ◽  
Young Won Yoon ◽  
In-Soo Kim ◽  
Jong-Youn Kim ◽  
Pil-Ki Min ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Septal Defect ◽  
Pulmonary Arterial Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Device Closure ◽  
Post Procedure ◽  
Pulmonary Arterial ◽  
One Year ◽  
Pressure Changes

Abstract Background: The age of candidates for device closure of atrial septal defect (ASD) has been increasing. Thus, concerns exist about dyspnea aggravation or atrial fibrillation development after device closure due to augmentation of left ventricular (LV) and left atrial (LA) preload. This study aimed to examine patterns and determinants of serial pulmonary arterial pressure and left ventricular filling pressure changes after device closure of ASD. Methods: Among the 86 consecutive patients who underwent percutaneous device closure of ASD, those without pre- or post-procedural Doppler data and end-stage renal disease were excluded. The clinical, transesophageal, and transthoracic echocardiographic findings of 78 patients were collected at baseline, one day post-procedure, and one year follow-up. Results: The mean age of study patients was 49.8 ± 15.0 years and the average maximal defect diameter and device size was 20.2 ± 6.0 mm and 23.8 ± 6.4 mm. Some patients (n = 21; 27%) exhibited paradoxically increased tricuspid regurgitant velocity (TRV) one-day post-procedure; they also were older with lower e’, glomerular filtration rate, and LV ejection fraction and a higher LA volume index. However, even in these patients, TRV deceased below baseline levels one-year later. Both E/e’ (9.0 ± 3.5 vs. 11.4 ± 4.3; p < 0.001) and LA volume index significantly increased immediately after device closure, but all decreased one-year later. Larger defect size and higher TRV were significantly correlated with immediate E/e’ elevation. Conclusion: In older, renal, diastolic and systolic dysfunctional patients with larger LA, scheduled for larger device implantation, peri-interventional preload reduction therapy would be beneficial.

PAF increases vascular permeability without increasing pulmonary arterial pressure in the rat

2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Microvascular Permeability ◽  
Blue Dye ◽  
E Coli ◽  
Pulmonary Arterial

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.

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