Effects of chronically elevated pulmonary arterial pressure and flow on right ventricular afterload

1994 ◽  
Vol 267 (1) ◽  
pp. H155-H165 ◽  
Author(s):  
B. Ha ◽  
C. L. Lucas ◽  
G. W. Henry ◽  
E. G. Frantz ◽  
J. I. Ferreiro ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Pulmonary Arterial Pressure ◽  
Systolic Pressure ◽  
Arterial Blood Flow ◽  
Pulmonary Hemodynamics ◽  
Reflected Wave ◽  
Arterial Blood ◽  
Pulmonary Arterial

The effects of pulsatile hemodynamics on right ventricle-pulmonary circulation interactions were studied in control lambs and in two lamb models of altered pulmonary hemodynamics induced at infancy: elevated pulmonary arterial pressure (PAP) was created by the infusion of monocrotaline pyrrole (MCTP), and elevated pulmonary arterial blood flow was obtained by the creation of an arteriovenous fistula (Shunt). High-fidelity PAP, midvessel Doppler blood velocity (PAV), and cardiac output (CO) were measured in open-chest, anesthetized lambs. PAV waveforms were normalized to match the measured CO. Measured pressure and flow signals were separated in the time domain into forward and backward components. Pulmonary input impedance and indexes quantifying the timing of the reflected wave pulse (beginning of reflected pulse, duration of reflected pulse in systole, and duration of reflected wave in diastole) were calculated for each group. Results indicate that in control animals the reflected wave returned late in systole and extended through much of diastole, thereby increasing diastolic pressure like a counterpulsation balloon. No significant differences in the timing indexes were found between Shunt and control animals. In the MCTP group, the reflected wave returned significantly earlier than normal with the peak reflected pulse occurring before valve closure. The resulting augmentation of systolic pressure and, therefore, large pulse pressure is consistent with pressure waveforms observed in clinical pulmonary hypertension. We conclude that early wave reflection exerts a detrimental effect in pulmonary hypertension by unfavorably loading the still-ejecting right ventricle.

Thromboxane does not mediate pulmonary hypertension in phorbol ester-induced acute lung injury in dogs

1990 ◽  
Vol 69 (1) ◽  
pp. 345-352 ◽  
Author(s):  
A. H. Stephenson ◽  
R. S. Sprague ◽  
T. E. Dahms ◽  
A. J. Lonigro
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
H2 Receptor Antagonist ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Relationship

Thromboxane (Tx) has been suggested to mediate the pulmonary hypertension of phorbol myristate acetate- (PMA) induced acute lung injury. To test this hypothesis, the relationship between Tx and pulmonary arterial pressure was evaluated in a model of acute lung injury induced with PMA in pentobarbital sodium-anesthetized male mongrel dogs. Sixty minutes after administration of PMA (20 micrograms/kg iv, n = 10), TxB2 increased 10-fold from control in both systemic and pulmonary arterial blood and 8-fold in bronchoalveolar lavage (BAL) fluid. Concomitantly, pulmonary arterial pressure (Ppa) increased from 14.5 +/- 1.0 to 36.2 +/- 3.5 mmHg, and pulmonary vascular resistance (PVR) increased from 5.1 +/- 0.4 to 25.9 +/- 2.9 mmHg.l-1.min. Inhibition of Tx synthase with OKY-046 (10 mg/kg iv, n = 6) prevented the PMA-induced increase in Tx concentrations in blood and BAL fluid but did not prevent or attenuate the increase in Ppa. OKY-046 pretreatment did, however, attenuate but not prevent the increase in PVR 60 min after PMA administration. Pretreatment with the TxA2/prostaglandin H2 receptor antagonist ONO-3708 (10 micrograms.kg-1.min-1 iv, n = 7) prevented the pressor response to bolus injections of 1-10 micrograms U-46619, a Tx receptor agonist, but did not prevent or attenuate the PMA-induced increase in Ppa. ONO-3708 also attenuated but did not prevent the increase in PVR. These results suggest that Tx does not mediate the PMA-induced pulmonary hypertension but may augment the increases in PVR in this model of acute lung injury.

Fetal pulmonary vasodilation after exogenous platelet-activating factor

1991 ◽  
Vol 70 (2) ◽  
pp. 778-787 ◽  
Author(s):  
F. J. Accurso ◽  
S. H. Abman ◽  
R. B. Wilkening ◽  
G. S. Worthen ◽  
P. Henson
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Ductus Arteriosus ◽  
Platelet Activating Factor ◽  
Vena Cava ◽  
Arterial Blood Flow ◽  
High Dose ◽  
Pulmonary Vasodilation ◽  
Arterial Blood ◽  
Pulmonary Arterial

To determine the fetal pulmonary vascular response to platelet-activating factor (PAF), we studied the hemodynamic effects of the infusion of PAF directly into the left pulmonary artery in 21 chronically catheterized fetal lambs. Left pulmonary arterial blood flow (Q) was measured with electromagnetic flow transducers. Ten-minute infusions of low-dose PAF (10-100 ng/min) produced increases in Q from a baseline of 71 +/- 5 to 207 +/- 20 ml/min (P less than 0.001) without changes in pulmonary arterial pressure. Pulmonary vasodilation with PAF was further confirmed through increases in Q with brief (15-s) infusions and increases in the slope of the pressure-flow relationship as assessed by rapid incremental compressions of the ductus arteriosus during PAF infusion. Infusion of Lyso-PAF had no effect on Q or pulmonary arterial pressure. Treatment with CV-3988, a selective PAF receptor antagonist, but not with meclofenamate, atropine, or diphenhydramine and cimetidine blocked the response to PAF infusion and did not affect baseline tone. Systemic infusion of high-dose PAF (300 ng/min) through the fetal inferior vena cava increased pulmonary arterial pressure (46.5 +/- 1.0 to 54.8 +/- 1.9 mmHg, P less than 0.01) and aorta pressure (44.3 +/- 1.0 to 52.7 +/- 2.2 mmHg, P less than 0.01) while also increasing Q. Neither PAF nor CV-3988 changed the gradient between pulmonary arterial and aorta pressures, suggesting that PAF does not affect ductal tone. We conclude that PAF is a potent fetal pulmonary vasodilator and that the effects are not mediated through cyclooxygenase products or by cholinergic or histaminergic effects.

Physiologic response to two endotracheal suctioning techniques in newborn lambs with and without acute pulmonary hypertension

1995 ◽  
Vol 4 (6) ◽  
pp. 453-459 ◽  
Author(s):  
BB Daicoff ◽  
Langham MRJr ◽  
TW Mullet ◽  
HN Yarandi
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Repeated Measures ◽  
Pulmonary Arterial Pressure ◽  
Endotracheal Suctioning ◽  
Repeated Measures Design ◽  
Arterial Blood ◽  
Acute Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Physiologic Responses

BACKGROUND: Endotracheal suctioning may cause sudden increases in pulmonary arterial pressure, which can result in hypoxia secondary to right ventricular failure and/or increased right-to-left shunting. An adaptor that allows suctioning without disconnecting the ventilator has been proposed to prevent these problems; however, its efficacy has not been rigorously studied. OBJECTIVE: To examine the physiologic responses to two endotracheal suctioning techniques in newborn lambs with and without acute pulmonary hypertension. METHODS: A repeated-measures design was used to compare two endotracheal suctioning techniques in seven newborn lambs with and without acute pulmonary hypertension. An adaptor was used in the ventilator-controlled technique, making disconnection of the ventilator during suctioning unnecessary. In the bag-controlled technique, the ventilator was disconnected and ventilation was done with a manual resuscitation bag. Physiologic variables, pulmonary and mean arterial pressure, peak inspiratory pressure, mixed venous oxygen saturation, cardiac index, and arterial blood gas values were recorded before, during, and after endotracheal suctioning. RESULTS: Endotracheal suctioning caused a statistically significant systemic hypertensive response in lambs with and without acute pulmonary hypertension, regardless of which suctioning technique was used. No statistically significant changes occurred in pulmonary arterial pressure using either technique. CONCLUSIONS: Use of an adaptor resulted in no differences in the physiologic responses to endotracheal suctioning. However, endotracheal suctioning was easier to perform using an adaptor because no extra equipment or person was needed.

Systemic and pulmonary vasomotor waves

1965 ◽  
Vol 209 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Ricardo Ferretti ◽  
Neil S. Cherniack ◽  
Guy Longobardo ◽  
O. Robert Levine ◽  
Eugene Morkin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Breathing Pattern ◽  
Pulmonary Arterial Pressure ◽  
Arterial Blood Flow ◽  
Mayer Waves ◽  
Arterial Blood ◽  
Vasomotor Activity ◽  
Pulmonary Arterial

Rhythmic oscillations in systemic arterial blood pressure (Mayer waves) were produced in the dog by metabolic acidosis; hypoxia generally augmented the amplitude of the Mayer waves. When the Mayer waves exceeded 20 mm Hg in amplitude, they were associated with rhythmic fluctuations in pulmonary arterial pressure. The pulmonary arterial waves resembled the Mayer waves with respect to frequency and independence of the breathing pattern but were generally smaller in amplitude Measurements of instantaneous pulmonary arterial blood flow indicate that the rhythmic fluctuations in pulmonary arterial pressure represent the passive effects of fluctuations in pulmonary blood flow rather than fluctuations in pulmonary vasomotor activity. In turn, the swings in pulmonary arterial blood flow appear to originate in rhythmic variations in systemic vasomotor activity.

Combination of nonspecific PDE inhibitors with inhaled prostacyclin in experimental pulmonary hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. L1361-L1368 ◽  
Author(s):  
Ralph Theo Schermuly ◽  
Axel Roehl ◽  
Norbert Weissmann ◽  
Hossein Ardeschir Ghofrani ◽  
Hanno Leuchte ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Hemodynamics ◽  
Shunt Flow ◽  
Pulmonary Vasodilation ◽  
Pde Inhibitors ◽  
Inhaled Prostacyclin ◽  
Pulmonary Arterial ◽  
Selective Pulmonary Vasodilation

Inhalation of aerosolized prostacyclin (PGI2) exerts selective pulmonary vasodilation, but its effect is rapidly lost after termination of nebulization. Amplification of the vasodilatory response to inhaled PGI2 might be achieved by phosphodiesterase (PDE) inhibitors to stabilize its second messenger, cAMP. We established stable pulmonary hypertension in perfused rabbit lungs by continuous infusion of U-46619. Short-term (10-min) aerosolization maneuvers of PGI2 effected a rapid, moderate decrease in pulmonary arterial pressure, with post-PGI2 vasorelaxation being lost within 10–15 min, accompanied by a marginal reduction in shunt flow. Preceding administration of subthreshold doses of the PDE inhibitors theophylline, dipyridamole, and pentoxifylline via the intravascular or inhalational route, which per se did not influence pulmonary hemodynamics, caused more than doubling of the immediate pulmonary arterial pressure drop in response to PGI2 and marked prolongation of the post-PGI2 vasorelaxation to >60 min (all PDE inhibitors via both routes of application). This was accompanied by a reduction in shunt flow in the case of aerosolized theophylline (27.5%), pentoxifylline (30.5%), and dipyridamole (33.4%). Coaerosolization of PGI2 and PDE inhibitors may be considered as a therapeutic strategy in pulmonary hypertension.

scholarly journals Effects of pulmonary endarterectomy on pulmonary hemodynamics in chronic thromboembolic pulmonary hypertension, evaluated by interventricular septum curvature

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401989750
Author(s):  
Takahiko Saito ◽  
Hajime Kasai ◽  
Toshihiko Sugiura ◽  
Yukiko Takahashi ◽  
Hiroshi Tajima ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Interventricular Septum ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Endarterectomy ◽  
Pulmonary Hemodynamics ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial

The interventricular septum curvature, measured in images of electrocardiogram-gated 320-slice multidetector computed tomography, is reportedly useful and less invasive than right heart catheterization, as it could provide clues regarding pulmonary arterial pressure in patients with chronic thromboembolic pulmonary hypertension. Although pulmonary endarterectomy is an efficient treatment for chronic thromboembolic pulmonary hypertension, the interventricular septum curvature in patients who have received pulmonary endarterectomy has not been evaluated. We evaluated whether the interventricular septum curvature on electrocardiogram-gated 320-slice multidetector computed tomography can predict pulmonary hemodynamics in chronic thromboembolic pulmonary hypertension even after pulmonary endarterectomy. We studied 40 patients with chronic thromboembolic pulmonary hypertension (60.5 ± 9.7 years; 30 females), who underwent pulmonary endarterectomy at Chiba University Hospital between December 2010 and July 2018. To measure the interventricular septum curvature, we prepared left ventricular short-axis tomographic images from 4D images of electrocardiogram-gated 320-slice multidetector computed tomography. We calculated the radius of interventricular septum and determined the interventricular septum curvature in both the systolic and diastolic phases. We compared the interventricular septum curvature with pulmonary hemodynamics measured by right heart catheterization before and after pulmonary endarterectomy. After pulmonary endarterectomy, the correlations of the interventricular septum curvature with mean pulmonary arterial pressure, systolic pulmonary arterial pressure, and pulmonary vascular resistance disappeared, although the interventricular septum curvature was correlated with these pulmonary hemodynamic parameters before pulmonary endarterectomy. Changes in systolic interventricular septum curvature revealed significant correlations with changes in mean pulmonary arterial pressure, systolic pulmonary arterial pressure and pulmonary vascular resistance. Diastolic interventricular septum curvature also showed significant correlations with preoperative pulmonary hemodynamics, but not with postoperative pulmonary hemodynamics. Changes in the interventricular septum curvature after pulmonary endarterectomy could estimate the efficacy of pulmonary endarterectomy, although the interventricular septum curvature after pulmonary endarterectomy showed no significant correlations with pulmonary hemodynamics. Additionally, our findings confirmed that the interventricular septum curvature before pulmonary endarterectomy could be used to evaluate the severity of disease.

Telemetry monitoring of pulmonary arterial pressure in freely moving rats

1996 ◽  
Vol 81 (2) ◽  
pp. 1027-1032 ◽  
Author(s):  
P. Hess ◽  
M. Clozel ◽  
J. P. Clozel
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Pulmonary Arterial Pressure ◽  
Telemetry System ◽  
Mean Pulmonary Arterial Pressure ◽  
Freely Moving Rats ◽  
Pulmonary Arterial ◽  
Freely Moving ◽  
The Right

Several rat models of pulmonary hypertension have been developed. However, up until now it has been difficult to monitor pulmonary arterial pressure for long periods of time. The goal of the present study was to develop a telemetry system allowing chronic monitoring of pulmonary arterial pressure in freely moving rats. For this purpose, while animals were under anesthesia, a sensing catheter was implanted into the pulmonary arterial trunk through the right ventricle. This catheter was connected to an emitter implanted in the abdomen. Validation of the system was performed in three steps. First, acutely, we controlled that the pressure signal transmitted by the telemetry system was accurate and corresponded to a signal obtained with a high-fidelity Millar catheter. Second, we evaluated the chronic consequences of implantation of the system. Third, we used the system to monitor pulmonary arterial pressure in a model of monocrotaline-induced hypertension in which the effects of bosentan, an endothelin-receptor antagonist, were evaluated. The telemetry system was reliable and did not lead to damage of the right ventricle and/or to chronic pulmonary embolism. After a recovery period of 8–10 days, mean pulmonary arterial pressure was stable. With the use of this telemetry system, it was possible to follow the increase of pulmonary arterial pressure induced by monocrotaline. In this model, bosentan decreased mean pulmonary arterial pressure by 13% (P = 0.07), suggesting a role of endothelin in this model of pulmonary hypertension. We conclude that it is possible to use this telemetry system to monitor pulmonary arterial pressure in freely moving conscious rats.

MO746CARDIAC REMODELING AND PULMONARY HYPERTENSION IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ekaterina Borodulina ◽  
Alexander M Shutov
Keyword(s):  
Pulmonary Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Hemodialysis Treatment ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Abstract Background and Aims An important predictor of cardiovascular mortality and morbidity in hemodialysis patients is left ventricular hypertrophy. Also, pulmonary hypertension is a risk factor for mortality and cardiovascular events in hemodialysis patients. The aim of this study was to investigate cardiac remodeling and the dynamics of pulmonary arterial pressure during a year-long hemodialysis treatment and to evaluate relationship between pulmonary arterial pressure and blood flow in arteriovenous fistula. Method Hemodialysis patients (n=88; 42 males, 46 females, mean age was 51.7±13.0 years) were studied. Echocardiography and Doppler echocardiography were performed in the beginning of hemodialysis treatment and after a year. Echocardiographic evaluation was carried out on the day after dialysis. Left ventricular mass index (LVMI) was calculated. Left ventricular ejection fraction (LVEF) was measured by the echocardiographic Simpson method. Arteriovenous fistula flow was determined by Doppler echocardiography. Pulmonary hypertension was diagnosed according to criteria of Guidelines for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology. Results Pulmonary hypertension was diagnosed in 47 (53.4%) patients. Left ventricular hypertrophy was revealed in 71 (80.7%) patients. Only 2 (2.3%) patients had LVEF<50%. At the beginning of hemodialysis correlation was detected between systolic pulmonary arterial pressure and LVMI (r=0.52; P<0.001). Systolic pulmonary arterial pressure negatively correlated with left ventricular ejection fraction (r=-0.20; P=0.04). After a year of hemodialysis treatment LVMI decreased from 140.49±42.95 to 123.25±39.27 g/m2 (р=0.006) mainly due to a decrease in left ventricular end-diastolic dimension (from 50.23±6.48 to 45.13±5.24 mm, p=0.04) and systolic pulmonary arterial pressure decreased from 44.83±14.53 to 39.14±10.29 mmHg (р=0.002). Correlation wasn’t found between systolic pulmonary arterial pressure and arteriovenous fistula flow (r=0.17; p=0.4). Conclusion Pulmonary hypertension was diagnosed in half of patients at the beginning of hemodialysis treatment. Pulmonary hypertension in hemodialysis patients was associated with left ventricular hypertrophy, systolic left ventricular dysfunction. After a year-long hemodialysis treatment, a regress in left ventricular hypertrophy and a partial decrease in pulmonary arterial pressure were observed. There wasn’t correlation between arteriovenous fistula flow and systolic pulmonary arterial pressure.

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