Treatment of Severe Pulmonary Embolism by Urokinase and Lysyl-Plasminogen

1979 ◽  
Author(s):  
H. Sors ◽  
A. Venet ◽  
P. Reynaud ◽  
D. Safran ◽  
P. Cornu ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Emboli ◽  
Thrombolytic Treatment ◽  
Mean Pulmonary Arterial Pressure ◽  
Group I ◽  
Pulmonary Arterial ◽  
Group Ii ◽  
Vascular Obstruction ◽  
The Uk

The effects of the heparin (H)-Urokinase (UK) treatment on pulmonary emboli (PE) are limited by the rapid disappearance of the plasminogen (Pig) contained in the clots. Two groups of patients with recent PE (less than 8 days) of equal severity (as judged by angiography) have been studied: Group I (15 patients) treated by H(500 IU/kg/24h) and UK (i.v. bolus 15,000 u. CTA/kg/20min) and Group II (15 patients) receiving H and a sequential treatment with a bolus of UK followed by Lysyl-Plg infusion (300 UI/kg/6h), then by a 2nd bolus of UK and finally by a Pig loading. Angiography and catheterization were performed before and 24 hours after the treatment. The vascular obstruction (VO%) was appreciated by the UPET method. In Group II, the values before treatment were : VO 57±11% ; mean pulmonary arterial pressure (PAP) : 30±5 torrs ; cardiac index (CI) ; 2.0±0.6 I/min/m2 ; pulmonary arterial resistances (PAR) 8.4±2.7 torrs/I/min/m2 ; PaO2 : 56±7 tors. The UK + Pig treatment elicited significant changes : 50% decrease in VO and PAR, 33% decrease in PAP and 30% increase in PaO2 and CI in 24 hours. One month later, hemodynamic was normal and the residual VO was less than 15%. In Croup I the initial hemodynamic values were similar but the 24 hours decrease in VO, PAP and FAR were respectively of 30, 22 and 29%, differing significantly of the Group II (F test). After one month, the residual VO was 25%. These observations suggest that Lys-Plg loading increases significantly the efficacy of thrombolytic treatment of massive and recent PE.

Starling resistor vs. distensible vessel models for embolic pulmonary hypertension

1995 ◽  
Vol 268 (2) ◽  
pp. H817-H827 ◽  
Author(s):  
C. Melot ◽  
M. Delcroix ◽  
J. Closset ◽  
P. Vanderhoeft ◽  
P. Lejeune ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Left Atrial ◽  
Glass Bead ◽  
Inflection Point ◽  
Pulmonary Arterial Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Closing Pressure

We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065–1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15–26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.

Right ventricular adaptation in the critical phase after acute intermediate-risk pulmonary embolism

2020 ◽  
pp. 204887262092525 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Gammelgaard Schultz ◽  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Intermediate Risk ◽  
Right Ventricular Afterload ◽  
Mean Pulmonary Arterial Pressure ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism ( n = 6) or sham ( n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased ( P < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( P < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( P < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( P = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo–arterial coupling was reduced ( P < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( P < 0.01) suggesting right ventricular failure. Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.

A computed method for noninvasive MRI assessment of pulmonary arterial hypertension

2004 ◽  
Vol 96 (2) ◽  
pp. 463-468 ◽  
Author(s):  
Eric Laffon ◽  
Christophe Vallet ◽  
Virginie Bernard ◽  
Michel Montaudon ◽  
Dominique Ducassou ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Cross Sectional Area ◽  
Physical Parameters ◽  
Sectional Area ◽  
Biophysical Parameters ◽  
Cross Sectional ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Mean

The present method enables the noninvasive assessment of mean pulmonary arterial pressure from magnetic resonance phase mapping by computing both physical and biophysical parameters. The physical parameters include the mean blood flow velocity over the cross-sectional area of the main pulmonary artery (MPA) at the systolic peak and the maximal systolic MPA cross-sectional area value, whereas the biophysical parameters are related to each patient, such as height, weight, and heart rate. These parameters have been measured in a series of 31 patients undergoing right-side heart catheterization, and the computed mean pulmonary arterial pressure value (PpaComp) has been compared with the mean pressure value obtained from catheterization (PpaCat) in each patient. A significant correlation was found that did not differ from the identity line PpaComp = PpaCat ( r = 0.92). The mean and maximal absolute differences between PpaComp and PpaCat were 5.4 and 11.9 mmHg, respectively. The method was also applied to compute the MPA systolic and diastolic pressures in the same patient series. We conclude that this computed method, which combines physical (whoever the patient) and biophysical parameters (related to each patient), improves the accuracy of MRI to noninvasively estimate pulmonary arterial pressures.

Endothelin effects in isolated, perfused lamb lungs: role of cyclooxygenase inhibition and vasomotor tone

1991 ◽  
Vol 261 (2) ◽  
pp. H443-H450 ◽  
Author(s):  
H. Toga ◽  
J. Usha Raj ◽  
R. Hillyard ◽  
B. Ku ◽  
J. Anderson
Keyword(s):  
Vasomotor Tone ◽  
Cyclooxygenase Inhibition ◽  
Group Iii ◽  
Group I ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Group Ii ◽  
Sites Of Action ◽  
Arteries And Veins

We have determined the sites of action of endothelin-1 (ET) in the lamb pulmonary circulation. The influence of cyclooxygenase inhibition and baseline vasomotor tone on ET effects was also studied. Lungs of 14 lambs (6-9 wk of age, 12.1 +/- 0.6 kg body wt) were isolated and perfused with blood. Group I lungs (n = 5) were untreated, group II lungs (n = 5) were treated with indomethacin to inhibit cyclooxygenase, and group III lungs (n = 4) were treated with indomethacin and a thromboxane A2 analogue, U-46619, to elevate vasomotor tone. All lungs were perfused with constant flow in zone 3, with left atrial and airway pressures being 8 and 6 cmH2O, respectively. We measured pulmonary arterial pressure and, by the micropuncture servo-null method, pressures in 20- to 50-microns diameter subpleural venules, both before and after each dose of ET was infused (50, 100, 250, and 500 ng/kg). Group I lungs, with high baseline vasomotor tone, exhibited a biphasic response to ET; 50-100 ng/kg of ET dilated both arteries and veins, whereas 500 ng/kg of ET constricted both arteries and veins. In group II lungs with low vasomotor tone, all doses of ET caused constriction of arteries only. In group III lungs (indomethacin treated with elevated vasomotor tone), 50-100 ng/kg of ET caused dilation of arteries and veins, whereas 500 ng/kg of ET induced constriction, this time only in arteries. We conclude that ET has both dilator and constrictor effects in arteries and veins of isolated, perfused lamb lungs. ET-induced arterial and venous dilation is dependent on initial vasomotor tone but not on cyclooxygenase metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Renal Vein Thrombosis and Pulmonary Embolism Secondary to Vaccine-induced Thrombotic Thrombocytopenia (VITT)

2021 ◽  
Author(s):  
Nikita Cliff-Patel ◽  
Lindsay Moncrieff ◽  
Veqas Ziauddin
Keyword(s):  
Pulmonary Embolism ◽  
General Hospital ◽  
Regulatory Agency ◽  
Renal Vein ◽  
District General Hospital ◽  
Renal Vein Thrombosis ◽  
The Other ◽  
Pulmonary Emboli ◽  
Vein Thrombosis ◽  
The Uk

The Medicines and Healthcare products Regulatory Agency (MHRA) of the UK has approved the use of three vaccines to combat COVID-19 (SARS-CoV-2). There have been rare reports of thrombosis after vaccination with the AstraZeneca vaccine. We present three cases of vaccine-induced thrombotic thrombocytopenia (VITT) in one UK district general hospital following administration of this vaccine. Two of the patients had asymptomatic pulmonary emboli, while the other is the first known case of both renal vein thrombosis and pulmonary embolism.

scholarly journals Mean pulmonary arterial pressure after percutaneous mitral valvuloplasty predicts long-term adverse outcomes

2012 ◽  
Vol 31 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Elisabete Jorge ◽  
Rui Baptista ◽  
Henrique Faria ◽  
João Calisto ◽  
Vítor Matos ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Adverse Outcomes ◽  
Mitral Valvuloplasty ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

scholarly journals Pulmonary Vasodilator Therapy in Children with Single Ventricle Physiology: Effects on Saturation and Pulmonary Arterial Pressure

2020 ◽  
Vol 41 (8) ◽  
pp. 1651-1659
Author(s):  
Ida Jeremiasen ◽  
Karin Tran-Lundmark ◽  
Nikmah Idris ◽  
Phan-Kiet Tran ◽  
Shahin Moledina
Keyword(s):  
Arterial Pressure ◽  
Single Ventricle ◽  
Pulmonary Arterial Pressure ◽  
Vasodilator Therapy ◽  
Single Ventricle Physiology ◽  
Pulmonary Vasodilators ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial ◽  
Stage 1

AbstractIn children with single ventricle physiology, increased pulmonary vascular resistance may impede surgical progression or result in failing single ventricle physiology. The use of pulmonary vasodilators has been suggested as a potential therapy. However, knowledge on indication, dosage, and effect is limited. A retrospective case notes review of all (n = 36) children with single ventricle physiology, treated with pulmonary vasodilators by the UK Pulmonary Hypertension Service for Children 2004–2017. Therapy was initiated in Stage 1 (n = 12), Glenn (n = 8), or TCPC (n = 16). Treatment indications were high mean pulmonary arterial pressure, cyanosis, reduced exercise tolerance, protein-losing enteropathy, ascites, or plastic bronchitis. Average dose of sildenafil was 2.0 mg/kg/day and bosentan was 3.3 mg/kg/day. 56% had combination therapy. Therapy was associated with a reduction of the mean pulmonary arterial pressure from 19 to 14 mmHg (n = 17, p < 0.01). Initial therapy with one or two vasodilators was associated with an increase in the mean saturation from 80 to 85%, (n = 16, p < 0.01). Adding a second vasodilator did not give significant additional effect. 5 of 12 patients progressed from Stage 1 to Glenn, Kawashima, or TCPC, and 2 of 8 from Glenn to TCPC during a mean follow-up time of 4.7 years (0–12.8). Bosentan was discontinued in 57% and sildenafil in 14% of treated patients and saturations remained stable. Pulmonary vasodilator therapy was well tolerated and associated with improvements in saturation and mean pulmonary arterial pressure in children with single ventricle physiology. It appears safe to discontinue when no clear benefit is observed.

Gestational resistance to the pulmonary vasoconstrictor effect of the TxA2 mimetic U-46619: possible mechanism

1997 ◽  
Vol 272 (6) ◽  
pp. R1734-R1739 ◽  
Author(s):  
G. Losonczy ◽  
G. Brown ◽  
I. Mucha ◽  
R. Klocke ◽  
V. Muller ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Vascular System ◽  
Late Gestation ◽  
Mechanically Ventilated ◽  
Mean Pulmonary Arterial Pressure ◽  
Vascular Sensitivity ◽  
Specific Receptors ◽  
Pulmonary Arterial ◽  
Dose Dependent

Pregnancy is associated with the reduction of vascular sensitivity to vasoconstrictor compounds. We have examined whether pregnancy in rabbits induces hyposensitivity of the pulmonary vascular system to U-46619. Anesthetized, mechanically ventilated nonpregnant (NP; n = 7) and late-pregnant (P; n = 7) rabbits were studied. The intravenous injection of 0.03, 0.1, and 0.3 microgram/kg U-46619 led to a dose-dependent elevation of mean pulmonary arterial pressure (MPAP) in NP rabbits from a baseline value of 15 +/- 1 to 22 +/- 1 mgHg. There was no significant MPAP response to intravenous administration of U-46619 in P rabbits. The pulmonary arterial pressure response of isolated, ventilated, and buffer-perfused lungs of P rabbits was also blunted (P < 0.001 vs. NP). Pulmonary arterial membrane binding of [125I]BOP, another thromboxane (Tx)A2 analog, indicated 48 +/- 16 fmol receptors/mg protein in P rabbits and 193 +/- 48 fmol receptors/mg protein in NP samples (P < 0.025). Receptor affinity [1/dissociation constant (KD)] was also lower in the tissue of P rabbits (P < 0.01 vs. NP). The urinary excretion of the stable TxA2 metabolite 11-dehydro-TxB2 was lower in P than in NP rabbits (P < 0.02), which made homologous desensitization an unlikely explanation for the changes of vascular TxA2 receptors. These results show that, in late gestation, rabbit pulmonary vascular sensitivity to U-46619 is reduced simultaneously with, and as a possible consequence of, downregulation of specific receptors.

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