scholarly journals Acute Pulmonary Hypertension Caused by Tumor Embolism: A Report of Two Cases

2015 ◽  
Vol 5 (3) ◽  
pp. 577-579 ◽  
Author(s):  
Caroline Mury ◽  
Antoine G. Schneider ◽  
Antoine Nobile ◽  
Samuel Rotman ◽  
Lucas Liaudet
Keyword(s):  
Pulmonary Hypertension ◽  
Tumor Embolism ◽  
Acute Pulmonary Hypertension

scholarly journals Pulmonary Tumor Embolism: A Rare Cause of Acute Pulmonary Hypertension

Cureus ◽  
2020 ◽  
Author(s):  
Timothy Chong ◽  
Joseph Park ◽  
Hafiz M Aslam ◽  
Shahryar Ansari ◽  
Sara L Wallach
Keyword(s):  
Pulmonary Hypertension ◽  
Tumor Embolism ◽  
Pulmonary Tumor ◽  
Acute Pulmonary Hypertension

Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension

1998 ◽  
Vol 84 (2) ◽  
pp. 435-441 ◽  
Author(s):  
Christophe Adrie ◽  
Fumito Ichinose ◽  
Alexandra Holzmann ◽  
Larry Keefer ◽  
William E. Hurford ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Half Life ◽  
Hemodynamic Effects ◽  
Pulmonary Vasodilation ◽  
Short Half Life ◽  
Acute Pulmonary Hypertension ◽  
Inhaled No

Adrie, Christophe, Fumito Ichinose, Alexandra Holzmann, Larry Keefer, William E. Hurford, and Warren M. Zapol. Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension. J. Appl. Physiol. 84(2): 435–441, 1998.—Sodium 1-( N, N-diethylamino)diazen-1-ium-1,2-diolate {DEA/NO; Et2N[N(O)NO]Na} is a compound that spontaneously generates nitric oxide (NO). Because of its short half-life (2.1 min), we hypothesized that inhaling DEA/NO aerosol would selectively dilate the pulmonary circulation without decreasing systemic arterial pressure. We compared the pulmonary selectivity of this new NO donor with two other reference drugs: inhaled NO and inhaled sodium nitroprusside (SNP). In seven awake sheep with pulmonary hypertension induced by the infusion of U-46619, we compared the hemodynamic effects of DEA/NO with those of incremental doses of inhaled NO gas. In seven additional awake sheep, we examined the hemodynamic effects of incremental doses of inhaled nitroprusside (i.e., SNP). Inhaled NO gas selectively dilated the pulmonary vasculature. Inhaled DEA/NO produced nonselective vasodilation; both systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were reduced. Inhaled SNP selectively dilated the pulmonary circulation at low concentrations (≤10−2 M), inducing a decrease of PVR of up to 42% without any significant decrease of SVR (−5%), but nonselectively dilated the systemic circulation at larger doses (>10−2 M). In conclusion, despite its short half-life, DEA/NO is not a selective pulmonary vasodilator compared with inhaled NO. Inhaled SNP appears to be selective to the pulmonary circulation at low doses but not at higher levels.

An artificial lung reduces pulmonary input impedance in acute pulmonary hypertension

2000 ◽  
Vol 191 (4) ◽  
pp. S61
Author(s):  
Jonathan Haft ◽  
J.Patrick Montoya ◽  
Osamma Alnajjar ◽  
Steven Posner ◽  
Joseph Bull ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Input Impedance ◽  
Artificial Lung ◽  
Acute Pulmonary Hypertension

scholarly journals Controversies in the identification and management of acute pulmonary hypertension in preterm neonates

2017 ◽  
Vol 82 (6) ◽  
pp. 901-914 ◽  
Author(s):  
Regan E Giesinger ◽  
Kiran More ◽  
Jodie Odame ◽  
Amish Jain ◽  
Robert P Jankov ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Preterm Neonates ◽  
Acute Pulmonary Hypertension

Effect of platelet depletion on lung vasoconstriction in heparin-protamine reactions

1989 ◽  
Vol 66 (5) ◽  
pp. 2344-2350 ◽  
Author(s):  
G. Montalescot ◽  
E. Kreil ◽  
K. Lynch ◽  
E. M. Greene ◽  
A. Torres ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Platelet Aggregation ◽  
Fold Increase ◽  
Bovine Thrombin ◽  
Thromboxane Production ◽  
Acute Pulmonary Hypertension ◽  
Arterial Plasma ◽  
Arterial Po2 ◽  
Platelet Depletion

In six awake sheep the control heparin-protamine reaction was associated with a 150-fold rise in arterial plasma thromboxane B2 (TxB2) levels, a 4.5-fold increase in pulmonary vascular resistance, a 20% decrease in cardiac output, a 30% decrease in arterial PO2, and a 30% reduction in arterial white blood cell concentrations. Depletion of 99% of circulating platelets by antibodies did not prevent either acute and severe pulmonary hypertension or increased plasma TxB2 levels induced by heparin-protamine administration. We produced sheep platelet aggregation in vitro with bovine thrombin and measured marked TxB2 release (36.3 +/- 16.3 ng/10(9) platelets). In contrast, neither heparin, protamine, nor heparin-protamine complexes over a 10,000-fold range of concentrations induced platelet aggregation and release of thromboxane in vitro. Therefore sheep platelets are not the source of thromboxane production associated with acute pulmonary hypertension during the heparin-protamine reaction, and other cells must produce the thromboxane.

scholarly journals Thiamine-Responsive Acute Pulmonary Hypertension of Early Infancy (TRAPHEI)—A Case Series and Clinical Review

Children ◽  
2020 ◽  
Vol 7 (11) ◽  
pp. 199
Author(s):  
Nalinikanta Panigrahy ◽  
Dinesh Kumar Chirla ◽  
Rakshay Shetty ◽  
Farhan A. R. Shaikh ◽  
Poddutoor Preetham Kumar ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Case Reports ◽  
Case Series ◽  
Early Infancy ◽  
Right Atrial ◽  
Voice Leading ◽  
Vasodilator Therapy ◽  
Polished Rice ◽  
Pulmonary Vasodilator ◽  
Acute Pulmonary Hypertension

Persistent pulmonary hypertension of the newborn (PPHN) is a syndrome of high pulmonary vascular resistance (PVR) commonly seen all over the world in the immediate newborn period. Several case reports from India have recently described severe pulmonary hypertension among infants in the postneonatal period. These cases typically present with respiratory distress in 1–6-month-old infants, breastfed by mothers on a polished rice-based diet. Predisposing factors include respiratory tract infection such as acute laryngotracheobronchitis with change in voice, leading to pulmonary hypertension, right atrial and ventricular dilation, pulmonary edema and hepatomegaly. Mortality is high without specific therapy. Respiratory support, pulmonary vasodilator therapy, inotropes, diuretics and thiamine infusion have improved the outcome of these infants. This review outlines four typical patients with thiamine-responsive acute pulmonary hypertension of early infancy (TRAPHEI) due to thiamine deficiency and discusses pathophysiology, clinical features, diagnostic criteria and therapeutic options.

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