Influence of Acute Pulmonary Hypertension on the Protamine-induced Systemic Hypotension in the Heparinized Dog

1998 ◽  
Vol 35 (3) ◽  
pp. 404
Author(s):  
Kyung Yeon Yoo ◽  
Seung Jin Shim ◽  
Jong Eun Park ◽  
Woong Mo Im
Keyword(s):  
Pulmonary Hypertension ◽  
Systemic Hypotension ◽  
Acute Pulmonary Hypertension

scholarly journals Maternal and neonatal risk factors for neonatal respiratory distress syndrome in term neonates in Cyprus: a prospective case–control study

2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Paraskevi Stylianou-Riga ◽  
Theodora Boutsikou ◽  
Panayiotis Kouis ◽  
Paraskevi Kinni ◽  
Marina Krokou ◽  
...  
Keyword(s):  
Risk Factors ◽  
Pulmonary Hypertension ◽  
Caesarean Section ◽  
Distress Syndrome ◽  
Elective Caesarean Section ◽  
Case Control ◽  
Male Gender ◽  
Term Neonates ◽  
Systemic Hypotension ◽  
Neonatal Respiratory Distress

Abstract Background Neonatal respiratory distress syndrome (NRDS) is strongly associated with premature birth, but it can also affect term neonates. Unlike the extent of research in preterm neonates, risk factors associated with incidence and severity of NRDS in term neonates are not well studied. In this study, we examined the association of maternal and neonatal risk factors with the incidence and severity of NRDS in term neonates admitted to Neonatal Intensive Care Unit (NICU) in Cyprus. Methods In a prospective, case-control design we recruited term neonates with NRDS and non-NRDS admitted to the NICU of Archbishop Makarios III hospital, the only neonatal tertiary centre in Cyprus, between April 2017–October 2018. Clinical data were obtained from patients’ files. We used univariate and multivariate logistic and linear regression models to analyse binary and continuous outcomes respectively. Results During the 18-month study period, 134 term neonates admitted to NICU were recruited, 55 (41%) with NRDS diagnosis and 79 with non-NRDS as controls. In multivariate adjusted analysis, male gender (OR: 4.35, 95% CI: 1.03–18.39, p = 0.045) and elective caesarean section (OR: 11.92, 95% CI: 1.80–78.95, p = 0.01) were identified as independent predictors of NRDS. Among neonates with NRDS, early-onset infection tended to be associated with increased administration of surfactant (β:0.75, 95% CI: − 0.02-1.52, p = 0.055). Incidence of pulmonary hypertension or systemic hypotension were associated with longer duration of parenteral nutrition (pulmonary hypertension: 11Vs 5 days, p < 0.001, systemic hypotension: 7 Vs 4 days, p = 0.01) and higher rate of blood transfusion (pulmonary hypertension: 100% Vs 67%, p = 0.045, systemic hypotension: 85% Vs 55%, p = 0.013). Conclusions This study highlights the role of elective caesarean section and male gender as independent risk factors for NRDS in term neonates. Certain therapeutic interventions are associated with complications during the course of disease. These findings can inform the development of evidence-based recommendations for improved perinatal care.

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.

Search for an animal model to investigate selective pulmonary vasodilation

2016 ◽  
Vol 51 (4) ◽  
pp. 376-387
Author(s):  
Bodil Petersen ◽  
Thilo Busch ◽  
Katharina Noreikat ◽  
Lorenz Homeister ◽  
Ralf Regenthal ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Animal Models ◽  
Vascular Tone ◽  
Acute Hypoxia ◽  
Haemodynamic Instability ◽  
Time Interval ◽  
Systemic Hypotension ◽  
Pulmonary Vasodilation ◽  
Selective Pulmonary Vasodilation

Pulmonary arterial hypertension is a life-threatening disease with a poor prognosis. Oral treatment with vasodilators is often limited by systemic hypotension. Inhalation of vasodilators offers the opportunity for selective pulmonary vasodilation. Testing selective pulmonary vasodilation by inhaled nitric oxide or alternative substances in animal models requires an increased pulmonary vascular tone. The aim of this study was to identify animal models that are suitable for investigating selective pulmonary vasodilation. To do so, a haemodynamic stable pulmonary hypertension was initiated, with a 30 min duration deemed to be a sufficient time interval before and after a possible intervention. In anaesthetized and mechanically-ventilated Sprague–Dawley rats pulmonary hypertension was induced either by acute hypoxia due to reduction of the inspired oxygen fraction from 0.21 to 0.1 ( n = 6), a fixed infusion rate of the thromboxane analogue U46619 (240 ng/min; n = 6) or a monocrotaline injection (MCT; 60 mg/kg applied 23 days before the investigation; n = 7). The animals were instrumented to measure right ventricular and systemic arterial pressures. Acute hypoxia caused a short, and only transient, increase of pulmonary artery pressure as well as profound systemic hypotension which suggested haemodynamic instability. U46619 infusion induced variable changes in the pulmonary and systemic vascular tone without sufficient stabilization within 30 min. MCT provoked sustained pulmonary hypertension with normal systemic pressure values and inhalation of nitric oxide caused selective pulmonary vasodilation. In conclusion, out of the three examined rat animal models only MCT-induced pulmonary hypertension is a solid and reliable model for investigating selective pulmonary vasodilation.

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