Influence of Indomethacin on the Systemic and Pulmonary Vascular Resistance in Man

1978 ◽  
Vol 54 (2) ◽  
pp. 141-145 ◽  
Author(s):  
Å. Wennmalm
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Total Oxygen ◽  
Related Substances ◽  
Blood Pressures ◽  
Pulmonary Arterial ◽  
Oxygen Difference ◽  
Relaxing Effect

1. Indomethacin, an inhibitor of the cyclo-oxygenase system that converts arachidonic acid into prostaglandins and related substances, was infused intravenously in 12 healthy volunteer subjects. 2. Systemic systolic and diastolic blood pressures and heart rate were recorded in all subjects, and in most of them also the systemic arteriovenous oxygen difference, the total oxygen uptake and the pulmonary arterial and wedge pressures. 3. The infusion of indomethacin was followed by a decreased cardiac output (from 7·3 ± 0·3 to 6·3 ± 0·3 litres/min) and an increased mean systemic blood pressure (from 92 ± 1 to 102 ± 1 mmHg), indicating an elevation of the total systemic vascular resistance (from 98 ± 4 to 124 ± 5 kPa)l−1 s) by indomethacin. The ventilation and the pulmonary vascular resistance did not change after the infusion of indomethacin. 4. The results suggest that products formed by the cyclo-oxygenase system at rest exert a relaxing effect in certain parts of the systemic vascular bed, thereby lowering the systemic vascular resistance.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

Effects of a perfluorocarbon emulsion for enhanced O2 solubility on hemodynamics and O2 transport in dogs

1995 ◽  
Vol 79 (5) ◽  
pp. 1777-1786 ◽  
Author(s):  
E. C. Johnson ◽  
B. K. Erickson ◽  
A. Podolsky ◽  
E. K. Birks ◽  
P. E. Keipert ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Pulmonary Gas Exchange ◽  
Perfluorocarbon Emulsion ◽  
Mean Pulmonary Arterial Pressure ◽  
O2 Transport ◽  
Airway Pressures ◽  
Pulmonary Arterial

Perfluorocarbon emulsions raise blood O2 solubility and thus augment O2 transport, but their cardiopulmonary effects at higher doses may limit their use. We therefore examined effects of increasing doses of perfluorooctylbromide emulsion (Oxy) on 1) pulmonary gas exchange, 2) pulmonary and systemic hemodynamics, and 3) mixed venous PO2 (PVO2). After hematocrit reduction to 24–26% by exchange with 5% albumin, anesthetized ventilated dogs breathing 100% O2 were given Oxy (n = 6) or 5% albumin (n = 5) intravenously in four successive 3 ml/kg doses. After each dose, arterial and venous PO2, PCO2, and pH, [O2], hematocrit, heart rate, and systemic, pulmonary arterial, and airway pressures were measured. Ventilation-perfusion relationships and cardiac output (QT) were determined by the multiple inert gas method. Oxy at 12 ml/kg almost doubled blood O2 solubility, increasing arterial [O2] by 1.28 ml/100 ml but did not affect O2 consumption and ventilation-perfusion relationships. QT rose by 21% after 3 ml/kg, then fell with increasing doses (-18% from baseline after 12 ml/kg); O2 delivery remained constant. Oxy at > 6 ml/kg increased systemic blood pressure and systemic vascular resistance considerably. Mean pulmonary arterial pressure and pulmonary vascular resistance increased slightly. Airway pressures were unaffected. PVO2 rose from 66 to 77 Torr (6 ml/kg), then fell to 72 Torr (12 ml/kg), in accord with theoretical-predictions. In this model, Oxy 1) dose not impair pulmonary gas exchange in doses up to 12 ml/kg, 2) leads to progressively higher systemic vascular resistance and fall in QT at > 3–6 ml/kg, possibly because of increased blood viscosity, and 3) augments PVO2, as predicted from the increase in plasma O2 solubility.

scholarly journals Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 779
Author(s):  
Daria S. Kostyunina ◽  
Paul McLoughlin
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Sex Chromosomes ◽  
Bone Morphogenetic Protein 2 ◽  
Sex Dimorphism ◽  
Pulmonary Arterial ◽  
The Impact

Pulmonary hypertension (PH) is a condition characterised by an abnormal elevation of pulmonary artery pressure caused by an increased pulmonary vascular resistance, frequently leading to right ventricular failure and reduced survival. Marked sexual dimorphism is observed in patients with pulmonary arterial hypertension, a form of pulmonary hypertension with a particularly severe clinical course. The incidence in females is 2–4 times greater than in males, although the disease is less severe in females. We review the contribution of the sex chromosomes to this sex dimorphism highlighting the impact of proteins, microRNAs and long non-coding RNAs encoded on the X and Y chromosomes. These genes are centrally involved in the cellular pathways that cause increased pulmonary vascular resistance including the production of reactive oxygen species, altered metabolism, apoptosis, inflammation, vasoconstriction and vascular remodelling. The interaction with genetic mutations on autosomal genes that cause heritable pulmonary arterial hypertension such as bone morphogenetic protein 2 (BMPR2) are examined. The mechanisms that can lead to differences in the expression of genes located on the X chromosomes between females and males are also reviewed. A better understanding of the mechanisms of sex dimorphism in this disease will contribute to the development of more effective therapies for both women and men.

Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary Vascular Resistance in Patients with Chronic Emphysema

Respiration ◽  
2000 ◽  
Vol 67 (5) ◽  
pp. 502-506 ◽  
Author(s):  
Akira Nakamura ◽  
Norio Kasamatsu ◽  
Ikko Hashizume ◽  
Takushi Shirai ◽  
Suguru Hanzawa ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Inhaled nitric oxide partially reverses hypoxic pulmonary vasoconstriction in the dog

1994 ◽  
Vol 76 (3) ◽  
pp. 1350-1355 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Vasomotor Tone ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmonary vasomotor tone decreases pulmonary arterial pressure (Ppa). We conducted this study to better characterize the hemodynamic effects induced by NO inhalation during hypoxic pulmonary vasoconstriction in 11 anesthetized ventilated dogs. Arterial and venous systemic and pulmonary pressures and aortic flow probe-derived cardiac output were recorded, and nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) were measured. The effects of 5 min of NO inhalation at 0, 17, 28, 47, and 0 ppm during hyperoxia (inspiratory fraction of O2 = 0.5) and hypoxia (inspiratory fraction of O2 = 0.16) were observed. NO inhalation has no measurable effects during hyperoxia. Hypoxia induced an increase in Ppa that reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO induced an immediate (< 30 s) decrease in Ppa and calculated pulmonary vascular resistance (P < 0.05 each) but did not return either to baseline hyperoxic values. Increasing the concentration of NO to 74 and 145 ppm in two dogs during hypoxia did not induce any further decreases in Ppa. Reversing hypoxia while NO remained at 47 ppm further decreased Ppa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systemic arterial pressure. MetHb remained low, and NO-Hb was unmeasurable. We concluded that NO inhalation only partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective to the pulmonary circulation.

scholarly journals PULMONARY ARTERIAL HYPEROXIA PRODUCING INCREASED PULMONARY VASCULAR RESISTANCE

1960 ◽  
Vol 40 (5) ◽  
pp. 588-601 ◽  
Author(s):  
Peter V. Moulder ◽  
Joseph R. Lancaster ◽  
Robert W. Harrison ◽  
Stephen L. Michel ◽  
Mark Snyder ◽  
...  
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial

scholarly journals Estimating afterload, systemic vascular resistance and pulmonary vascular resistance in an intensive care setting

2012 ◽  
Vol 45 (18) ◽  
pp. 501-506
Author(s):  
David J. Stevenson ◽  
James Revie ◽  
Geoffrey J. Chase ◽  
Geoffrey M. Shaw ◽  
Bernard Lambermont ◽  
...  
Keyword(s):  
Intensive Care ◽  
Pulmonary Vascular Resistance ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Care Setting ◽  
Intensive Care Setting
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