scholarly journals Effects of hydralazine and nitroprusside on cardiopulmonary function when a decrease in cardiac output complicates a short-term increase in pulmonary vascular resistance.

Circulation ◽  
1983 ◽  
Vol 68 (6) ◽  
pp. 1299-1303 ◽  
Author(s):  
K Y Lee ◽  
D W Molloy ◽  
L Slykerman ◽  
R M Prewitt
Keyword(s):  
Cardiac Output ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Short Term ◽  
Cardiopulmonary Function

Increased pulmonary vascular resistance and reduced stroke volume in association with CO2retention and inferior vena cava dilatation

2006 ◽  
Vol 101 (3) ◽  
pp. 866-872 ◽  
Author(s):  
Darija Baković ◽  
Davor Eterović ◽  
Zoran Valic ◽  
Žana Saratlija-Novaković ◽  
Ivan Palada ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Inferior Vena Cava ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Inferior Vena ◽  
Vena Cava ◽  
Arterial Oxygen ◽  
Breath Holding ◽  
Oxygen Saturation Level ◽  
The Impact

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO2and O2were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO2increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (∼4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO2retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.

Modulation of Pulmonary Vascular Resistance and Edema Formation by Short-Term Infusion of a 10% Fish Oil Emulsion

1993 ◽  
Vol 20 (6) ◽  
pp. 291-300 ◽  
Author(s):  
T. Koch ◽  
H.P. Duncker ◽  
A. Klein ◽  
E. Schlotzer ◽  
B.M. Peskar ◽  
...  
Keyword(s):  
Fish Oil ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Short Term ◽  
Edema Formation ◽  
Oil Emulsion

Low exercise pulmonary resistance is not dependent on vasodilator prostaglandins

1983 ◽  
Vol 55 (2) ◽  
pp. 558-561 ◽  
Author(s):  
J. Lindenfeld ◽  
J. T. Reeves ◽  
L. D. Horwitz
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Cyclooxygenase Inhibitors ◽  
Pulmonary Resistance ◽  
Before And After ◽  
Pulmonary Arterial

In resting conscious dogs, administration of cyclooxygenase inhibitors results in modest increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that vasodilator prostaglandins play a role in maintaining the low vascular resistance in the pulmonary bed. To assess the role of these vasodilator prostaglandins on pulmonary vascular resistance during exercise, we studied seven mongrel dogs at rest and during exercise before and after intravenous meclofenamate (5 mg/kg). Following meclofenamate, pulmonary vascular resistance rose both at rest (250 24 vs. 300 +/- 27 dyn . s . cm-5, P less than 0.01) and with exercise (190 +/- 9 vs. 210 +/- 12 dyn . s . cm-5, P less than 0.05). Systemic vascular resistance rose slightly following meclofenamate both at rest and during exercise. There were no changes in cardiac output. The effects of cyclooxygenase inhibition, although significant, were less during exercise than at rest. This suggests that the normal fall in pulmonary vascular resistance during exercise depends largely on factors other than vasodilator prostaglandins.

Effects of Acutely Induced Changes in Arterial pH on Pulmonary Vascular Resistance during Normoxia and Hypoxia in Awake Dogs

1972 ◽  
Vol 42 (3) ◽  
pp. 277-287 ◽  
Author(s):  
O. G. Thilenius ◽  
Carol Derenzo
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Main Pulmonary Artery ◽  
Compensatory Mechanisms ◽  
Artery Pressure ◽  
Arterial Ph ◽  
Small Rise

1. Awake dogs with chronically implanted catheters (pulmonary artery, left atrium, aorta) and electromagnetic flow probe (main pulmonary artery) underwent five types of experiments in succession: (1) slow infusion of 0·4 m-hydrochloric acid; (2) rapid infusion of 1·0 m-sodium bicarbonate; (3) exposure to 30 min of hypoxia (10% O2); (4) exposure to hypoxia after arterial pH had been lowered to 7·30; (5) exposure to hypoxia after pH had been increased to 7·55. Intravascular pressures, pulmonary vascular resistance, cardiac output, arterial gas tension and pH were studied. 2. Acute acidosis (pH 7·21) resulted in a small rise in pulmonary artery pressure, cardiac output and pulmonary vascular resistance, associated with a decrease in Pa,co2. Acute alkalosis (pH 7·61) was accompanied by a small rise in pulmonary artery pressure, marked increase in cardiac output, a fall in pulmonary vascular resistance and mild elevation in Pa,co2. During acidosis hypoxia resulted in a more pronounced rise in pulmonary vascular resistance than during alkalosis (P < 0·01). 3. The study provides evidence that in the intact, awake dog with its compensatory mechanisms acute alkalosis decreases pulmonary vascular resistance by decreasing vascular tone and/or recruitment of pulmonary vascular channels; it diminishes the vasoconstrictive response to hypoxia; conversely, mild acidosis increases the pulmonary vascular resistance slightly and enhances vasoconstriction during hypoxia to a small extent.

Multipoint pulmonary vascular pressure-cardiac output plots in conscious dogs

1985 ◽  
Vol 249 (2) ◽  
pp. H351-H357 ◽  
Author(s):  
R. F. Lodato ◽  
J. R. Michael ◽  
P. A. Murray
Keyword(s):  
Cardiac Output ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Vasomotor Tone ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Induced Changes ◽  
Arterial Po2

To characterize quantitatively the relationships among pulmonary vascular pressures (P) and cardiac output (Q) in conscious dogs, multipoint plots of pulmonary arterial (PAP), pulmonary capillary wedge (PCWP), PAP - PCWP, and left atrial (LAP) pressure versus Q were generated by graded constriction of the thoracic inferior vena cava (IVC) to vary Q. Slopes and extrapolated pressure intercepts from linear regression fits to the P/Q plots were determined for three inspired oxygen tensions: normoxia, hyperoxia, and hypoxia. During normoxia (arterial Po2 87 +/- 1 Torr), the extrapolated pressure intercepts for PAP, PCWP, and PAP - PCWP were virtually 0 mmHg, and for LAP, substantially negative (-5.5 +/- 1.1 mmHg; P less than 0.01). Hyperoxia (Po2 365 +/- 28 Torr) had no effect on any of the P/Q plots. In contrast, hypoxia (Po2 51 +/- 1 Torr) significantly increased the intercepts (P less than 0.01) as well as the slopes (P less than 0.05) of PAP and PAP - PCWP versus Q, but produced only minor changes in PCWP and LAP versus Q. These hypoxia-induced changes in intercepts, perhaps related to changes in critical closing pressures, demonstrate the limitations of pulmonary vascular resistance calculations (quotient of pressure gradient and Q) in quantifying changes in pulmonary vasomotor tone. In this way, the IVC constriction technique provides a more complete description of P/Q relationships than that permitted by simple calculations of pulmonary vascular resistance. We conclude that this technique can be utilized to investigate the effects of other physiological and pharmacological interventions on pulmonary vasomotor tone in conscious dogs.

Monocrotaline model of noncardiogenic pulmonary edema in dogs

1978 ◽  
Vol 45 (6) ◽  
pp. 962-965 ◽  
Author(s):  
W. C. Miller ◽  
D. L. Rice ◽  
R. G. Kreusel ◽  
C. W. Bedrossian
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Intravenous Injection ◽  
Vascular Resistance ◽  
Endothelial Damage ◽  
Lung Water

Monocrotaline, a plant alkaloid shown histologically to produce pulmonary endothelial damage and edema, was used in dogs to produce an acute model of noncardiogenic pulmonary edema. Following intravenous injection there was no change in pulmonary vascular pressures or heart rate; cardiac output fell and pulmonary vascular resistance increased. After 2 h measurement of lung water demonstrated modest pulmonary edema in all animals. The degree of edema produced was more consistent and reproducible than that following alloxan or alpha-naphthylthiourea.

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