scholarly journals Action of Promethazine on Systemic Blood Pressure, Pulmonary Artery Pressure, and Pulmonary Blood-flow

BMJ ◽  
1954 ◽  
Vol 2 (4899) ◽  
pp. 1266-1267 ◽  
Author(s):  
S. Howarth ◽  
S. G. Owen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Artery Pressure

scholarly journals Progressive dysfunction of nitric oxide synthase in a lamb model of chronically increased pulmonary blood flow: a role for oxidative stress

2008 ◽  
Vol 295 (5) ◽  
pp. L756-L766 ◽  
Author(s):  
Peter E. Oishi ◽  
Dean A. Wiseman ◽  
Shruti Sharma ◽  
Sanjiv Kumar ◽  
Yali Hou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Lung Tissue ◽  
Pulmonary Blood Flow ◽  
Artery Pressure ◽  
Oxide Synthase ◽  
Inhaled No

Cardiac defects associated with increased pulmonary blood flow result in pulmonary vascular dysfunction that may relate to a decrease in bioavailable nitric oxide (NO). An 8-mm graft (shunt) was placed between the aorta and pulmonary artery in 30 late gestation fetal lambs; 27 fetal lambs underwent a sham procedure. Hemodynamic responses to ACh (1 μg/kg) and inhaled NO (40 ppm) were assessed at 2, 4, and 8 wk of age. Lung tissue nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), neuronal NOS (nNOS), inducible NOS (iNOS), and heat shock protein 90 (HSP90), lung tissue and plasma nitrate and nitrite (NOx), and lung tissue superoxide anion and nitrated eNOS levels were determined. In shunted lambs, ACh decreased pulmonary artery pressure at 2 wk ( P < 0.05) but not at 4 and 8 wk. Inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). In control lambs, ACh and inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). Total NOS activity did not change from 2 to 8 wk in control lambs but increased in shunted lambs (ANOVA, P < 0.05). Conversely, NOxlevels relative to NOS activity were lower in shunted lambs than controls at 4 and 8 wk ( P < 0.05). eNOS protein levels were greater in shunted lambs than controls at 4 wk of age ( P < 0.05). Superoxide levels increased from 2 to 8 wk in control and shunted lambs (ANOVA, P < 0.05) and were greater in shunted lambs than controls at all ages ( P < 0.05). Nitrated eNOS levels were greater in shunted lambs than controls at each age ( P < 0.05). We conclude that increased pulmonary blood flow results in progressive impairment of basal and agonist-induced NOS function, in part secondary to oxidative stress that decreases bioavailable NO.

Physiological alterations in increased pulmonary blood flow with and without pulmonary hypertension

1961 ◽  
Vol 16 (2) ◽  
pp. 305-308 ◽  
Author(s):  
Lois T. Ellison ◽  
David P. Hall ◽  
Thomas Yeh ◽  
H. Mobarhan ◽  
Joseph Rossi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Function ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Artery Hypertension ◽  
Systolic Pulmonary Artery Pressure ◽  
Venous Admixture ◽  
Artery Pressure ◽  
Physiological Alterations

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960

Pressure-Flow Relationships in the Dog Lung During Acute, Subtotal Pulmonary Vascular Occlusion

1958 ◽  
Vol 192 (3) ◽  
pp. 613-619 ◽  
Author(s):  
Michael T. Lategola
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Vascular Occlusion ◽  
Percentage Change ◽  
Artery Pressure ◽  
Vascular Bed ◽  
Change In Mean ◽  
Pulmonary Vascular Bed

The relationship of pulmonary artery pressure to pulmonary blood flow was studied in the dog by means of occlusive shifting of blood flow within the pulmonary vascular bed. All experiments were performed using the closed-chest preparation. The range of blood flow increases studied was 25–388%. A graphical plot of the percentage change in blood flow versus the percentage change in mean pulmonary artery pressure is presented. A visually estimated curve of this latter data is presented, discussed and compared to four other curves from previous pulmonary vascular studies. A comparison of these curves suggests that the relative maximum capacity of the pulmonary vascular bed of man and dog are similar. These curves plus certain assumptions allow the speculative delineation of a graphical area representing the ‘active’ vasomotor component of exercise at different levels of pulmonary blood flow increase.

Acute effects of partial compression of ductus arteriosus on fetal pulmonary circulation

1989 ◽  
Vol 257 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Base Line ◽  
Acute Effects ◽  
Artery Pressure

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute increases in anastomotic bronchial systemic to pulmonary blood flow due to generalized lung injury

1987 ◽  
Vol 62 (6) ◽  
pp. 2358-2361 ◽  
Author(s):  
S. Lakshminarayan ◽  
S. K. Jindal ◽  
W. Kirk ◽  
J. Butler
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Autologous Blood ◽  
Lower Lobe ◽  
Lung Ventilation ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pulmonary Vessels ◽  
Lung Lobe

Since pulmonary blood flow to regions involved in adult respiratory disease syndrome (ARDS) is reduced by hypoxic vasoconstriction, compression by cuffs of edema, and local thromboses, we postulated that the bronchial circulation must enlarge to provide for the inflammatory response. We measured anastomotic bronchial systemic to pulmonary blood flow [QBr(s-p)] serially in a lung lobe in 31 open-chest dogs following a generalized lobar injury simulating ARDS. The pulmonary circulation of the weighed left lower lobe (LLL) was isolated and perfused (zone 2) with autologous blood in anesthetized dogs. QBr(s-p) was measured from the amount of blood which overflowed from this closed vascular circuit corrected by any changes in the lobe weight. The LLL was ventilated with 5% CO2 in air. The systemic blood pressure (volume infusion), gases, and acid-base status (right lung ventilation) were kept constant. We injured the LLL via the airway by instilling either 0.1 N HCl or a mixture of glucose and glucose oxidase or via the pulmonary vessels by injecting either alpha-naphthylthiourea or oleic acid into the LLL pulmonary artery. In both types of injury, there was a prompt rise in QBr(s-p) (mean rise = 247% compared with control), which was sustained for the 2 h of observation. The cause of this increase in flow was studied. Control instillation of normal saline into the airways or into the pulmonary vessels did not change QBr(s-p) nor did a similar increase in lobar fluid (weight) due to hydrostatic edema. Neither cardiac output nor systemic blood pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)

The Use of Histamine Questioned

PEDIATRICS ◽  
1976 ◽  
Vol 58 (5) ◽  
pp. 776-777
Author(s):  
Shyamal K. Sanyal
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Cardiac Catheterization ◽  
Pulmonary Blood Flow ◽  
Pathogenetic Mechanism ◽  
Artery Pressure

The pathogenetic mechanism proposed by Levin et al.1 to explain the persistence of fetal cardiopulmonary circulatory pathway (PFCCP) during infancy if of interest. However, their suggestion that use of histamine injected directly into the pulmonary artery may be beneficial in such patients raises some questions. The initial cardiac catheterization data in their patient at the age of 33 days show hypoxia and hypercarbia. The authors have indicated in Table II that both of these factors could produce a decrease in pulmonary blood flow as well as an increase in pulmonary artery pressure and pulmonary vascular resistance.

VENTILATION-PERFUSION RELATIONSHIPS IN CHILDREN WITH HEART DISEASE AND DIMINISHED PULMONARY BLOOD FLOW

PEDIATRICS ◽  
1968 ◽  
Vol 42 (5) ◽  
pp. 778-785
Author(s):  
Martin H. Lees ◽  
Richard H. Burnell ◽  
Clarence L. Morgan ◽  
Benjamin B. Ross
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Pulmonary Function ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Alveolar Ventilation ◽  
Uneven Distribution ◽  
Artery Pressure ◽  
Major Abnormality

Pulmonary function of infants and children with diminished pulmonary blood flow was studied by measurement of alveolar ventilation and alveolar-arterial gas tension differences of O2, CO2, and N2. The increased ventilation of these subjects was found to be effective in CO2 elimination (arterial CO2 tension, 31 mm Hg), but there was evidence of considerable unevenness of distribution of ventilation/perfusion ratios (VAQ). A measure of the degree of VA/Q unevenness was obtained by use of the urine-alveolar nitrogen tension difference. It is likely, under the prevailing conditions of hyperventilation and hypoperfusion, that maldistribution of perfusion is the major abnormality. Uneven distribution of perfusion is most probably due to the effects of gravity enhanced by low pulmonary artery pressure and blood flow—an exaggenation of the normal physiologic relative overperfusion of the lower-most parts of the lung.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

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