Effect of lung inflation and hypoxia on pulmonary arterial blood volume

1977 ◽  
Vol 43 (1) ◽  
pp. 8-13 ◽  
Author(s):  
E. J. Quebbeman ◽  
C. A. Dawson
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Transpulmonary Pressure ◽  
The Other ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

Isolated cat lungs were perfused with constant blood flow. During control conditions (Pa02, 100 Torr), pulmonary artery pressure increased as the lungs were inflated. Hypoxia (Pa02, 22 Torr) increased arterial pressure. However, as the lungs were inflated arterial pressure fell. Thus, the magnitude of the hypoxic pressor response was reduced by inflation. During control conditions, arterial volume (ether bolus method) increased with increasing transpulmonary pressure. Hypoxia decreased arterial volume, and the increase in arterial volume with inflation was somewhat less than that during control conditions. When the influences of vascular and transpulmonary pressures were examined independently by changing one while holding the other constant, increasing transpulmonary pressure increased arterial volume beyond that which could be accounted for by changes in the differences between arterial and pleural pressure. However, this influence of transpulmonary pressure did not appear to be altered by hypoxia. Thus, while hypoxia decreased arterial volume at all levels of lung inflation, it had relatively little effect on the influence of interdependence between the pulmonary arterial bed and the surrounding lung tissue.

Effects of lung inflation on pulmonary arterial blood volume in intact dogs

1975 ◽  
Vol 38 (4) ◽  
pp. 675-680 ◽  
Author(s):  
A. Wanner ◽  
S. Zarzecki ◽  
M. A. Sackner
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Valsalva Maneuver ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Mueller Maneuver ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

The isolated effects of alterations of lung inflation and transmural pulmonary arterial pressure (pressure difference between intravascular and pleural pressure) on pulmonary arterial blood volume (Vpa) were investigated in anesthetized intact dogs. Using transvenous phrenic nerve stimulation, changes in transmural pulmonary arterial pressure (Ptm) at a fixed transpulmonary pressure (Ptp) were produced by the Mueller maneuver, and increases in Ptp at relatively constant Ptm by a quasi-Valsalva maneuver. Also, both Ptm and Ptp were allowed to change during open airway lung inflation. Vpa was determined during these three maneuvers by multiplying pulmonary blood flow by pulmonary arterial mean transit time obtained by an ether plethysmographic method. During open airway lung inflation, mean (plus or minus SD) Ptp increased by 7.2 (plus or minus 3.7) cmH2O and Ptm by 4.3 (plus or minus 3.4) cmH2O for a mean increase in Vpa by 26.2 (plus or minus 10.7) ml. A pulmonary arterial compliance term (Delta Vpa/Delta Ptm) calculated from the Mueller maneuver was 3.9 ml/cmH2O and an interdependence term (Delta Vpa/Delta Ptp) calculated from the quasi-Valsalva maneuver was 2.5 ml/cmH2O for a 19% increase in lung volume, and 1.2 ml/cmH2O for an increase in lung volume from 19% to 35%. These findings indicate that in normal anesthetized dogs near FRC for a given change in Ptp and Ptm the latter results in a greater increase of Vpa.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

Thromboxane does not mediate pulmonary hypertension in phorbol ester-induced acute lung injury in dogs

1990 ◽  
Vol 69 (1) ◽  
pp. 345-352 ◽  
Author(s):  
A. H. Stephenson ◽  
R. S. Sprague ◽  
T. E. Dahms ◽  
A. J. Lonigro
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
H2 Receptor Antagonist ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Relationship

Thromboxane (Tx) has been suggested to mediate the pulmonary hypertension of phorbol myristate acetate- (PMA) induced acute lung injury. To test this hypothesis, the relationship between Tx and pulmonary arterial pressure was evaluated in a model of acute lung injury induced with PMA in pentobarbital sodium-anesthetized male mongrel dogs. Sixty minutes after administration of PMA (20 micrograms/kg iv, n = 10), TxB2 increased 10-fold from control in both systemic and pulmonary arterial blood and 8-fold in bronchoalveolar lavage (BAL) fluid. Concomitantly, pulmonary arterial pressure (Ppa) increased from 14.5 +/- 1.0 to 36.2 +/- 3.5 mmHg, and pulmonary vascular resistance (PVR) increased from 5.1 +/- 0.4 to 25.9 +/- 2.9 mmHg.l-1.min. Inhibition of Tx synthase with OKY-046 (10 mg/kg iv, n = 6) prevented the PMA-induced increase in Tx concentrations in blood and BAL fluid but did not prevent or attenuate the increase in Ppa. OKY-046 pretreatment did, however, attenuate but not prevent the increase in PVR 60 min after PMA administration. Pretreatment with the TxA2/prostaglandin H2 receptor antagonist ONO-3708 (10 micrograms.kg-1.min-1 iv, n = 7) prevented the pressor response to bolus injections of 1-10 micrograms U-46619, a Tx receptor agonist, but did not prevent or attenuate the PMA-induced increase in Ppa. ONO-3708 also attenuated but did not prevent the increase in PVR. These results suggest that Tx does not mediate the PMA-induced pulmonary hypertension but may augment the increases in PVR in this model of acute lung injury.

Effect of tonsillectomy and/or adenoidectomy on pulmonary arterial pressure in adults

Open Medicine ◽  
2008 ◽  
Vol 3 (4) ◽  
pp. 482-486
Author(s):  
Saeed Abdelwhab ◽  
Khaled. Dessoukey ◽  
Gamal Lotfy ◽  
Ashraf Alsaeed ◽  
Hesham Anwar
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Arterial Oxygen ◽  
Artery Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Group 1

AbstractThe aim of the study was to determine the mean pulmonary pressure in adult with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy has any effect on mean pulmonary arterial pressure of these adult. The study was carried out on 50 patients with diagnosis of upper airway obstruction resulting from hypertrophied tonsils and adenoids (group1). 25 adults were assigned as control with similar age and sex distribution (group2). For study subjects Routine general Examinations, BMI, ECG, Chest X ray, Arterial blood gases and Echocardiography were done. Mean pulmonary arterial pressure was measured by using Doppler Echocardiography preoperatively and mean 3–4 months postoperatively in all subjects. Elevated PAP (pulmonary artery pressure) was found in 15 patients (30%) in group 1 preoperatively. Mean PAP was 28.34 ±5.11 mmHg preoperative in group 1 and 19.84 ± 5.0 mmHg in group 2 (p <0.001). PAP decrease to 22.38 ±4.28 mmHg postoperatively in group 1 (p <0.001). Arterial oxygen saturation (spo2%) increase from 93.5 ± 1.9% preoperatively to 95.3 ± 1.3% post operatively (p < 0.001). percent reduction of PAP postoperatively correlates to age (t=−2.3, p= 0.02), preoperative PAP (p =0.01) but no correlation was found with BMI. In conclusions, this Study showed that obstructed adenoid and hypertrophy of tonsils causes higher mean pulmonary artery pressure in adult & revealed that tonsil& adenoid is effective therapeutic measure in such patients. With early intervention is necessary to avoid progressive cardiopulmonary disease.

Influence of state of inflation of the lung on pulmonary vascular resistance

1960 ◽  
Vol 15 (5) ◽  
pp. 878-882 ◽  
Author(s):  
James L. Whittenberger ◽  
Maurice McGregor ◽  
Erik Berglund ◽  
Hans G. Borst
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Flow Resistance ◽  
Transpulmonary Pressure ◽  
Lung Inflation ◽  
Pulmonary Arterial ◽  
Low Levels ◽  
The Relationship ◽  
Complete Collapse

The relationship between the degree of pulmonary inflation and the pulmonary vascular resistance was studied in an open-chested dog preparation. It was possible to control the state of inflation and the blood flow to the lung under study. Vascular resistance could then be observed under controlled conditions. In most cases the resistance at complete collapse was very slightly higher than at moderate levels of inflation. In a few instances collapse was associated with a more marked elevation of resistance. Higher levels of inflation resulted in elevation of vascular resistance. At high levels of pulmonary blood flow and pulmonary arterial pressure, the flow resistance curve is lower than at low levels of blood flow. The resistance values obtained during deflation of the lung were consistently different at equal transpulmonary pressures from those obtained during inflation. The possible reasons for this hysteresis are discussed. Evidence is presented that the increased resistance at high levels of lung inflation is due to the effect of transpulmonary pressure on the vessels surrounding the alveoli. Submitted on January 11, 1960

scholarly journals THE EFFECT OF MULTIPLE EMBOLI OF THE CAPILLARIES AND ARTERIOLES OF ONE LUNG

1927 ◽  
Vol 45 (4) ◽  
pp. 643-653 ◽  
Author(s):  
Carl A. L. Binger ◽  
Douglas Boyd ◽  
Richmond L. Moore
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Respiratory Rate ◽  
Potato Starch ◽  
Left Lung ◽  
Carbon Dioxide Tension ◽  
The Other ◽  
Arterial Blood ◽  
Shallow Breathing ◽  
The Right

1. Injection of a suspension of potato starch cells into the left branch of the pulmonary artery, in quantity sufficient ordinarily to give rise to markedly accelerated respirations, resulted in no change in respiratory rate. 2. A method for injecting substances into the pulmonary artery or its branches without interfering with the blood flow to the lungs has been described. 3. Injection of similar material into one lung when the other is excluded from the circulation either by ligation or by temporary clamping does give rise to rapid and shallow breathing (from a rate of 10 to 15 per minute to one of 60 or over) identical in character to that brought about by introducing emboli into both lungs. 4. A method for clamping and releasing the pulmonary artery or its branches in a dog breathing normally with closed thorax has been devised. This is described in detail in another paper. 5. After rapid breathing has been initiated by the effect of emboli lodged in the arterioles and capillaries of the right lung, reestablishing the circulation in the other lung by releasing the clamp on its artery may or may not restore the respiratory rate to its original, normal level. 6. This discrepancy in results has not been correlated with any difference in oxygen saturation of the arterial blood, or in carbon dioxide tension or pH of its plasma. 7. It is, however, believed to be related to the gross and microscopic anatomy of the lung of which the artery has been temporarily clamped. Photomicrographs are published, showing in one dog (No. 3), in which the respiratory rate returned to normal, a normal histological picture of the left lung, and in another dog (No. 4), in which the rate remained rapid after release of the clamp, a picture characterized by congestion and dilatation of arterioles and capillaries. 8. The fact that accelerated respirations result from emboli in the pulmonary capillaries and arterioles only after a certain quantity of material has been introduced, and the fact that emboli in one lung do not occasion accelerated respirations unless the circulation through the other lung is occluded or abnormal, leads us to the conclusion that the phenomenon is not an irritative stimulus due to foreign bodies, but is in some manner related to (a) diminution of the pulmonary vascular bed, (b) resistance to the blood flow through the lungs or (c) congestion or dilatation of the arterioles and capillaries of the lungs.

Pulmonary vasoconstrictor responses to graded decreases in precapillary blood PO2 in intact-chest cat

1981 ◽  
Vol 51 (4) ◽  
pp. 1009-1016 ◽  
Author(s):  
A. L. Hyman ◽  
R. T. Higashida ◽  
E. W. Spannhake ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Venous Blood ◽  
Pulmonary Veins ◽  
Right Atrial ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Pulmonary Arterial ◽  
Alveolar Capillary

The effects of graded changes in pulmonary lobar arterial blood PO2 and ventilatory hypoxia were investigated in the intact-chest cat under conditions of controlled lobar blood flow. A reduction in precapillary PO2 from systemic arterial levels to below 60 Torr increased lobar arterial pressure. Ventilation with 10% O2 increased lobar arterial pressure, and responses to ventilatory hypoxia and precapillary hypoxemia were independent but additive. The magnitude of the pressor response to precapillary hypoxemia was similar in experiments in which the lung was autoperfused with right atrial blood or cross-perfused with aortic blood from a donor cat breathing 10% O2. During retrograde perfusion of the ventilated lung, a reduction in pulmonary venous PO2 to 40 Torr did not affect inflow pressure. The present data suggest that sensor sites upstream to the alveolar-capillary region in segments of lobar artery unexposed to alveolar gas sense a reduction in precapillary blood PO2 and elicit a pulmonary vasoconstrictor response. The sensor site in the precapillary segment is independent of sensors in the alveolar-capillary-exposed segment region, and the effects of stimulation of both sensors on the pulmonary vascular bed are additive. In addition, the present data indicate that sensors in the pulmonary veins do not sense a reduction in PO2 in venous blood and elicit a vasoconstrictor response. These data suggest that the mixed venous blood PO2 may exert an important regulatory role in controlling pulmonary arterial pressure and pulmonary vascular resistance in the cat under normal and pathological conditions.

Systemic and pulmonary vasomotor waves

1965 ◽  
Vol 209 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Ricardo Ferretti ◽  
Neil S. Cherniack ◽  
Guy Longobardo ◽  
O. Robert Levine ◽  
Eugene Morkin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Breathing Pattern ◽  
Pulmonary Arterial Pressure ◽  
Arterial Blood Flow ◽  
Mayer Waves ◽  
Arterial Blood ◽  
Vasomotor Activity ◽  
Pulmonary Arterial

Rhythmic oscillations in systemic arterial blood pressure (Mayer waves) were produced in the dog by metabolic acidosis; hypoxia generally augmented the amplitude of the Mayer waves. When the Mayer waves exceeded 20 mm Hg in amplitude, they were associated with rhythmic fluctuations in pulmonary arterial pressure. The pulmonary arterial waves resembled the Mayer waves with respect to frequency and independence of the breathing pattern but were generally smaller in amplitude Measurements of instantaneous pulmonary arterial blood flow indicate that the rhythmic fluctuations in pulmonary arterial pressure represent the passive effects of fluctuations in pulmonary blood flow rather than fluctuations in pulmonary vasomotor activity. In turn, the swings in pulmonary arterial blood flow appear to originate in rhythmic variations in systemic vasomotor activity.

Interaction of vasopressin and opioids during rapid hemorrhage in conscious rabbits

1991 ◽  
Vol 260 (2) ◽  
pp. R373-R381 ◽  
Author(s):  
J. C. Schadt ◽  
E. M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Endogenous Opioids ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Conscious Rabbits

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

Factors influencing pulmonary and cutaneous arterial blood flow in the toad, Bufo marinus

1984 ◽  
Vol 247 (5) ◽  
pp. R884-R894 ◽  
Author(s):  
N. H. West ◽  
W. W. Burggren
Keyword(s):  
Blood Flow ◽  
Gas Flow ◽  
Lung Ventilation ◽  
Bufo Marinus ◽  
Arterial Blood Flow ◽  
Lung Inflation ◽  
Response Characteristics ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Toad Bufo

In the conscious, undisturbed toad, Bufo marinus, pulmonary arterial blood flow increased during periods of lung ventilation and decreased in intervening periods of pulmonary apnea. In unidirectionally ventilated, anesthetized toads, lung inflation produced by increasing the outflow resistance to pulmonary gas flow to 3 cmH2O caused a significant increase in pulmonary arterial blood flow and a significant decrease in cutaneous arterial blood flow. Changes in flow were associated with reciprocal changes in calculated vascular resistance. Mean pulmocutaneous pressure and cardiac frequency did not change significantly. Thus lung inflation (in the absence of changes in the composition of intrapulmonary gases) increased the proportion of total pulmocutaneous flow routed to the lungs and decreased the proportion directed to the skin. Unidirectional ventilation with air + 5% CO2 at constant lung volume produced a significant decrease in pulmonary arterial blood flow, an increase in calculated pulmonary arterial flow resistance, and a small increase in the flow to the cutaneous artery. Concomitant mild hypoxia potentiated the effects of pulmonary hypercapnia, although hypoxia alone was less effective than hypercapnia alone in decreasing pulmonary flow. Pulmonary arterial blood flow was decreased by infusion of acetylcholine into the pulmocutaneous artery, but epinephrine had no effect on either the pulmonary or cutaneous artery at doses below those that produced systemic effects. Atropine blocked all changes in pulmonary arterial blood flow. This and other evidence suggest that calculated arterial resistance changes are due to reflex changes in the tone of vascular smooth muscle. Intrapulmonary CO2-sensitive mechanoreceptors possess appropriate response characteristics to mediate the afferent limb of the reflex.

Sign in / Sign up

Export Citation Format

Share Document