Effect of continuous postive-pressure ventilation (CPPV) on edema formation in dog lung

1975 ◽  
Vol 39 (4) ◽  
pp. 672-679 ◽  
Author(s):  
P. Caldini ◽  
J. D. Leith ◽  
M. J. Brennan
Keyword(s):  
Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Arterial Oxygen Tension ◽  
Lung Parenchyma ◽  
Arterial Oxygen ◽  
Morphometric Measurements ◽  
Edema Formation ◽  
Significant Difference ◽  
Pulmonary Arterial

The effect of CPPV on edema formation in lungs perfused at constant blood flow was studied in whole dogs and in isolated dog lungs. In intact animals, subjected to an increase in left atrial pressure relative to pleural pressure of 40 Torr, pulmonary shunts correlate inversely (r = -0.82) with the level of end-expiratory pressure (PEE). CPPV had no significant effect on total extravasation of liquid even though PEE higher than 20 Torr was effective in preventing liquid from accumulating in the airways. In isolated lobes, perfused at constant blood flow and at a venous pressure of zero, accumulation of liquid occurred when PEE was increased above 8–10 Torr. At comparable levels of pulmonary arterial pressure, an increase in PEE resulted in lesser accumulation of liquid than when pulmonary venous pressure was elevated. Morphometric measurements revealed no significant difference in the distribution of accumulated liquid within the lung parenchyma between lobes made edematous either by raising venous pressuure or by raising PEE. It would appear that CPPV, while beneficial in improving arterial oxygen tension in pulmonary edema, does not prevent extravasation of liquid in lungs perfused at constant blood flow. High levels of PEE appear to damage the lung by favoring accumulation of liquid in the extravascular spaces of the lung.

Pulmonary arterial and venous constriction during hypoxia in 3- to 5-wk-old and adult ferrets

1990 ◽  
Vol 69 (6) ◽  
pp. 2183-2189 ◽  
Author(s):  
J. U. Raj ◽  
R. Hillyard ◽  
P. Kaapa ◽  
M. Gropper ◽  
J. Anderson
Keyword(s):  
Blood Flow ◽  
Pressure Drop ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Pressure Profile ◽  
Fluid Filtration ◽  
Pressure Drops ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial

We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.

Lowered pulmonary arterial pressure prevents edema after endotoxin in sheep

1987 ◽  
Vol 63 (3) ◽  
pp. 1008-1011 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
J. Katz ◽  
J. C. Gabel ◽  
G. A. Laine
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Dry Weight ◽  
Base Line ◽  
Capillary Membrane ◽  
Significant Difference ◽  
Pulmonary Arterial ◽  
The Difference

Escherichia coli endotoxin causes increased capillary membrane permeability and increased pulmonary arterial pressure (PAP) in sheep. If the pulmonary hypertension extends to the level of the microvasculature, then the increased microvascular pressure may contribute to the pulmonary edema caused by endotoxin. We tested the hypothesis that reducing the pulmonary hypertension would reduce the amount of edema caused by endotoxin. Twelve sheep were chronically instrumented with catheters to measure PAP, left atrial pressure, and central venous pressure. The sheep were divided into two groups. One group (E) of six sheep received an intravenous infusion of 4 micrograms/kg of E. coli endotoxin. The second group (E + SNP) received the same dose of endotoxin as well as a continuous infusion of sodium nitroprusside (SNP) to reduce PAP. Three hours after the endotoxin infusions, the sheep were terminated and the extravascular fluid-to-blood-free dry weight ratios of the lungs were determined (EVF). The base-line PAP was 17.5 +/- 2.7 mmHg. A two-way analysis of variance demonstrated a significant difference (P less than 0.01) in PAP between the E and E + SNP groups. Although PAP in each group varied as a function of time, the difference between the two groups did not. The mean PAP for the E + SNP group (20.9 +/- 1.5 mmHg) was lower than the E group PAP of 27.3 +/- 2.1 mmHg after the endotoxin spike. Furthermore, the E + SNP group EVF (3.9 +/- 0.2) was significantly less than the EVF of the E group (4.7 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary blood flow distribution measured by radionuclide-computed tomography

1983 ◽  
Vol 54 (1) ◽  
pp. 225-233 ◽  
Author(s):  
H. Maeda ◽  
H. Itoh ◽  
Y. Ishii ◽  
G. Todo ◽  
T. Mukai ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Flow Distribution ◽  
Mitral Valve Stenosis ◽  
Blood Flow Distribution ◽  
Pulmonary Arterial

Distributions of pulmonary blood flow per unit lung volume were measured with subjects in the prone, supine, and sitting positions by means of radionuclide-computed tomography of intravenously administered 99mTc-labeled macroaggregates of human serum albumin. The blood flow was greater in the direction of gravity in all 31 subjects except one with severe mitral valve stenosis. With the subject in a sitting position, four different types of distribution were distinguished. One type had a three-zonal blood flow distribution as previously reported by West and co-workers (J. Appl. Physiol. 19: 713–724, 1964). Pulmonary arterial pressure and venous pressure estimated from this model showed reasonable agreement with pulmonary arterial pressure and capillary wedge pressure measured by Swan-Ganz catheter in 17 supine patients and in 2 sitting patients. The method makes possible noninvasive assessment of pulmonary vascular pressures.

Achieving optimal pulmonary blood flow in the first-stage of palliation in early infancy for complex cardiac defects with hypoplastic left ventricles

1995 ◽  
Vol 5 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Tetsuya Kitagawa ◽  
Itsuo Katoh ◽  
Yoshiaki Fukumura ◽  
Masanori Yoshizumi ◽  
Yutaka Masuda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Arterial Oxygen Tension ◽  
Postoperative Mortality ◽  
Arterial Oxygen ◽  
Optimal Size ◽  
Mean Airway Pressure ◽  
Rigid Model ◽  
Pulmonary Arterial ◽  
Left Heart Syndrome

AbstractThe aim of the study was to determine the optimal size and technique for construction of the systemic-to-pulmonary arterial shunt which will provide suitable pulmonary blood flow in first-stage Norwood palliation for hypoplastic left heart syndrome in neonates. Our clinical experience suggested that an arterial oxygen tension of about 30 mm Hg immediately after cardiopulmonary bypass, with the patients being ventilated at the lowest possible mean airway pressure with an FiO2of 1.0, provided a suitable pulmonary-to-systemic flow ratio. We also aimed to clarify the characteristics of pulmonary blood flow in accordance with the size of the shunt and the change in the pulmonary vascular resistance in a simplified rigid model of the Norwood procedure. A hole of2.0 mm diameter proved adequate to provide a suitable pulmonary blood flow of 200−300 mlx002F;min in the presence of a pressure gradient of 20−40 mm Hg between the systemic and pulmonary circulations in neonates weighing 3 kg. A short central shunt with a prosthesis of4 mm in diameter produced an excessive flow of pulmonary blood. Our data suggest that using a smaller shunt than that commonly used is necessary to decrease the early and intermediate postoperative mortality. A prosthesis of 3.0 or 3.5 mm in diameter arising from the brachiocephalic artery would be acceptable and can be recommended for first-stage Norwood palliation in small infants, especially in view of the operative difficulties encountered in taking down the shunt at the time of subsequent operations.

scholarly journals A scoring system to predict the elevation of mean pulmonary arterial pressure in idiopathic pulmonary fibrosis

2018 ◽  
Vol 51 (1) ◽  
pp. 1701311 ◽  
Author(s):  
Taiki Furukawa ◽  
Yasuhiro Kondoh ◽  
Hiroyuki Taniguchi ◽  
Mitsuaki Yagi ◽  
Toshiaki Matsuda ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Arterial Pressure ◽  
Scoring System ◽  
Screening Tool ◽  
Pulmonary Arterial Pressure ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Elevated mean pulmonary arterial pressure (MPAP; ≥21 mmHg) is sometimes seen in patients with idiopathic pulmonary fibrosis (IPF) and has an adverse impact upon survival. Although early diagnosis is crucial, there is no established screening tool that uses a combination of noninvasive examinations.We retrospectively analysed IPF patients at initial evaluation from April 2007 to July 2015 and, using logistic regression analysis, created a screening tool to identify elevated MPAP. Internal validation was also assessed for external validity using a bootstrap method.Using right-heart catheterisation (RHC), elevation of MPAP was determined to be present in 55 out of 273 patients. Multivariate models demonstrated that % predicted diffusing capacity of the lung for carbon monoxide (DLCO) <50%, ratio of pulmonary artery diameter to aorta diameter (PA/Ao) on computed tomography (CT) ≥0.9 and arterial oxygen tension (PaO2) <80 Torr were independent predictors. When we assigned a single point to each variable, the prevalence of elevation of MPAP with a score of zero, one, two or three points was 6.7%, 16.0%, 29.1% and 65.4%, respectively. The area under curve (AUC) for the receiver operating characteristic (ROC) curve was good at 0.757 (95% CI 0.682–0.833).A simple clinical scoring system consisting of % predicted DLCO, PA/Ao ratio on CT and PaO2 can easily predict elevation of MPAP in patients with IPF.

Role of nitric oxide in porcine liver circulation under normal and endotoxemic conditions

1995 ◽  
Vol 78 (4) ◽  
pp. 1319-1329 ◽  
Author(s):  
T. Ayuse ◽  
N. Brienza ◽  
J. P. Revelly ◽  
J. K. Boitnott ◽  
J. L. Robotham
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Local Control ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Endotoxic Shock ◽  
Liver Blood Flow ◽  
Pulmonary Arterial

The role of nitric oxide (NO) in the liver vasculature during baseline and endotoxic shock states was evaluated in 17 anesthetized pigs. Mean systemic arterial pressure, pulmonary arterial pressure, and portal venous pressure and flow, hepatic arterial pressure and flow, and cardiac output were measured. Pressure-flow (P-Q) relationships defined resistances as a back pressure and a slope. Inhibition of nitric oxide synthase (NOS) with NG-nitro-L-arginine methyl ester (L-NAME) at baseline increased mean arterial pressure, pulmonary arterial pressure, hepatic arterial pressure, and the slopes of their P-Q relationships (P < 0.05) but had no effect on portal venous pressure or its P-Q relationship. After endotoxin (10 micrograms/kg iv), NO induced arterial dilation and attenuated increases in portal venous and pulmonary arterial resistances (P < 0.05) that were reversed by L-NAME. NOS inhibition was stereospecifically reversed by L-arginine. Local control of liver blood flow at baseline via the hepatic arterial buffer response and hepatic arterial autoregulation were increased in gain after L-NAME. Endotoxic shock ablated the hepatic arterial buffer response and autoregulation independent of either NO or an alpha-adrenergic-receptor agonist (P < 0.05). Under baseline conditions, NO modulates pulmonary, systemic, and hepatic arterial but not portal venous resistances. NO production during endotoxic shock induces arterial hypotension and hepatic arterial vasodilation and attenuates increases in both portal and pulmonary resistances. NOS inhibition in endotoxic shock could increase morbidity due to a loss of local control of liver blood flow and marked increases in resistance to venous return across both the liver and lungs.

Cardiovascular responses to vasoactive intestinal contractor, a novel endothelin-like peptide

1990 ◽  
Vol 259 (4) ◽  
pp. H1152-H1160
Author(s):  
R. K. Minkes ◽  
T. R. Higuera ◽  
G. F. Rogers ◽  
E. A. Sheldon ◽  
M. A. Langston ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Autonomic Reflexes ◽  
Pulmonary Arterial ◽  
Artery Flow ◽  
Higher Doses

Cardiovascular and pulmonary responses to vasoactive intestinal contractor (VIC), an endothelin (ET)-like peptide from the murine gastrointestinal tract, were investigated in the cat. VIC (0.1-1.0 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP) and increased central venous pressure, cardiac output, pulmonary arterial pressure, and left atrial pressure. VIC produced biphasic changes in systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). VIC increased heart rate (HR) and, at the 1 nmol/kg dose, a secondary decrease was observed. Hexamethonium blocked the changes in HR in response to VIC, whereas the ganglionic blocker, meclofenamate, or glybenclamide had no effect on changes in AP, SVR, and PVR elicited by the peptide. VIC caused small changes in right ventricular contractile force and increased distal aortic and carotid artery blood flow at all doses, with secondary decreases at the higher doses. VIC decreased superior mesenteric artery flow and decreased renal blood flow at the 1 nmol/kg dose. The changes in AP in response to VIC, ET-1, and ET-2 were similar, whereas those elicited by ET-3 and sarafotoxin 6b were similar. The present data show that VIC can produce both vasodilation and vasoconstriction in the systemic vascular bed and biphasic changes in PVR in the cat. These data show that VIC can produce complex cardiovascular responses similar to those elicited by the ET peptides and that these responses are largely independent of autonomic reflexes, release of cyclooxygenase products, and activation of ATP-regulated potassium channels. We conclude that VIC may act as an ET-like peptide.

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.

Lower vascular tone and larger plasma volume in Parkinson's disease with orthostatic hypotension

2011 ◽  
Vol 111 (2) ◽  
pp. 443-448 ◽  
Author(s):  
J. T. Groothuis ◽  
R. A. J. Esselink ◽  
J. P. H. Seeger ◽  
M. J. H. van Aalst ◽  
M. T. E. Hopman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Flow ◽  
Orthostatic Hypotension ◽  
Vascular Resistance ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Dilution Method ◽  
Significant Difference ◽  
Head Up Tilt

The pathophysiology of orthostatic hypotension in Parkinson's disease (PD) is incompletely understood. The primary focus has thus far been on failure of the baroreflex, a central mediated vasoconstrictor mechanism. Here, we test the role of two other possible factors: 1) a reduced peripheral vasoconstriction (which may contribute because PD includes a generalized sympathetic denervation); and 2) an inadequate plasma volume (which may explain why plasma volume expansion can manage orthostatic hypotension in PD). We included 11 PD patients with orthostatic hypotension (PD + OH), 14 PD patients without orthostatic hypotension (PD − OH), and 15 age-matched healthy controls. Leg blood flow was examined using duplex ultrasound during 60° head-up tilt. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. In a subset of 9 PD + OH, 9 PD − OH, and 8 controls, plasma volume was determined by indicator dilution method with radiolabeled albumin (125I-HSA). The basal leg vascular resistance was significantly lower in PD + OH (0.7 ± 0.3 mmHg·ml−1·min) compared with PD − OH (1.3 ± 0.6 mmHg·ml−1·min, P < 0.01) and controls (1.3 ± 0.5 mmHg·ml−1·min, P < 0.01). Leg vascular resistance increased significantly during 60° head-up tilt with no significant difference between the groups. Plasma volume was significantly larger in PD + OH (3,869 ± 265 ml) compared with PD − OH (3,123 ± 377 ml, P < 0.01) and controls (3,204 ± 537 ml, P < 0.01). These results indicate that PD + OH have a lower basal leg vascular resistance in combination with a larger plasma volume compared with PD − OH and controls. Despite the increase in leg vascular resistance during 60° head-up tilt, PD + OH are unable to maintain their blood pressure.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

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