Responses of pulmonary C-fibre and rapidly adapting receptor afferents to pulmonary congestion and edema in dogs

1992 ◽  
Vol 70 (1) ◽  
pp. 68-76 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda
Keyword(s):  
Pulmonary Edema ◽  
Extravascular Lung Water ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Control Value ◽  
Significant Stimulation ◽  
C Fibre ◽  
The Mean

The effects of cardiogenic and noncardiogenic pulmonary edema on the activities of rapidly adapting receptors (RARs) and pulmonary C-fibre receptors were investigated in dogs anaesthetized with chloralose. Cardiogenic pulmonary edema was produced by elevating the mean left atrial pressure by 25 mmHg (1 mmHg = 133.32 Pa) above the control value for a period of 45 min, by partial obstruction of the mitral valve. Noncardiogenic pulmonary edema was produced by injecting alloxan (100 mg/kg) intravenously. The effect of the latter was examined on RARs alone. Cardiogenic edema activated RARs (n = 8) and the activity was greatest during the first few minutes after elevation of mean left atrial pressure. The pulmonary C-fibre receptors (n = 6) were also activated by cardiogenic edema, but these responses were variable. Noncardiogenic pulmonary edema also activated RAR (n = 6), and this response was maintained during the entire recording period (20 min). The extravascular lung water (%), measured 15 min (n = 5) and 45 min (n = 5) after the elevation of the mean left atrial pressure, was significantly elevated above control values. However, these two values were not significantly different from each other. The extravascular lung water increased significantly after the injection of alloxan also (n = 5). These results show that during pulmonary edema, there is significant stimulation of the RARs and the pulmonary C-fibre receptors. It is suggested that the reflex respiratory responses observed in pulmonary edema may be due to the activation of both the RARs and the pulmonary C-fibre receptors.Key words: alloxan, cardiogenic edema, vagus.

Correlation of Extravascular Lung Water with Cardiac Output and Left Atrial Pressure in Man

1976 ◽  
Vol 51 (3) ◽  
pp. 5P-6P
Author(s):  
C. G. C. MacArthur ◽  
C. G. Rhodes ◽  
F. Fazio ◽  
T. Jones ◽  
J. M. B. Hughes
Keyword(s):  
Cardiac Output ◽  
Extravascular Lung Water ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water

Extravascular Lung Water: Effects of Using Ionic Contrast Media at Varying Levels of Left Atrial Pressure and During Myocardial Ischemia

Radiology ◽  
1984 ◽  
Vol 152 (3) ◽  
pp. 575-578 ◽  
Author(s):  
Robert A. Slutsky ◽  
Jeffrey J. Brown ◽  
Gideon Strich
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Media ◽  
Extravascular Lung Water ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Ionic Contrast ◽  
Water Effects

β-Adrenergic agonist therapy accelerates the resolution of hydrostatic pulmonary edema in sheep and rats

2000 ◽  
Vol 89 (4) ◽  
pp. 1255-1265 ◽  
Author(s):  
James A. Frank ◽  
Yibing Wang ◽  
Oscar Osorio ◽  
Michael A. Matthay
Keyword(s):  
Pulmonary Edema ◽  
Left Atrial ◽  
Experimental Studies ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Adrenergic Agonist ◽  
Agonist Therapy ◽  
Arterial Blood ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

To determine whether β-adrenergic agonist therapy increases alveolar liquid clearance during the resolution phase of hydrostatic pulmonary edema, we studied alveolar and lung liquid clearance in two animal models of hydrostatic pulmonary edema. Hydrostatic pulmonary edema was induced in sheep by acutely elevating left atrial pressure to 25 cmH2O and instilling 6 ml/kg body wt isotonic 5% albumin (prepared from bovine albumin) in normal saline into the distal air spaces of each lung. After 1 h, sheep were treated with a nebulized β-agonist (salmeterol) or nebulized saline (controls), and left atrial pressure was then returned to normal. β-Agonist therapy resulted in a 60% increase in alveolar liquid clearance over 3 h ( P< 0.001). Because the rate of alveolar fluid clearance in rats is closer to human rates, we studied β-agonist therapy in rats, with hydrostatic pulmonary edema induced by volume overload (40% body wt infusion of Ringer lactate). β-Agonist therapy resulted in a significant decrease in excess lung water ( P < 0.01) and significant improvement in arterial blood gases by 2 h ( P < 0.03). These preclinical experimental studies support the need for controlled clinical trials to determine whether β-adrenergic agonist therapy would be of value in accelerating the resolution of hydrostatic pulmonary edema in patients.

Lung fluid balance during acute renal failure in sheep

1986 ◽  
Vol 60 (4) ◽  
pp. 1333-1340 ◽  
Author(s):  
B. T. Peterson ◽  
J. A. Brooks ◽  
R. W. Hyde
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Water Volume ◽  
Bilateral Nephrectomy ◽  
Lung Water ◽  
Lung Fluid ◽  
Protein Clearance

To determine whether uremia changes lung vascular permeability, we measured the flow of lymph and proteins from the lungs of acutely uremic sheep. Acute renal failure was induced by either bilateral nephrectomy or by reinfusing urine. Both models of renal failure increased the plasma creatinine from 0.8 +/- 0.3 to 11 +/- 1 mg/dl in 3 days but caused no significant change in the flow of lymph from the lungs. To determine whether uremia increased the protein clearance response to elevated pulmonary microvascular pressures, we inflated a balloon in the left atrium for 2 h before and 3 days after inducing acute renal failure. In seven sheep, before removing the kidneys, the 20 cmH2O elevation of left atrial pressure increased the protein clearance 3.9 +/- 3.0 ml/h (from 9.5 +/- 4.9 to 13.4 +/- 5.4 ml/h). Three days after the bilateral nephrectomy the same increase in left atrial pressure increased the protein clearance 6.4 +/- 3.6 ml/h (from 6.1 +/- 2.1 to 12.5 +/- 5.2 ml/h), which was a significantly larger increase than that measured before the nephrectomy (P less than 0.05). Sham nephrectomy in seven sheep caused the protein clearance response to the elevated left atrial pressure to fall from 4.7 +/- 1.9 ml/h before the sham nephrectomy to 2.6 +/- 1.4 ml/h 3 days later (P less than 0.05). Uremia due to reinfusion of urine in five sheep did not affect the protein clearance response to elevations in left atrial pressure. Neither model of acute uremia increased the postmortem extravascular lung water volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of thoracic duct drainage on hydrostatic pulmonary edema and pleural effusion in sheep

1991 ◽  
Vol 71 (1) ◽  
pp. 314-316 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
G. A. Laine ◽  
J. C. Gabel
Keyword(s):  
Pleural Effusion ◽  
Central Venous Pressure ◽  
Pulmonary Edema ◽  
Thoracic Duct ◽  
Left Atrial ◽  
Venous Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Central Venous ◽  
Pulmonary Arterial

Positive end-expiratory pressure (PEEP) increases central venous pressure, which in turn impedes return of systemic and pulmonary lymph, thereby favoring formation of pulmonary edema with increased microvascular pressure. In these experiments we examined the effect of thoracic duct drainage on pulmonary edema and hydrothorax associated with PEEP and increased left atrial pressure in unanesthetized sheep. The sheep were connected via a tracheostomy to a ventilator that supplied 20 Torr PEEP. By inflation of a previously inserted intracardiac balloon, left atrial pressure was increased to 35 mmHg for 3 h. Pulmonary arterial, systemic arterial, and central venous pressure as well as thoracic duct lymph flow rate were continuously monitored, and the findings were compared with those in sheep without thoracic duct cannulation (controls). At the end of the experiment we determined the severity of pulmonary edema and the volume of pleural effusion. With PEEP and left atrial balloon insufflation, central venous and pulmonary arterial pressure were increased approximately threefold (P less than 0.05). In sheep with a thoracic duct fistula, pulmonary edema was less (extra-vascular fluid-to-blood-free dry weight ratio 4.8 +/- 1.0 vs. 6.1 +/- 1.0; P less than 0.05), and the volume of pleural effusion was reduced (2.0 +/- 2.9 vs. 11.3 +/- 9.6 ml; P less than 0.05). Our data signify that, in the presence of increased pulmonary microvascular pressure and PEEP, thoracic duct drainage reduces pulmonary edema and hydrothorax.

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation

1991 ◽  
Vol 70 (5) ◽  
pp. 1991-1995 ◽  
Author(s):  
S. A. Gu ◽  
J. Ducas ◽  
U. Schick ◽  
R. M. Prewitt
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Mean Value ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Response ◽  
Wide Range ◽  
Pulmonary Arterial ◽  
The Mean

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

Aerosolized Pseudomonas elastase and lung fluid balance in anesthetized sheep

1992 ◽  
Vol 72 (5) ◽  
pp. 1927-1933 ◽  
Author(s):  
B. T. Peterson ◽  
M. L. Collins ◽  
L. D. Gray ◽  
A. O. Azghani
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Water Volume ◽  
Lung Epithelium ◽  
Lung Water ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

The role of the lung epithelium in lung fluid balance was studied by ventilating anesthetized sheep with an aerosol of 20 mg of elastase from Pseudomonas aeruginosa (Ps. elastase) to increase lung epithelial permeability without affecting lung endothelial permeability or lung vascular pressures. Ps. elastase had no effect on the lung vascular pressures, the alveolar-arterial PO2 gradient (A-aPO2), the flow or protein concentration of the lung lymph, or the postmortem water volume of the lungs. The morphological alveolar flooding score in these sheep was 2.5 times the control level, but this was only marginally significant. Elevation of the left atrial pressure by 20 cmH2O alone increased the postmortem lung water volume but had no effect on A-aPO2, the alveolar flooding score, or the lung epithelial permeability assessed by the clearance of 99mTc-labeled human serum albumin. Addition of aerosolized Ps. elastase to these sheep had no effect on the total lung water volume, but it caused a redistribution of water into the air spaces, as evidenced by significant increases in the alveolar flooding score and A-aPO2 (P less than 0.01). Elevation of the left atrial pressure by 40 cmH2O without elastase caused the same response as elevation of the left atrial pressure by 20 cmH2O with elastase, except the higher pressure caused a greater increase in the total lung water volume. We conclude that alteration of the integrity of the lung epithelium with aerosolized Ps. elastase causes a redistribution of lung water into the alveoli without affecting the total lung water volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Specificity and sensitivity of noninvasive measurement of pulmonary vascular protein leak

1985 ◽  
Vol 59 (2) ◽  
pp. 564-574 ◽  
Author(s):  
I. M. Dauber ◽  
W. T. Pluss ◽  
A. VanGrondelle ◽  
R. S. Trow ◽  
J. V. Weil
Keyword(s):  
Lung Injury ◽  
Left Atrial ◽  
Low Dose ◽  
Gamma Probe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
High Dose ◽  
Lung Water ◽  
Specificity And Sensitivity ◽  
Rate Of Increase

Noninvasive techniques employing external counting of radiolabeled protein have the potential for measuring pulmonary vascular protein permeability, but their specificity and sensitivity remain unclear. We tested the specificity and sensitivity of a double-radioisotope method by injecting radiolabeled albumin (131I) and erythrocytes (99mTc) into anesthetized dogs and measuring the counts of each isotope for 150 min after injection with an external gamma probe fixed over the lung. We calculated the rate of increase of albumin counts measured by the probe (which reflects the rate at which protein leaks into the extravascular space). To assess permeability we normalized the rate of increase in albumin counts for changes in labeled erythrocyte signal to minimize influence of changes in vascular surface area and thus derived an albumin leak index. We measured the albumin leak index and gravimetric lung water during hydrostatic edema (acutely elevating left atrial pressure by left atrial balloon inflation: mean pulmonary arterial wedge pressure = 22.6 Torr) and in lung injury edema induced by high- (1.0 g/kg) and low-dose (0.25 g/kg) intravenous thiourea. To test specificity we compared hydrostatic and high-dose thiourea edema. The albumin leak index increased nearly fourfold from control after thiourea injury (27.2 +/- 2.3 X 10–4 vs. 7.6 +/- 0.9 X 10–4 min-1) but did not change from control levels after elevating left atrial pressure (8.9 +/- 1.2 X 10–4 min-1) despite comparable increases in gravimetric lung water. To test sensitivity we compared low-dose thiourea with controls. Following low-dose thiourea, the albumin leak index nearly doubled despite the absence of a measurable increase in lung water. We conclude that a noninvasive double radioisotope measurement of pulmonary vascular protein leak, employing external counting techniques and a simplified method of calculation, is specific for lung injury and is also sensitive enough to detect lung injury insufficient to produce detectable pulmonary edema.

Catecholamines increase lung edema clearance in rats with increased left atrial pressure

2001 ◽  
Vol 90 (3) ◽  
pp. 1088-1094 ◽  
Author(s):  
Zaher S. Azzam ◽  
Fernando J. Saldias ◽  
Alejandro Comellas ◽  
Karen M. Ridge ◽  
David H. Rutschman ◽  
...  
Keyword(s):  
Left Atrial ◽  
Sch 23390 ◽  
Alveolar Epithelium ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Edema ◽  
Atpase Inhibitor ◽  
Fluid Reabsorption ◽  
Control Value ◽  
Rat Lungs

During hydrostatic pulmonary edema, active Na+ transport and alveolar fluid reabsorption are decreased. Dopamine (DA) and isoproterenol (ISO) have been shown to increase active Na+ transport in rat lungs by upregulating Na+-K+-ATPase in the alveolar epithelium. We studied the effects of DA and ISO in isolated rat lungs with increased left atrial pressure (Pla = 15 cmH2O) compared with control rats with normal Pla (Pla = 0). Alveolar fluid reabsorption decreased from control value of 0.51 ± 0.02 to 0.27 ± 0.02 ml/h when Pla was increased to 15 cmH2O ( P < 0.001). DA and ISO increased the alveolar fluid reabsorption back to control levels. Treatment with the D1antagonist SCH-23390 inhibited the stimulatory effects of DA (0.30 ± 0.02 ml/h), whereas fenoldopam, a specific D1-receptor agonist, increased alveolar fluid reabsorption in rats exposed to Pla of 15 cmH2O (0.47 ± 0.04 ml/h). Propranolol, a β-adrenergic-receptor antagonist, blocked the stimulatory effects of ISO; however, it did not affect alveolar fluid reabsorption in control or DA-treated rats. Amiloride (a Na+ channel blocker) and ouabain (a Na+-K+-ATPase inhibitor), either alone or together, inhibited the stimulatory effects of DA. Colchicine, which disrupts the cellular microtubular transport of ion-transporting proteins to the plasma membrane, inhibited the stimulatory effects of DA, whereas the isomer β-lumicolchicine did not block the stimulatory effects of DA. These data suggest that DA and ISO increase alveolar fluid reabsorption in a model of increased Pla by regulating active Na+ transport in rat alveolar epithelium. The effects of DA and ISO are mediated by the activation of dopaminergic D1receptors and the β-adrenergic receptors, respectively.

Pulmonary Edema and Elevated Left Atrial Pressure: Four Hours and Beyond

Physiology ◽  
2002 ◽  
Vol 17 (6) ◽  
pp. 223-226 ◽  
Author(s):  
R. E. Drake ◽  
M. F. Doursout
Keyword(s):  
Connective Tissue ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Cardiogenic Pulmonary Edema ◽  
Left Heart ◽  
Fluid Accumulation ◽  
Increased Pressure

Cardiogenic pulmonary edema is caused by the increase in left atrial pressure when the left heart fails. The increased pressure causes rapid fluid accumulation within the lung interstitial spaces. However, over the following days to weeks, additional fluid may accumulate due to the deposition of excess lung connective tissue.

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