Assessment of alveolar-capillary membrane permeability of dogs by aerosolization

1981 ◽  
Vol 51 (4) ◽  
pp. 955-962 ◽  
Author(s):  
G. J. Huchon ◽  
J. W. Little ◽  
J. F. Murray
Keyword(s):  
Membrane Permeability ◽  
Left Atrial ◽  
Volume Of Distribution ◽  
The Body ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pressure Groups ◽  
Capillary Membrane ◽  
Anesthetized Dogs ◽  
Alveolar Capillary

We developed a method for measuring an index of alveolar-capillary membrane permeability (PI) by aerosolizing a mixture of 99mTc-diethylenetriaminepentaacetic acid (Tc-DTPA) and 125I-antipyrine (I-AP) and injecting 111In-DTPA (In-DTPA). The I-AP was used to compute the quantity of Tc-DTPA delivered and the In-DTPA the quantity of Tc-DTPA in the body. The PI was the ratio of the uptake of Tc-DTPA per minute to the amount deposited at the end of aerosolization. In 14 anesthetized dogs we measured the volume of distribution of I-AP (0.54 +/- 0.034 l/kg body wt) and/or showed that the volumes of distribution of Tc-DTPA and In-DTPA were similar. We measured PI in four groups of dogs: control (n = 5), oleic acid (n = 5), hydrochloric acid (n = 6), and high left atrial pressure (n = 5). The PI increased significantly in both groups with acid-induced increased permeability compared with the control and high left atrial pressure groups, which did not differ from each other. We conclude that the aerosolization method is suitable for differentiating increased from normal permeability.

Effect of lymphatic cannula outflow height on lung microvascular permeability estimations

1984 ◽  
Vol 57 (5) ◽  
pp. 1412-1416 ◽  
Author(s):  
G. A. Laine ◽  
R. E. Drake ◽  
F. G. Zavisca ◽  
J. C. Gabel
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lymph Vessel ◽  
Percent Change ◽  
Permeability Surface ◽  
Percent Increase ◽  
Anesthetized Dogs ◽  
Area Product ◽  
Lung Lymph

Estimates of the pulmonary microvascular membrane reflection coefficient (sigma) and permeability-surface area product (PS) are frequently made with the assumption that a percent change in transmicrovascular fluid flux (Jv) will be represented by an equal percent change in the lymph flow rate (QL) from a single cannulated lung lymph vessel. To test this, we measured QL in seven anesthetized dogs with the outflow end of the lymph cannula set at several heights (H) above and below the lung hilus. The left atrial pressure was then elevated to increase Jv, and QL was again measured at several H's. The percent increase in QL at elevated left atrial pressure depended on H. We used the QL data and lymph and plasma protein concentrations to estimate sigma and PS with a modified form of the Kedem and Katchalsky equations. The calculated values varied considerably with H. Our results indicate that changes in Jv are not represented by equal changes in QL. Therefore, techniques for estimating permeability that depend upon QL as an estimate of Jv may lead to erroneous estimates of sigma and PS.

Vasopressin-induced changes in cardiac vagal tone and oxygen consumption in dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R838-R849
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Beta Blockade ◽  
Cardiac Denervation ◽  
Anesthetized Dogs ◽  
Atropine Treatment

Experiments were conducted in 63 dogs to determine whether stimulation of vagal tone contributes to the decrease in O2 consumption (VO2) that results from arginine vasopressin (AVP) administration. Vagal stimulation with pilocarpine did not reduce VO2 in conscious dogs. In anesthetized dogs, bilateral electrical cervical efferent vagal stimulation lowered both cardiac output (CO; by 46%) and VO2 (by 22%) over the first 5 min. Between 7 and 11 min of stimulation, CO remained decreased, but VO2 returned to control. Significant increases in left atrial pressure, bradycardia, and a fall in mean arterial pressure accompanied vagal stimulation. All these effects of cervical vagal stimulation were abolished by cardiac denervation and also by pacing. Administration of a selective AVP V1 agonist led to significant reductions of CO and VO2. Cardiac denervation prevented the decrease in VO2 induced by AVP infusion, but not the decrease in CO. During AVP infusions, pacing at a rate slightly higher than control heart rate did not prevent the fall in CO or in VO2, whereas pacing at 150 beats/min prevented part of the fall in VO2. Sinoaortic denervation or atropine treatment prevented the decrease in VO2 resulting from AVP infusion. The combination of alpha- and beta-blockade did not affect the CO or the VO2 response to AVP infusion, nor did naloxone treatment. The administration of atrial or ventricular extracts, but not that of alpha-human atrial natriuretic peptide, led to a significant reduction in VO2. These results are compatible with the hypothesis that AVP infusion increases vagal tone to the heart, which, possibly as a result of increased left atrial pressure and reduced heart rate, may release a factor reducing VO2.

Mechanism of diuretic response associated with atrial tachycardia

1975 ◽  
Vol 229 (6) ◽  
pp. 1486-1491 ◽  
Author(s):  
J Boykin ◽  
P Cadnapaphornchai ◽  
KM McDonald ◽  
RW Schrier
Keyword(s):  
Left Atrial ◽  
Atrial Tachycardia ◽  
Free Water ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Atrial Pacing ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.

Changes in microvascular permeability with acceleration of edema in dog lungs

1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Left Atrial ◽  
Membrane Filtration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Edema Formation ◽  
Before And After

Elevation of left atrial pressure to 25–40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5–120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

Inhibition of hypoxic pulmonary vasoconstriction by increased left atrial pressure in dogs

1990 ◽  
Vol 259 (1) ◽  
pp. H93-H100 ◽  
Author(s):  
P. Lejeune ◽  
J. M. De Smet ◽  
P. de Francquen ◽  
M. Leeman ◽  
S. Brimioulle ◽  
...  
Keyword(s):  
Left Atrial ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Experimental Conditions ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
The Mean

To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.

Effect of increased left atrial pressure on breathing frequency in anesthetized dog

1990 ◽  
Vol 69 (6) ◽  
pp. 1973-1980 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Breathing Frequency ◽  
Anesthetized Dogs ◽  
The Right

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.

Lung microvascular pressure profile measured by micropuncture in anesthetized dogs

1988 ◽  
Vol 64 (2) ◽  
pp. 874-879 ◽  
Author(s):  
J. M. Shepard ◽  
M. A. Gropper ◽  
G. Nicolaysen ◽  
N. C. Staub ◽  
J. Bhattacharya
Keyword(s):  
Left Atrial ◽  
Left Lung ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Alveolar Pressure ◽  
Pressure Zone ◽  
Isolated Lung ◽  
Anesthetized Dogs

We have micropunctured the lung in the open thorax of 17 anesthetized dogs to measure microvascular pressure. After intravenous pentobarbital sodium (25 mg/kg), we exposed the left lung through a wide left thoracotomy, which required rib excision. Through a double-lumen endotracheal tube, we ventilated the right lung to maintain normal blood gases and pH while we held the left lung motionless at an inflation pressure of 5 cmH2O. To reduce motion on the surface of the left lower lobe, we resected the left upper lobe, placed a Plexiglas baffle between the lobe and the heart, and held the lobe surface in a suction ring. In accordance with procedures we have previously described, we micropunctured subpleural vessels to measure microvascular pressure. At base line when alveolar pressure exceeded left atrial pressure (zone 2 conditions), 21, 38, and 41% of the total pressure drop occurred, respectively, in the arterial, microvascular, and venous segments. When we raised left atrial pressure above alveolar pressure (zone 3 conditions), the corresponding pressure drops were 30, 55, and 20% of total. The blood flow in the superficial layer of the lung averaged 15% less than the flow in the deeper layers as measured by distribution of 99mTc-albumin macroaggregates. We conclude that the intact and the isolated lung preparations in dog exhibit similar distributions of subpleural microvascular pressure.

Regional atrial distensibility

1992 ◽  
Vol 262 (5) ◽  
pp. H1356-H1360 ◽  
Author(s):  
B. D. Hoit ◽  
R. A. Walsh
Keyword(s):  
Left Atrial ◽  
Regional Differences ◽  
The Body ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Wide Range ◽  
Intravenous Saline ◽  
Strain Relationship ◽  
Systolic And Diastolic Function

We studied 12 open-chest dogs to determine whether there are regional differences in left atrial distensibility. Sonomicrometer crystal pairs were used to measure the anteroposterior diameters of the left atrial body and appendage simultaneously over a wide range of intracardiac pressures and volumes obtained by intravenous saline infusion. Left atrial pressure-natural strain data for the body and appendage were fitted to an exponential function. The mean coefficient of the left atrial monoexponential pressure-strain relationship was greater for the body than appendage (3.1 +/- 1.1 vs. 1.9 +/- 0.7 mmHg, P less than 0.01). The Y-intercepts were not significantly different (5.2 +/- 1.7 vs 4.9 +/- 1.8 mmHg). The maximum minus minimum left atrial dimension, an index of the reservoir function of the atrium, increased with volume infusion in both the body and appendage and was significantly greater in the appendage than body at each level of left atrial pressure. Similarly, atrial systolic shortening fraction increased with volume infusion, and regional shortening was greater in the appendage than the body at each level of left atrial pressure. We conclude that regional differences in atrial distensibility exist in vivo and may play an important role in modulating systolic and diastolic function of the left atrium.

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs

1996 ◽  
Vol 270 (4) ◽  
pp. H1217-H1224 ◽  
Author(s):  
N. B. Ingels ◽  
G. T. Daughters ◽  
S. D. Nikolic ◽  
A. DeAnda ◽  
M. R. Moon ◽  
...  
Keyword(s):  
Pressure Gradient ◽  
Left Atrial ◽  
Ambient Pressure ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Systolic Volume ◽  
Open Chest ◽  
End Systolic Volume ◽  
Anesthetized Dogs

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

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