Biomedical subjects

M A Gropper

Publications and source records attributed to M A Gropper.

29 records · Page 2Linked to original sources

PubMed1989

Lung expansion and the perialveolar interstitial pressure gradient.

We have determined the combined effects of lung expansion and increased extravascular lung water (EVLW) on the perialveolar interstitial pressure gradient. In the isolated perfused lobe of dog lung, we measured interstitial pressures by micropuncture at alveolar junctions (Pjct) and in adventitia of 30- to 50-microns microvessels (Padv) with stopped blood flow at vascular pressure of 3-5 cmH2O. We induced edema by raising vascular pressures. In nonedematous lobes (n = 6, EVLW = 3.1 +/- 0.3 g/g dry wt) at alveolar pressure of 7 cmH2O, Pjct averaged 0.5 +/- 0.8 (SD) cmH2O and the Pjct-Padv gradient averaged 0.9 +/- 0.5 cmH2O. After increase of alveolar pressure to 23 cmH2O the gradient was abolished in nonedematous lobes, did not change in moderately edematous lobes (n = 9, EVLW = 4.9 +/- 0.6 g/g dry wt), and increased in severely edematous lobes (n = 6, EVLW = 7.6 +/- 1.4 g/g dry wt). Perialveolar interstitial compliance decreased with increase of alveolar pressure. We conclude that increase of lung volume may reduce perialveolar interstitial liquid clearance by abolishing the Pjct-Padv gradient in nonedematous lungs and by compressing interstitial liquid channels in edematous lungs.

Animals↗

PubMed1989

[Estimation of the filtration variables in the rat lung].

The filtration variables, filtration coefficient (K), perimicrovascular pressure (Ppmv) and reflection coefficient (sigma) were estimated independently in previous reports using the Starling Equation or the micropuncture method. We estimated these variables simultaneously. We measured filtration rate by a gravimetric method in isolated rat lung lobes in zone 1 conditions (alveolar pressure = 20 cmH2O) at two vascular pressures, Pvasc = 15 or 8 cmH2O and perfused the lobes with plasma containing a low or high concentration of protein. By extrapolating the log of the rate of weight gain to time = 0, we obtain the initial filtration rate. Assuming that protein filtered into perimicrovascular space only by convection, we substituted into the Starling Equation as follows: Q = K[(Pmv-Ppmv)-sigma 2 pi mv], where Pmv and pi mv are hydrostatic and plasma protein osmotic pressures in microvascular space. pi mv was estimated by Yamada's equation. We obtained K = 26.3 +/- 8.7 mg/(min.cmH2O.g), PPMV = 6.2 +/- 0.7 cmH2O, sigma = 0.46 +/- 0.07. The chief advantages of this method are that it does not require a separate estimation of isogravimetric pressure or a direct measurement of interstitial pressure, and that all variables are obtained simultaneously.

Animals↗

PubMed1988

Lung microvascular pressure profile measured by micropuncture in 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.

Animals↗

PubMed1988

Filtration profile in isolated zone 1 and zone 3 dog lungs at constant high alveolar pressure.

We measured the rate of liquid filtration in isolated dog lung lobes inflated to a constant alveolar pressure of 25 cmH2O and with all open vessels filled with plasma. We measured lung weight gain at vascular pressures ranging from 5 to 40 cmH2O relative to pleural pressure. We confirmed that under zone 1 conditions the "arterial" and "venous" extra-alveolar segments have essentially the same filtration characteristics. Using the combined extra-alveolar vascular system, we determined when recruitment of filtration surface area occurred as we increased vascular pressure from 0 to 40 cmH2O. Based on an abrupt increase in filtration rate as vascular pressure approached the zone 1/3 boundary, we infer that a sudden recruitment of exchange surface area occurred at that point. Based on the slopes of the zone 1 and zone 3 filtration profiles, we conclude that extra-alveolar vascular segments contribute approximately 25% of total to filtration in the lung under zone 3 conditions, although the exact vessels filtering under zone 1 conditions have yet to be determined. Our analysis of the data supports the concept that there is a difference in the perimicrovascular pressure around alveolar and extra-alveolar vessels, which in part may account for the apparent high filtration fraction apportioned to extra-alveolar vessels.

Animals↗

PubMed1988

Alveolar liquid and protein clearance from normal dog lungs.

To determine whether liquid and protein clearance from the air spaces and lungs of anesthetized and unanesthetized dogs is the same as in sheep, we quantified these variables at three different time periods (4, 8, and 12 h) by instilling heparinized plasma (3 ml/kg) labeled with 125I-albumin into one lower lobe. Protein clearance, measured from the residual 125I-albumin in the lung homogenate, was slow and monoexponential (approximately 1%/h), similar to our previous data for protein clearance from the lungs in sheep. Lung liquid clearance in dogs, however, was 50% less than in previous experiments in sheep. Residual lung liquid (as percent of instilled) was 88.7 +/- 7.0 at 4 h, 70.5 +/- 9.1 at 8 h, and 64.0 +/- 5.8 at 12 h. At each time period, alveolar protein concentration increased by 0.6 +/- 0.4 g/dl at 4 h, 1.3 +/- 1.2 g/dl at 8 h, and 2.1 +/- 0.8 g/dl at 12 h. This increase in alveolar protein concentration was proportional to the volume of liquid removed from the lungs. beta-Adrenergic agonist therapy with terbutaline (10(-5) M mixed with the instilled plasma) doubled the volume of liquid cleared from the lungs over 4 h, and the alveolar protein concentration increased proportionally. However, lung liquid clearance in dogs that were treated with beta-agonists was proportionally (50%) less than in sheep treated with beta-agonists. The slower liquid clearance in dogs compared with sheep cannot be explained by differences in hemodynamics, pulmonary blood flow, anesthesia, mode of ventilation, or alveolar surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Relationship of pleural effusions to increased permeability pulmonary edema in anesthetized sheep.

We studied anesthetized sheep to determine the relationship between increased permeability pulmonary edema and the development and mechanism of pleural effusion formation. In 12 sheep with intact, closed thoraces, we studied the time course of pleural liquid formation after 0.12 ml/kg i.v. oleic acid. After 1 h, there were no pleural effusions, even though extravascular lung water increased 50% to 6.0 +/- 0.7 g/g dry lung. By 3 h pleural effusions had formed, they reached a maximum at 5 h (48.5 +/- 16.9 ml/thorax), and at 8 h there was no additional accumulation of pleural liquid (45.5 +/- 16.9 ml). Morphologic studies by light and electron microscopy demonstrated subpleural edema but no detectable injury to the visceral pleura, suggesting that the pleural liquid originated from the lung and not the pleura. In nine sheep, we quantified the rate of formation of pleural liquid by enclosing one lung in a plastic bag. By comparing in the same sheep the volume of pleural liquid collected from the enclosed lung to the volume found in the opposite intact chest, we estimated the rate of liquid absorption from the intact chest to be 0.32 ml/(kg.h); we had previously reported a liquid absorption rate of 0.28 ml/(kg.h) in normal sheep. These studies also supported the conclusion that the majority of the pleural liquid originated from the lung because we could account for all of the pleural liquid that was formed and cleared. The volume of pleural liquid collected from the enclosed lungs was equal to 21% of the excess lung liquid that formed after oleic acid-induced lung injury. Thus, the pleural space and parietal pleural lymphatic pathways are important pathways for the clearance of pulmonary edema liquid after experimentally induced increased permeability pulmonary edema.

Animals↗

PubMed1987

Direct measurement of blood pressure within the long hypophysial portal blood vessels.

The microvascular pressures that perfuse the anterior pituitary gland with blood were not known. We now report the direct measurement of these pressures in the urethane-anesthetized rat. The infundibular stalk and ventral surface of the anterior pituitary gland were surgically exposed via a parapharyngeal approach and a micropressure transducer inserted into the lumen of hypophysial portal vessels under direct microscopic observation. A Weiderhielm-type servo-controlled pressure system was used to record the pressures. Continuous pressure recordings up to 30 min in duration were made in long hypophysial portal vessels ranging in diameter from 10 to 50 micron in adult, female Sprague-Dawley rats. The mean pressure recorded from these vessels was 4.0 cm H2O (2.7 mm Hg). A small increase in systemic pressure produced by a rapid saline infusion into a cannulated femoral vein resulted in a mirrored but much greater magnitude increase in pressure to the hypophysial portal vessels. This finding suggests that pressure within the portal vessels is in some instances closely coupled to systemic blood pressure. The low pressures recorded in hypophysial portal vessels correlate well with pressures measured in the hepatic portal vasculature. The porosity of fenestrated capillaries surrounding anterior pituitary cells is hemodynamically essential, since the low hydrostatic pressures alone would be inappropriate for rapid and thorough exchange.

Animals↗

PubMed1985

Pleural liquid pressure in dogs measured using a rib capsule.

We have developed a minimally invasive method for measuring the hydrostatic pressure in the pleural space liquid. A liquid-filled capsule is bonded into a rib and a small hole is cut in the parietal pleura to allow direct communication between the liquid in the capsule and the pleural space. The pressure can be measured continuously by a strain gauge transducer connected to the capsule. The rib capsule does not distort the pleural space or require removal of intercostal muscle. Pneumothoraces are easily detected when they occur inadvertently on puncturing the parietal pleura. We examined the effect of height on pleural pressure in 15 anesthetized spontaneously breathing dogs. The vertical gradients in pleural pressure were 0.53, 0.42, 0.46, and 0.23 cmH2O/cm height for the head-up, head-down, supine, and prone body positions, respectively. These vertical gradients were much less than the hydrostatic value (1 cmH2O/cm), indicating that the pleural liquid is not in hydrostatic equilibrium. In most body positions the magnitudes of pleural liquid pressure interpolated to midchest level were similar to the mean transpulmonary (surface) pressure determined postmortem. This suggests that pleural liquid pressure is closely related to the lung static recoil.

Animals↗

PubMed1984

Interstitial fluid pressure gradient measured by micropuncture in excised dog lung.

We have directly measured lung interstitial fluid pressure at sites of fluid filtration by micropuncturing excised left lower lobes of dog lung. We blood-perfused each lobe after cannulating its artery, vein, and bronchus to produce a desired amount of edema. Then, to stop further edema, we air-embolized the lobe. Holding the lobe at a constant airway pressure of 5 cmH2O, we measured interstitial fluid pressure using beveled glass micropipettes and the servo-null method. In 31 lobes, divided into 6 groups according to severity of edema, we micropunctured the subpleural interstitium in alveolar wall junctions, in adventitia around 50-micron venules, and in the hilum. In all groups an interstitial fluid pressure gradient existed from the junctions to the hilum. Junctional, adventitial, and hilar pressures, which were (relative to pleural pressure) 1.3 +/- 0.2, 0.3 +/- 0.5, and -1.8 +/- 0.2 cmH2O, respectively, in nonedematous lobes, rose with edema to plateau at 4.1 +/- 0.4, 2.0 +/- 0.2, and 0.4 +/- 0.3 cmH2O, respectively. We also measured junctional and adventitial pressures near the base and apex in each of 10 lobes. The pressures were identical, indicating no vertical interstitial fluid pressure gradient in uniformly expanded nonedematous lobes which lack a vertical pleural pressure gradient. In edematous lobes basal pressure exceeded apical but the pressure difference was entirely attributable to greater basal edema. We conclude that the presence of an alveolohilar gradient of lung interstitial fluid pressure, without a base-apex gradient, represents the mechanism for driving fluid flow from alveoli toward the hilum.

Animals↗

PubMed1984

Micropuncture measurement of lung microvascular pressure profile during hypoxia in cats.

To determine the lung microvascular pressure profile during hypoxia, we micropunctured the subpleural microcirculation of isolated perfused cat lungs. Our procedures involved exsanguinating a cat, then cannulating its pulmonary artery, left atrium, and trachea. Using the cat's own blood, we perfused the lungs at pulmonary artery and left atrial pressures of 18 and 9 cm water, respectively, to obtain lung blood flow of 81 +/- 29 ml/(kg body weight x min), which we held constant throughout the experiment. We stabilized the lung surface with a vacuum ring and micropunctured 30- to 50-micrometers arterioles and venules to measure microvascular pressure by the servo-null method. During micropuncture, we held the lungs at constant inflation using airway pressure of 8 cm water. We varied the oxygen concentration of the inflation gas from 30% during baseline to 2% during hypoxia. We studied groups with high (more than 7.5) or normal pH. During normoxia, 27, 44, and 29% of the pressure drop occurred in the arterial, capillary and venous segments, respectively. During hypoxia, the increase in pulmonary vascular resistance, which was marked in both groups, was significantly greater in the normal pH group. All segmental pressure drops increased significantly during hypoxia. However, the predominant increase occurred in the arteries where segmental pressure drop increased by 148% and 210%, respectively, in the high and normal pH groups. We conclude that the major site of hypoxic vasoconstriction is in the pulmonary arteries.

Acid-Base Equilibrium↗

PubMed1983

Effect of lung inflation on alveolar-airway barrier protein permeability in dog lung.

To determine the leakiness to protein of the barrier that separates the air space and interstitial compartment of the lung, we measured perivascular interstitial fluid cuff protein concentration and volume in 10 isolated and 9 intact closed-chest dog lung lobes, which we degassed and inflated to 25, 50, 75, or 100% of capacity with 5% bovine serum albumin labeled with Evans blue dye. After 1 h we froze the lobes in liquid N2 and made color transparencies of 20 randomly selected frozen samples of each lobe. We measured Evans blue dye-albumin concentrations from absorption by cuff images of a 50-micron-diam red (lambda = 620 nm) microspot. We measured absolute cuff volume (ml/g dry lung) by point counting on the transparencies. Using specific Evans blue-albumin fluorescence we determined that the dye was protein bound in airways and cuffs. Cuff protein concentration averaged 37% of instillate concentration and did not vary with inflation volume or between isolated and intact lobes. Cuff volume was 3.4 ml/g dry lung at total lung capacity in both isolated and intact lobes. We conclude that at some point the barrier is permeable to albumin as well as liquid at all lung volumes in dogs and that the protein sieving properties of the barrier do not change with lung expansion over the range examined. The liquid storage capacity of the cuffs can increase as much as 20-fold between low and high lung volumes.

Albumins↗