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R K Albert

Publications and source records attributed to R K Albert.

At least 55 records · Page 3Linked to original sources
PubMed1993

Lung inflation distends small arteries (< 1 mm) in excised dog lungs.

We utilized microfocal fluoroscopic angiography to study the influence of lung inflation on small (0.2- to 1.3-mm-diam) pulmonary arteries in isolated left lower lobes from dog lungs during both flow and no-flow conditions. Alveolar pressure, which in this preparation was equal to transpulmonary pressure, was set at 2, 8, or 14 mmHg while vascular pressure was varied from 0 to 24 mmHg. The diameters of these small arterial vessels increased with lung inflation. No differences were observed between the results obtained during flow and no-flow conditions. Thus, arteries in this diameter range can be considered as extra-alveolar, and the effect of lung inflation on these small extra-alveolar arteries was qualitatively similar to that previously described for larger extra-alveolar vessels. Quantitatively, the degree of vessel distension was about the same per unit increase in transpulmonary pressure at constant vascular pressure as for a change in vascular pressure at constant transpulmonary pressure. Accordingly, inflation produced a decrease in perivascular pressure surrounding these small arteries that was approximately equal to the increase in transpulmonary pressure.

Air Pressure↗
PubMed1992

Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs.

The effect of severe generalized edema on respiratory system mechanics is not well described. We measured airway pressure, gastric pressure, and four vertical pleural pressures in 13 anesthetized paralyzed pigs ventilated in the upright position. Pressure-volume relationships of the respiratory system, chest wall, and lung were measured on deflation from total lung capacity to residual volume and during tidal breathing both before (control) and 50 min after one of two interventions. In one series of experiments, a volume equal to 15-20% of the pig's body weight was infused intravenously. In a second series, a balloon was placed in the peritoneal space to distend the abdomen to the same gastric pressures as achieved in the first series. Measurements were compared before and after either abdominal balloon inflation or volume infusion. Volume infusion increased the pleural pressure in dependent lung regions, decreased both total lung capacity (34%) and functional residual capacity (62%) (both P less than 0.05), and markedly shifted the respiratory system and chest wall pressure-volume curves to the right, but it only moderately affected the lung deflation curve. Tidal compliances of the respiratory system, chest wall, and lung decreased 36, 31, and 49%, respectively (all P less than 0.05). The effect of abdominal balloon inflation on respiratory system mechanics was similar to that of volume infusion. We conclude that infusing large volumes of fluid markedly alters chest wall mechanics, mainly by causing abdominal distension that prohibits descent of the diaphragm.

Abdomen↗
PubMed1992

Pulmonary artery occlusion is sufficient to increase pulmonary vascular permeability in rabbits.

Unilateral pulmonary artery obstruction (PAO) for 24-48 h, followed by reperfusion, results in pulmonary edema and lung inflammation. We hypothesized that lung injury actually occurred during the period of PAO but, because of low microvascular pressures during the period of occlusion, was not detected until perfusion was reestablished. To test this hypothesis, we studied 14 rabbits divided into three groups: group I rabbits underwent sham occlusion of the left pulmonary artery for 24 h; group II rabbits underwent PAO but were not reperfused; and group III rabbits were subjected to PAO and then reperfused for 4 h. The fluid filtration coefficient measured during a zone 3 no-flow hydrostatic stress (pulmonary arterial pressure = pulmonary venous pressure, both greater than alveolar pressure) in group I lungs was less than that of lungs in either group II or III [0.52 +/- 0.02 (SE) ml.min-1.cmH2O.100 g wet wt-1 vs. 0.94 +/- 0.11 and 0.86 +/- 0.13 for groups II and III, respectively, P less than 0.05]. The wet-to-dry weight ratio of the left lung measured after the zone 3 stress was applied for 20 min was 6.90 +/- 0.09 in group I rabbits and 9.21 +/- 0.75 and 11.75 +/- 0.44 in groups II and III, respectively (P less than 0.05). Radiolabeled microspheres demonstrated that flow to the left lung was diminished after the period of PAO (38 +/- 4, 9 +/- 5, and 2 +/- 1% of cardiac output in groups I, II, and III, respectively; P less than 0.05 for group I vs. groups II and III).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Prone position alters the effect of volume overload on regional pleural pressures and improves hypoxemia in pigs in vivo.

Oxygenation improves in patients with adult respiratory distress syndrome and in animals with oleic acid-induced lung injury when they are turned from the supine to the prone position. Dependent and nondependent pleural pressures (Ppl) were measured in six pigs ventilated in the supine and prone positions before and after volume infusion (VI). Before VI the mean +/- SEM AaPO2 difference was 26 +/- 8 mm Hg when the animals were supine and 10 +/- 2 mm Hg when they were prone (p > 0.05). After VI the AaPO2 was 64 +/- 6 mm Hg when the animals were supine (p < 0.05) and 43 +/- 7 mm Hg when they were prone (p < 0.05). VI increased the Ppl gradient from 0.53 +/- 0.1 to 0.71 +/- 0.1 cm H2O/cm when the animals were supine (p < 0.05) and from 0.17 +/- 0.1 to 0.27 +/- 0.1 cm H2O/cm when they were prone (p < 0.05). Dependent Ppl at FRC was much less positive when the animals were prone versus supine (0.9 +/- 0.3 versus 3.0 +/- 0.5 cm H2O, p < 0.05), suggesting that the airways in these dependent regions would narrow and/or close and that ventilation to these regions would diminish as a result of VI.

Abdomen↗
PubMed1992

Expression and function of beta 2 integrins on alveolar macrophages from human and nonhuman primates.

The alveolar macrophage (AM) participates in diverse, adherence-related activities required for host defense and the inflammatory response. The beta 2 integrins (the CD11/CD18 heterodimer) mediate some of these activities on circulating leukocytes and peritoneal macrophages. We investigated expression of the CD11/CD18 leukocyte integrin subunits on AMs obtained by bronchoalveolar lavage of human and nonhuman primates. We also determined the role of the CD11/CD18 complex in AM chemotaxis and adherence to A549 alveolar epithelial cell monolayers. Immunofluorescence flow cytometry indicated that the CD11a/CD18 complex was expressed in high levels and CD11b/CD18 and CD11c/CD18 in lower levels on the AM surface. Northern blot analysis indicated the presence of CD11a, CD11c, and CD18 mRNA in the AMs. Smaller quantities of CD11b mRNA were also found. AM chemotaxis to zymosan-activated serum was markedly inhibited by a monoclonal antibody to CD18. In addition, adherence of AMs to A549 cells (stimulated by tumor necrosis factor to upregulate intercellular adhesion molecule-1 expression) was decreased from 30.3 +/- 5.0 to 20.8 +/- 2.4% (P less than 0.05) by the same monoclonal antibody. We conclude that: (1) AMs obtained from human and nonhuman primates constitutively express predominantly CD11a/CD18 surface antigen and mRNA, (2) chemotaxis of AMs is CD18 dependent, and (3) adhesion of AMs to an alveolar epithelial cell monolayer is partly but not completely dependent on the beta 2 integrins.

Animals↗
PubMed1991

Flow through zone 1 lungs utilizes alveolar corner vessels.

We have previously observed flows equivalent to 15% of the resting cardiac output of rabbits occurring through isolated lungs that were completely in zone 1. To distinguish between alveolar corner vessels and alveolar septal vessels as a possible zone 1 pathway, we made in vivo microscopic observations of the subpleural alveolar capillaries in five anesthetized dogs. Videomicroscopic recordings were made via a transparent thoracic window with the animal in the right lateral position. From recordings of the uppermost surface of the left lung, alveolar septal and corner vessels were classified depending on whether they were located within or between alveoli, respectively. Observations were made with various levels of positive end-expiratory pressure (PEEP) applied only to the left lung via a double-lumen endotracheal tube. Consistent with convention, flow through septal vessels stopped when PEEP was raised to the mean pulmonary arterial pressure (the zone 1-zone 2 border). However, flow through alveolar corner vessels continued until PEEP was 8-16 cmH2O greater than mean pulmonary arterial pressure (8-16 cm into zone 1). These direct observations support the idea that alveolar corner vessels rather than patent septal vessels provide the pathway for blood flow under zone 1 conditions.

Animals↗
PubMed1991

Abdominal distension alters regional pleural pressures and chest wall mechanics in pigs in vivo.

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.

Abdomen↗
PubMed1991

Gravity is a minor determinant of pulmonary blood flow distribution.

Regional pulmonary blood flow in dogs under zone 3 conditions was measured in supine and prone postures to evaluate the linear gravitational model of perfusion distribution. Flow to regions of lung that were 1.9 cm3 in volume was determined by injection of radiolabeled microspheres in both postures. There was marked perfusion heterogeneity within isogravitational planes (coefficient of variation = 42.5%) as well as within gravitational planes (coefficient of variation = 44.2 and 39.2% in supine and prone postures, respectively; P = 0.02). On average, vertical height explained only 5.8 and 2.4% of the flow variability in the supine and prone postures, respectively. Whereas the gravitational model predicts that regional flows should be negatively correlated when measured in supine and prone postures, flows in the two postures were positively correlated, with an r2 of 0.708 +/- 0.050. Regional perfusion as a function of distance from the center of a lung explained 13.4 and 10.8% of the flow variability in the supine and prone postures, respectively. A linear combination of vertical height and radial distance from the centers of each lung provided a better-fitting model but still explained only 20.0 and 12.0% of the flow variability in the supine and prone postures, respectively. The entire lung was searched for a region of contiguous lung pieces (22.8 cm3) with high flow. Such a region was found in the dorsal area of the lower lobes in six of seven animals, and flow to this region was independent of posture. Under zone 3 conditions, neither gravity nor radial location is the principal determinant of regional perfusion distribution in supine and prone dogs.

Animals↗
PubMed1991

Extra-alveolar veins are contiguous with, and leak fluid into, periarterial cuffs in rabbit lungs.

We previously observed physiological evidence that arterial and venous extra-alveolar vessels shared a common interstitial space. The purpose of the present investigation was to determine the site of this continuity to improve our understanding of interstitial fluid movement in the lung. Orange G and Evans blue dyes were added to the arterial and venous reservoirs, respectively, of excised rabbit lungs as they were placed 20 cmH2O into zone 1 (pulmonary arterial and venous pressures = 5 cmH2O, alveolar pressure = 25 cmH2O). After 10 s or 4 h the lungs were fixed by immersion in liquid N2, freeze-dried, cut into 5-mm serial slices, and examined by light macroscopy. Serial sections of 0.25-0.5 mm were subsequently examined by scanning electron microscopy. In the animals subjected to the zone 1 stress for 4 h, arterial and venous extra-alveolar vessels were surrounded by cuffs of edema. The edema ratio (cuff area divided by vessel lumen area) was greater around arteries than veins and decreased with increasing vessel size. Periarterial cuffs usually contained orange dye and frequently contained both orange and blue dye. Lymphatics containing orange or blue dye were frequently seen in periarterial cuffs. Scanning electron microscopy demonstrated that extra-alveolar veins of approximately 100 microns diameter were anatomically contiguous with arterial extra-alveolar vessel cuffs. In rabbit lungs, both arterial and venous extra-alveolar vessels (and/or alveolar corner vessels) leak fluid into perivascular cuffs surrounding arterial extra-alveolar vessels, and lymphatics located in the periarterial cuff contain fluid that originates from both the arterial and venous extra-alveolar vessels.

Air Pressure↗
PubMed1991

AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli.

The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.

Blood Pressure↗
PubMed1990

Prone position reverses gravitational distribution of perfusion in dog lungs with oleic acid-induced injury.

Although oxygenation improves in patients with the adult respiratory distress syndrome and in animals with oleic acid- (OA) induced acute lung injury when they are turned from the supine to the prone position, the mechanism(s) by which this improvement occurs is not known. Several groups have speculated that this improvement results from preferential edema accumulation in the dorsal lung regions and redistribution of perfusion away from these regions when the patients are turned to the prone position. We used radiolabeled microspheres to measure the regional distribution of perfusion (Qr) to the dorsal, mid, and ventral lungs of eight dogs in vivo in the supine and prone positions, before and after inducing acute lung injury with OA, and correlated the Qr observed after injury with the degree of regional extravascular lung water (EVLWr). Before OA, Qr increased along the gravitational gradient when the animals were supine but was more uniformly distributed when they were prone. After OA, Qr again followed a gravitational gradient when the animals were supine but was preferentially distributed to the nondependent regions when they were prone. EVLWr was similar in all regions, regardless of whether OA was injected when the animals were supine or prone. The gravitational Qr gradient is markedly reduced in the prone position, both before and after lung injury. The prone position-induced improvement in oxygenation is not the result of redistribution of Qr away from areas in which edema preferentially develops.

Animals↗
PubMed1990

Surfactant replacement improves lung recoil in rabbit lungs after acid aspiration.

We tested the hypothesis that surfactant replacement would be beneficial in the acid-aspiration model of acute lung injury. HCl (0.1 N, 2 ml/kg) was injected into the trachea of excised rabbit lungs (n = 8). Control lungs (n = 4) had no intervention. All were perfused with Tyrode's solution mixed 1:1 with autologous whole blood at 40 ml/min/kg for 30 min, and then degassed. A modified natural surfactant (Survanta, Ross Laboratories) was then injected into the trachea of four lungs injured with HCl (100 mg/kg at 25 mg/ml). Two quasi-static pressure-volume curves were determined. The mean alveolar pressures at 50, 60, 70, 80, and 90% of TLC were greater in the HCl group than in the control group (p less than 0.05). However, no difference was observed between the control lungs and those that received HCl + Survanta. In 13 anesthetized, paralyzed, and ventilated rabbits, deflation pressure-volume curves were determined from TLC to FRC (measured by helium dilution). Then, 0.1 N HCl (3 ml/kg) was injected into the trachea and, in seven, Survanta was instilled 5 min later. The mean alveolar pressures at 60, 70, 80, and 90% TLC were higher at 15 and 60 min in the HCl group compared with their pre-HCl time point (p less than 0.05). In the HCl + Survanta group, no differences were seen at 15 min, and only slight increased were seen at 60 min. No effect of surfactant replacement on arterial blood gases was observed. HCl aspiration increased recoil in both excised and in vivo lungs, and surfactant replacement with Survanta returned recoil to normal.

Animals↗
PubMed1989

Effect of leukotrienes B4, C4, and D4 on segmental pulmonary vascular pressures.

Leukotrienes (LTs) C4 and D4 are vasoconstrictors and are thought to increase both systemic and pulmonary vascular permeability. However, we and others have observed that LTC4 and LTD4 cause pulmonary vasoconstriction but do not increase the fluid filtration coefficient of excised guinea pig lungs perfused with a cell-depleted perfusate. To determine what vascular segments were exposed to an LT-induced increase in intravascular hydrostatic pressure we measured pulmonary arterial (Ppa), pulmonary arterial occlusion (Po,a), venous (Po,v) and double occlusion (Pdo) pressures in isolated guinea pig lungs perfused with a cell-depleted buffered salt solution before and after injecting 4 micrograms of LTB4, LTC4, or LTD4 into the pulmonary artery. All three LTs increased airway pressures and also increased Ppa, Po,a, and Pdo. Histamine (15 micrograms) as well as serotonin (20 or 200 micrograms) had the same effect. In excised rabbit lungs, histamine and serotonin increased only Ppa, and Po,a. LTC4 had no vasoactivity. There are marked species variations with regard to the activity and site of action of histamine, serotonin, and LTC4 on the pulmonary circulation.

Animals↗
PubMed1989

Flow characteristics of open vessels in zone 1 rabbit lungs.

To describe the flow characteristics of vessels open in zone 1, we perfused isolated rabbit lungs with Tyrode's solution containing 1% albumin, 4% dextran, and papaverine (0.05 mg/ml). Lungs were expanded by negative pleural pressure (Ppl) of -10, -15, -20, and -25 cmH2O. Pulmonary arterial (Ppa) and venous (Ppv) pressures were varied relative to alveolar pressure (PA = 0) and measured 5-10 mm inside the pleura (i) and outside (o) of the lungs. With Ppa(o) at -2.5 cmH2O, we constructed pressure-flow (P-Q) curves at each Ppl by lowering Ppv(o) until Q reached a maximum, indicating fully developed zone 1 choke flow. Maximum flows were negligible until Ppl fell below -10 cmH2O, then increased rapidly at Ppl of -15 and -20 cmH2O, and at Ppl of -25 cmH2O reached about 15 ml.min-1.kg body wt-1. The Ppv(o) at which flow became nearly constant depended on degree of lung inflation and was 5-8 cmH2O more positive than Ppl. As Ppv(o) was lowered below Ppa(o), Ppv(i) remained equal to Ppv(o) until Ppv(i) became fixed at a pressure 2-3 cmH2O more positive than Ppl. At this point the choke flow was therefore located in veins near the pleural boundary. No evidence of choke flow (only ohmic resistance) was seen in the intrapulmonary segment of the vessels remaining open in zone 1. With Ppv(o) held roughly at Ppl, Q could be stopped by lowering Ppa(o), at which time Ppa(i) was several cmH2O above Ppv(i), showing that intrapulmonary vessel closure had occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of lung inflation on fluid flux in zone 1 lungs.

Because of conflicting data in the literature, we studied the effect of positive-pressure inflation on transvascular fluid filtration in zone 1 lungs. Lungs from New Zealand White rabbits (n = 10) were excised, perfused with saline and autologous whole blood (1:1), ventilated, and continuously weighed. Pulmonary arterial and venous pressures (Pvas) were referenced to the most dependent part of the lung. A change in vascular volume (delta Vvas) and a fluid filtration rate (FFR) were calculated from the change in lung weight that occurred from 0 to 30 s and from 3 to 5 and 5 to 10 min, respectively, after changing alveolar pressure (PA). FFR's and delta Vvas's were measured with Pvas equal to 2 or 10 cmH2O and PA changing from 15 to 30 cmH2O when the lungs were normal and after they were made edematous. When Pvas = 2 cmH2O, increasing PA increased the Vvas and the FFR in both normal and edematous lungs. However, when Pvas = 10 cmH2O, increasing PA only slightly changed the Vvas and reduced the FFR in the normal lungs, and decreased Vvas and markedly decreased the FFR in the presence of edema. Inflating zone 1 lungs by positive pressure has an effect on transvascular fluid flux that depends on the Pvas. The results suggest that the sites of leakage in zone 1 also vary depending on Pvas and PA.

Animals↗
PubMed1988

Sites of leakage in three models of acute lung injury.

Fluid leaking from arterial and venous extra-alveolar vessels (EAV's) may account for up to 60% of the total transvascular fluid flux when edema occurs in the setting of normal vascular permeability. We determined if the permeability and relative contribution of EAV's was altered after inducing acute lung injury in rabbits by administering oleic acid (0.1 ml/kg) into the pulmonary artery, HCl (5 ml/kg of 0.1 N) into the trachea, or air emboli (0.03 ml.kg-1.min-1) into the right atrium for 90 min. Subsequently, the lungs were excised and continuously weighed while they were maintained in a warmed, humidified chamber with alveolar and pulmonary vascular pressures controlled and the lungs either ventilated or distended with 5% CO2 in air. The vascular system was filled with autologous blood and saline (1:1) to which papaverine (0.1 mg/ml) was added to inhibit vasospasm. Vascular pressures were referenced to the lung base. After a transient hydrostatic stress to maximize recruitment, vascular pressures were set at 5 cmH2O, and lungs were allowed to become isogravimetric (30-60 min). A fluid filtration coefficient (Kf) was determined by the use of a modification of the method of Drake and colleagues [Am. J. Physiol. 234 (Heart Circ. Physiol. 3): H266-H274, 1978]. EAV's were isolated by zoning techniques. In control preparations arterial and venous EAV's accounted for 26% (n = 9) and 38% (n = 11) of the total leakage, respectively. In all three models Kf increased two- to fourfold when the lungs were in zone 3 (alveolar vessels and arterial and venous EAV's contributing to the leakage).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Glycolysis is not required for fluid homeostasis in isolated rabbit lungs.

We investigated whether glycolysis was necessary to maintain the integrity of vascular endothelial and alveolar epithelial barriers in continually weighed isolated rabbit lungs. Lungs were perfused with a cell-free buffered salt solution, and glycolysis was inhibited with a glucose analogue (alpha-methyl glucoside, alpha-MG) or one of two glycolysis inhibitors (iodoacetic acid, IAA, or NaF). Fluid filtration rates (FFR's, the change in lung weight/time) in response to a 7.5-min zone 3 hydrostatic stress (pulmonary arterial and venous pressures raised from 8 to 15 cmH2O, alveolar pressure kept constant at 4 cm on the deflation limb) were repeatedly measured for 120 min after which the lungs were lavaged. The total protein concentration was measured in the bronchoalveolar lavage fluid (BALP). Lactate production was measured to verify inhibition of glycolysis. Lower concentrations of IAA and alpha-MG eliminated lactate production but did not affect FFR or BALP. NaF also had no effect on the FFR or BALP. Only high concentrations of IAA increased FFR and BALP, seemingly by causing nonspecific membrane injury that was unrelated to its specific effects on glycolysis. The glycolytic pathway for energy production is not necessary to maintain the integrity of the pulmonary endothelial-epithelial barrier.

Animals↗