Why do the lungs clear ultrasonic contrast?

Meltzer, Richard S.; Tickner, E. Glenn; Popp, Richard L.

doi:10.1016/0301-5629(80)90022-8

Cited by 141 publications

(49 citation statements)

References 16 publications

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“…The sieving effect of the pulmonary microcirculation theoretically should prevent the passage of particles 8 ~m or greater in diameter [15]. However, this size limitation may apply only to rigid structures such as microspheres or microbubbles.…”

Section: Discussionmentioning

confidence: 99%

Experimental carbon dioxide pulmonary embolization after vena cava laceration under pneumoperitoneum

1995

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The potential for pulmonary embolization following major venous laceration occurring during laparoscopic surgery has never been evaluated. Five anesthetized dogs were hemodynamically monitored with an arterial line and Swan-Ganz catheter. Observation by transesophageal echocardiography (TEE) allowed comparison with pulmonary artery pressure (PAP) recording. Under pneumoperitoneum, a 1-cm venotomy was performed in the infrarenal vena cava and a total of 11 events were evaluated upon unclamping the venotomy. These results were compared with intravenous (i.v.) bolus injections of 15 cc of CO2 (15 events) and of 100 cc of CO2 (12 events). The animals were maintained euvolemic. In 2 out of the 11 (18%) events which followed unclamping the venotomies, a few CO2 bubbles were seen in the right heart cavities. However, the quantity of gas was much less important than that seen after i.v. injection of 15 cc and 100 cc of CO2. There was no significant elevation of the PAP from pre-event values after venotomy or after i.v. injection of 15 cc of CO2. However, there was a significant difference (P < 0.05) when these results were compared to the PAP values recorded after i.v. injection of 100 cc of CO2. No dog died after these episodes of embolization. Massive i.v. injection of CO2 (> 300 cc) led to appearance of gas bubbles in the left heart cavities and death. This experiment suggests that caution should be exerted when laparoscopic surgery is performed beside large veins. Nevertheless, the observation that no gas embolism occurred in 82% of the cases after unclamping venotomies was unexpected. In contrast, many more gas bubbles were detected in the right heart after i.v. injection of only 15 cc of CO2. TEE is a more sensitive indicator of pulmonary embolization than elevation of PAP.

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Section: Discussionmentioning

confidence: 99%

Experimental carbon dioxide pulmonary embolization after vena cava laceration under pneumoperitoneum

1995

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“…Although the actual size of the saline contrast microbubbles is not known, theoretical and experimental data have estimated that the size distribution of microbubbles that survive to enter the pulmonary microcirculation to be 60 to 90 m in diameter (8,10,16,31,32). These estimates prompted Eldridge et al (5) to suggest that these inducible intrapulmonary arteriovenous pathways must be at least 60 m in diameter.…”

mentioning

confidence: 99%

Direct demonstration of 25- and 50-μm arteriovenous pathways in healthy human and baboon lungs

Lovering

Stickland²,

Kelso³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Lovering AT, Stickland MK, Kelso AJ, Eldridge MW. Direct demonstration of 25-and 50-m arteriovenous pathways in healthy human and baboon lungs. Am J Physiol Heart Circ Physiol 292: H1777-H1781, 2007. First published December 1, 2006; doi:10.1152/ajpheart.01024.2006.-Postmortem microsphere studies in adult human lungs have demonstrated the existence of intrapulmonary arteriovenous pathways using nonphysiological conditions. The aim of the current study was to determine whether large diameter (Ͼ25 and 50 m) intrapulmonary arteriovenous pathways are functional in human and baboon lungs under physiological perfusion and ventilation pressures. We used fresh healthy human donor lungs obtained for transplantion and fresh lungs from baboons (Papio c. anubis). Lungs were ventilated with room air by using a peak inflation pressure of 15 cmH 2O and a positive end-expiratory pressure of 5 cmH2O. Lungs were perfused between 10 and 20 cmH2O by using a phosphate-buffered saline solution with 5% albumin. We infused a mixture of 25-and 50-m microspheres (0.5 and 1 million total for baboons and human studies, respectively) into the pulmonary artery and collected the entire pulmonary venous outflow. Under these conditions, evidence of intrapulmonary arteriovenous anastomoses was found in baboon (n ϭ 3/4) and human (n ϭ 4/6) lungs. In those lungs showing evidence of arteriovenous pathways, 50-m microspheres were always able to traverse the pulmonary circulation, and the fraction of transpulmonary passage ranged from 0.0003 to 0.42%. These data show that intrapulmonary arteriovenous pathways Ͼ50 m in diameter are functional under physiological ventilation and perfusion pressures in the isolated lung. These pathways provide an alternative conduit for pulmonary blood flow that likely bypasses the areas of gas exchange at the capillary-alveolar interface that could compromise both gas exchange and the ability of the lung to filter out microemboli.intrapulmonary arteriovenous anastomoses; shunt; baboon; pulmonary circulation RECENT WORK has demonstrated the transpulmonary passage of saline contrast microbubbles during exercise, but not at rest, in healthy adult human subjects without cardiac anomalies, suggesting that intrapulmonary arteriovenous pathways are recruited during hyperdynamic conditions (5,14,22). Although the actual size of the saline contrast microbubbles is not known, theoretical and experimental data have estimated that the size distribution of microbubbles that survive to enter the pulmonary microcirculation to be 60 to 90 m in diameter (8,10,16,31,32). These estimates prompted Eldridge et al. (5) to suggest that these inducible intrapulmonary arteriovenous pathways must be at least 60 m in diameter. Postmortem studies in adult human lungs have documented the existence of intrapulmonary arteriovenous pathways for more than 100 years (20). More recent studies using microspheres have demonstrated that these vessels are functional under various conditions. For example, Tobin and Zariquiey (25) demonstrated that arteriove...

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“…This lack of contrast in the left ventricle is probably due to both the "sieve" effect in which the lung capillaries filter out large microbubbles (Meltzer et al 1980), and increased dissolution rates as the microbubbles pass through the lungs (Wible et al 1996;Kabalnov et al 1998). As a result, few microbubbles survive the transit through the lung vasculature to provide contrast in the left ventricle.…”

Section: In Vivo Imagingmentioning

confidence: 98%

In vivo imaging of microfluidic-produced microbubbles

Dhanaliwala

Dixon

Lin

et al. 2015

Biomed Microdevices

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Microfluidics-based production of stable microbubbles for ultrasound contrast enhancement or drug/gene delivery allows for precise control over microbubble diameter but at the cost of a low production rate. In situ microfluidic production of microbubbles directly in the vasculature may eliminate the necessity for high microbubble production rates, long stability, or small diameters. Towards this goal, we investigated whether microfluidic-produced microbubbles directly administered into a mouse tail vein could provide sufficient ultrasound contrast. Microbubbles composed of nitrogen gas and stabilized with 3 % bovine serum albumin and 10 % dextrose were injected for 10 seconds into wild type C57BL/6 mice, via a tail-vein catheter. Short-axis images of the right and left ventricle were acquired at 12.5 MHz and image intensity over time was analyzed. Microbubbles were produced on the order of 10(5) microbubbles/s and were observed in both the right and left ventricles. The median rise time, duration, and decay time within the right ventricle were 2.9, 21.3, and 14.3 s, respectively. All mice survived the procedure with no observable respiratory or heart rate distress despite microbubble diameters as large as 19 μm.

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Why do the lungs clear ultrasonic contrast?

Cited by 141 publications

References 16 publications

Experimental carbon dioxide pulmonary embolization after vena cava laceration under pneumoperitoneum

Experimental carbon dioxide pulmonary embolization after vena cava laceration under pneumoperitoneum

Direct demonstration of 25- and 50-μm arteriovenous pathways in healthy human and baboon lungs

In vivo imaging of microfluidic-produced microbubbles

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