Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia

Robert C. King, Oliver A.R. Binns, R. Chai Kanithanon, Patrick E. Parrino, T. Brett Reece, James D. Maliszewskyj, Kimberly S. Shockey, Curtis G. Tribble, Irving L. Kron

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background. We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4°C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20% whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia. Methods. We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4°C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients. Results. The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 ± 65.1 versus 145.3 ± 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 ± 48.4 versus 70.7 ± 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 ± 0.96 versus 55.52 ± 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 ± 1,291 versus 67,594 ± 9,467 dynes · s · cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups. Conclusions. Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.

Original languageEnglish (US)
Pages (from-to)795-800
Number of pages6
JournalAnnals of Thoracic Surgery
Volume64
Issue number3
DOIs
StatePublished - Sep 1 1997
Externally publishedYes

Fingerprint

Dextrans
Potassium
Ischemia
Lung
Cold Ischemia
Rabbits
Vascular Resistance
Pulmonary Artery
Pressure
Atrial Pressure
Tidal Volume
Compliance
Reperfusion

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

King, R. C., Binns, O. A. R., Kanithanon, R. C., Parrino, P. E., Reece, T. B., Maliszewskyj, J. D., ... Kron, I. L. (1997). Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia. Annals of Thoracic Surgery, 64(3), 795-800. https://doi.org/10.1016/S0003-4975(97)00595-X

Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia. / King, Robert C.; Binns, Oliver A.R.; Kanithanon, R. Chai; Parrino, Patrick E.; Reece, T. Brett; Maliszewskyj, James D.; Shockey, Kimberly S.; Tribble, Curtis G.; Kron, Irving L.

In: Annals of Thoracic Surgery, Vol. 64, No. 3, 01.09.1997, p. 795-800.

Research output: Contribution to journalArticle

King, RC, Binns, OAR, Kanithanon, RC, Parrino, PE, Reece, TB, Maliszewskyj, JD, Shockey, KS, Tribble, CG & Kron, IL 1997, 'Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia', Annals of Thoracic Surgery, vol. 64, no. 3, pp. 795-800. https://doi.org/10.1016/S0003-4975(97)00595-X
King RC, Binns OAR, Kanithanon RC, Parrino PE, Reece TB, Maliszewskyj JD et al. Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia. Annals of Thoracic Surgery. 1997 Sep 1;64(3):795-800. https://doi.org/10.1016/S0003-4975(97)00595-X
King, Robert C. ; Binns, Oliver A.R. ; Kanithanon, R. Chai ; Parrino, Patrick E. ; Reece, T. Brett ; Maliszewskyj, James D. ; Shockey, Kimberly S. ; Tribble, Curtis G. ; Kron, Irving L. / Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia. In: Annals of Thoracic Surgery. 1997 ; Vol. 64, No. 3. pp. 795-800.
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abstract = "Background. We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4°C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20{\%} whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia. Methods. We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4°C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients. Results. The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 ± 65.1 versus 145.3 ± 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 ± 48.4 versus 70.7 ± 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 ± 0.96 versus 55.52 ± 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 ± 1,291 versus 67,594 ± 9,467 dynes · s · cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups. Conclusions. Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.",
author = "King, {Robert C.} and Binns, {Oliver A.R.} and Kanithanon, {R. Chai} and Parrino, {Patrick E.} and Reece, {T. Brett} and Maliszewskyj, {James D.} and Shockey, {Kimberly S.} and Tribble, {Curtis G.} and Kron, {Irving L.}",
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T1 - Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia

AU - King, Robert C.

AU - Binns, Oliver A.R.

AU - Kanithanon, R. Chai

AU - Parrino, Patrick E.

AU - Reece, T. Brett

AU - Maliszewskyj, James D.

AU - Shockey, Kimberly S.

AU - Tribble, Curtis G.

AU - Kron, Irving L.

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Y1 - 1997/9/1

N2 - Background. We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4°C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20% whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia. Methods. We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4°C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients. Results. The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 ± 65.1 versus 145.3 ± 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 ± 48.4 versus 70.7 ± 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 ± 0.96 versus 55.52 ± 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 ± 1,291 versus 67,594 ± 9,467 dynes · s · cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups. Conclusions. Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.

AB - Background. We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4°C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20% whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia. Methods. We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4°C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients. Results. The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 ± 65.1 versus 145.3 ± 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 ± 48.4 versus 70.7 ± 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 ± 0.96 versus 55.52 ± 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 ± 1,291 versus 67,594 ± 9,467 dynes · s · cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups. Conclusions. Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.

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