Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study

Autores
Dubin, Arnaldo; Pozo, Mario Omar; Kanoore Edul, Vanina Siham; Murias, Gastón; Canales, Héctor Saúl; Barán, Marcelo; Maskin, Bernardo; Ferrara, Gonzalo; Laporte, Mercedes; Estenssoro, Elisa
Año de publicación
2005
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Introduction: Continuous monitoring of bladder partial carbon dioxide tension (PCO₂) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO₂. Our hypothesis was that bladder PCO₂, measured using saline tonometry, will be similar to ileal PCO₂ during ischaemia and reperfusion. Method: Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO₂ gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO2 were measured using saline tonometry. Results: After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO₂ gradients when compared with baseline values (all values in mmHg; bladder ∆PCO₂ 3 ± 3 versus 12 ± 5, ileal ∆PCO₂ 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO₂ 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO₂ 4 ± 2 versus 14 ± 4; P < 0.05 versus basal for all). After blood reinfusion, PCO₂ gradients returned to basal values except for bladder ∆PCO₂, which remained at ischaemic levels (13 ± 7 mmHg). Conclusion: Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO₂ might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO₂gradients occurred in gut mucosa. Moreover, the fact that ileal ∆PCO₂ was greater than the mesenteric venous–arterial PCO₂ suggests that tonometrically measured PCO₂ reflects mucosal rather than transmural PCO₂. Ileal ∆PCO₂ appears to be the more sensitive marker of ischaemia.
Facultad de Ciencias Médicas
Materia
Ciencias Médicas
Partial carbon dioxide tension
Tissue perfusion
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/128600

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network_name_str SEDICI (UNLP)
spelling Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational studyDubin, ArnaldoPozo, Mario OmarKanoore Edul, Vanina SihamMurias, GastónCanales, Héctor SaúlBarán, MarceloMaskin, BernardoFerrara, GonzaloLaporte, MercedesEstenssoro, ElisaCiencias MédicasPartial carbon dioxide tensionTissue perfusionIntroduction: Continuous monitoring of bladder partial carbon dioxide tension (PCO₂) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO₂. Our hypothesis was that bladder PCO₂, measured using saline tonometry, will be similar to ileal PCO₂ during ischaemia and reperfusion. Method: Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO₂ gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO2 were measured using saline tonometry. Results: After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO₂ gradients when compared with baseline values (all values in mmHg; bladder ∆PCO₂ 3 ± 3 versus 12 ± 5, ileal ∆PCO₂ 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO₂ 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO₂ 4 ± 2 versus 14 ± 4; P &lt; 0.05 versus basal for all). After blood reinfusion, PCO₂ gradients returned to basal values except for bladder ∆PCO₂, which remained at ischaemic levels (13 ± 7 mmHg). Conclusion: Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO₂ might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO₂gradients occurred in gut mucosa. Moreover, the fact that ileal ∆PCO₂ was greater than the mesenteric venous–arterial PCO₂ suggests that tonometrically measured PCO₂ reflects mucosal rather than transmural PCO₂. Ileal ∆PCO₂ appears to be the more sensitive marker of ischaemia.Facultad de Ciencias Médicas2005info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/128600enginfo:eu-repo/semantics/altIdentifier/issn/1466-609Xinfo:eu-repo/semantics/altIdentifier/issn/1364-8535info:eu-repo/semantics/altIdentifier/pmid/16277718info:eu-repo/semantics/altIdentifier/doi/10.1186/cc3797info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:30:57Zoai:sedici.unlp.edu.ar:10915/128600Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:58.115SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
title Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
spellingShingle Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
Dubin, Arnaldo
Ciencias Médicas
Partial carbon dioxide tension
Tissue perfusion
title_short Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
title_full Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
title_fullStr Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
title_full_unstemmed Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
title_sort Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study
dc.creator.none.fl_str_mv Dubin, Arnaldo
Pozo, Mario Omar
Kanoore Edul, Vanina Siham
Murias, Gastón
Canales, Héctor Saúl
Barán, Marcelo
Maskin, Bernardo
Ferrara, Gonzalo
Laporte, Mercedes
Estenssoro, Elisa
author Dubin, Arnaldo
author_facet Dubin, Arnaldo
Pozo, Mario Omar
Kanoore Edul, Vanina Siham
Murias, Gastón
Canales, Héctor Saúl
Barán, Marcelo
Maskin, Bernardo
Ferrara, Gonzalo
Laporte, Mercedes
Estenssoro, Elisa
author_role author
author2 Pozo, Mario Omar
Kanoore Edul, Vanina Siham
Murias, Gastón
Canales, Héctor Saúl
Barán, Marcelo
Maskin, Bernardo
Ferrara, Gonzalo
Laporte, Mercedes
Estenssoro, Elisa
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Partial carbon dioxide tension
Tissue perfusion
topic Ciencias Médicas
Partial carbon dioxide tension
Tissue perfusion
dc.description.none.fl_txt_mv Introduction: Continuous monitoring of bladder partial carbon dioxide tension (PCO₂) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO₂. Our hypothesis was that bladder PCO₂, measured using saline tonometry, will be similar to ileal PCO₂ during ischaemia and reperfusion. Method: Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO₂ gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO2 were measured using saline tonometry. Results: After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO₂ gradients when compared with baseline values (all values in mmHg; bladder ∆PCO₂ 3 ± 3 versus 12 ± 5, ileal ∆PCO₂ 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO₂ 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO₂ 4 ± 2 versus 14 ± 4; P &lt; 0.05 versus basal for all). After blood reinfusion, PCO₂ gradients returned to basal values except for bladder ∆PCO₂, which remained at ischaemic levels (13 ± 7 mmHg). Conclusion: Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO₂ might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO₂gradients occurred in gut mucosa. Moreover, the fact that ileal ∆PCO₂ was greater than the mesenteric venous–arterial PCO₂ suggests that tonometrically measured PCO₂ reflects mucosal rather than transmural PCO₂. Ileal ∆PCO₂ appears to be the more sensitive marker of ischaemia.
Facultad de Ciencias Médicas
description Introduction: Continuous monitoring of bladder partial carbon dioxide tension (PCO₂) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO₂. Our hypothesis was that bladder PCO₂, measured using saline tonometry, will be similar to ileal PCO₂ during ischaemia and reperfusion. Method: Six anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO₂ gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO2 were measured using saline tonometry. Results: After bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO₂ gradients when compared with baseline values (all values in mmHg; bladder ∆PCO₂ 3 ± 3 versus 12 ± 5, ileal ∆PCO₂ 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO₂ 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO₂ 4 ± 2 versus 14 ± 4; P &lt; 0.05 versus basal for all). After blood reinfusion, PCO₂ gradients returned to basal values except for bladder ∆PCO₂, which remained at ischaemic levels (13 ± 7 mmHg). Conclusion: Tissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO₂ might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO₂gradients occurred in gut mucosa. Moreover, the fact that ileal ∆PCO₂ was greater than the mesenteric venous–arterial PCO₂ suggests that tonometrically measured PCO₂ reflects mucosal rather than transmural PCO₂. Ileal ∆PCO₂ appears to be the more sensitive marker of ischaemia.
publishDate 2005
dc.date.none.fl_str_mv 2005
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info:eu-repo/semantics/altIdentifier/doi/10.1186/cc3797
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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