Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia

Autores
Dubin, Arnaldo; Murias, Gastón; Estenssoro, Elisa; Canales, Héctor Saúl; Badie, Julio Ezequiel; Pozo, Mario Omar; Sottile, Juan Pablo; Barán, Marcelo; Pálizas, Fernando; Laporte, Mercedes
Año de publicación
2002
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
Introduction. An elevation in intramucosal-arterial PCO2 gradient (ΔPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO2 should not be altered. Methods. In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. Results. Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO2 increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant). Discussion. In this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO2 might be determined primarily by blood flow.
Facultad de Ciencias Médicas
Materia
Ciencias Médicas
Blood flow
Carbon dioxide
Hypoxia
Oxygen consumption
Tonometry
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:10915/84975

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oai_identifier_str oai:sedici.unlp.edu.ar:10915/84975
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxiaDubin, ArnaldoMurias, GastónEstenssoro, ElisaCanales, Héctor SaúlBadie, Julio EzequielPozo, Mario OmarSottile, Juan PabloBarán, MarceloPálizas, FernandoLaporte, MercedesCiencias MédicasBlood flowCarbon dioxideHypoxiaOxygen consumptionTonometryIntroduction. An elevation in intramucosal-arterial PCO<SUB>2</SUB> gradient (ΔPCO<SUB>2</SUB>) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> should not be altered. Methods. In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO<SUB>2</SUB> by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO<SUB>2</SUB>. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. Results. Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO<SUB>2</SUB> increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant). Discussion. In this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO<SUB>2</SUB> might be determined primarily by blood flow.Facultad de Ciencias Médicas2002info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdf514-520http://sedici.unlp.edu.ar/handle/10915/84975enginfo:eu-repo/semantics/altIdentifier/issn/1364-8535info:eu-repo/semantics/altIdentifier/doi/10.1186/cc1813info: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:UNLP2025-09-03T10:48:36Zoai:sedici.unlp.edu.ar:10915/84975Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 10:48:36.34SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
title Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
spellingShingle Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
Dubin, Arnaldo
Ciencias Médicas
Blood flow
Carbon dioxide
Hypoxia
Oxygen consumption
Tonometry
title_short Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
title_full Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
title_fullStr Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
title_full_unstemmed Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
title_sort Intramucosal-arterial PCO<sub>2</sub> gap fails to reflect intestinal dysoxia in hypoxic hypoxia
dc.creator.none.fl_str_mv Dubin, Arnaldo
Murias, Gastón
Estenssoro, Elisa
Canales, Héctor Saúl
Badie, Julio Ezequiel
Pozo, Mario Omar
Sottile, Juan Pablo
Barán, Marcelo
Pálizas, Fernando
Laporte, Mercedes
author Dubin, Arnaldo
author_facet Dubin, Arnaldo
Murias, Gastón
Estenssoro, Elisa
Canales, Héctor Saúl
Badie, Julio Ezequiel
Pozo, Mario Omar
Sottile, Juan Pablo
Barán, Marcelo
Pálizas, Fernando
Laporte, Mercedes
author_role author
author2 Murias, Gastón
Estenssoro, Elisa
Canales, Héctor Saúl
Badie, Julio Ezequiel
Pozo, Mario Omar
Sottile, Juan Pablo
Barán, Marcelo
Pálizas, Fernando
Laporte, Mercedes
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Blood flow
Carbon dioxide
Hypoxia
Oxygen consumption
Tonometry
topic Ciencias Médicas
Blood flow
Carbon dioxide
Hypoxia
Oxygen consumption
Tonometry
dc.description.none.fl_txt_mv Introduction. An elevation in intramucosal-arterial PCO<SUB>2</SUB> gradient (ΔPCO<SUB>2</SUB>) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> should not be altered. Methods. In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO<SUB>2</SUB> by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO<SUB>2</SUB>. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. Results. Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO<SUB>2</SUB> increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant). Discussion. In this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO<SUB>2</SUB> might be determined primarily by blood flow.
Facultad de Ciencias Médicas
description Introduction. An elevation in intramucosal-arterial PCO<SUB>2</SUB> gradient (ΔPCO<SUB>2</SUB>) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> should not be altered. Methods. In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO<SUB>2</SUB> by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO<SUB>2</SUB>. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. Results. Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO<SUB>2</SUB> increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant). Discussion. In this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO<SUB>2</SUB> might be determined primarily by blood flow.
publishDate 2002
dc.date.none.fl_str_mv 2002
dc.type.none.fl_str_mv info:eu-repo/semantics/review
info:eu-repo/semantics/publishedVersion
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dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/1364-8535
info:eu-repo/semantics/altIdentifier/doi/10.1186/cc1813
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
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instname_str Universidad Nacional de La Plata
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institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
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