Gut and muscle tissue Po2 in endotoxemic dogs during shock and resuscitation

Vallet, B.; Lund, N.; Curtis, SE; Kelly, Denis; Sm, Cain

doi:10.1016/0300-9572(95)94137-x

Cited by 28 publications

(36 citation statements)

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“…Vasomotion reduces resistance and in-summation of cardiac responses and individual vascular beds. Our laboratory and others have demonstrated creases blood flow compared to a static vessel with the same average diameter, regulates delivery of nutrients that individual vascular beds react differently to the same septic challenge [3]. Visceral beds, such as intesand elimination of metabolites, and may control capillary filtration [21].…”

Section: Methodsmentioning

confidence: 99%

“…OcAltered vascular responsiveness is the hallmark of cult mucosal ischemia is thought to be central to the septic shock. Recently, these changes have frequently development of gut-derived sepsis [3]. Farquhar et been attributed to increased production of nitric oxide al.…”

mentioning

confidence: 99%

“…This is especially true in the small resis-of the intestinal villi, with countercurrent oxygen extance arterioles of the viscera. We used in vivo micros-change, makes the mucosa very susceptible to hypcopy of the rat small intestine to assess (1) endothelial-oxia [3, 6]. While altered vascular responsiveness is …”

mentioning

confidence: 99%

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Differential Intestinal Microvascular Dysfunction Occurs during Bacteremia

Spain

Wilson

Krysztopik

et al. 1997

Journal of Surgical Research

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential Intestinal Microvascular Dysfunction Occurs during Bacteremia

Spain

Wilson

Krysztopik

et al. 1997

Journal of Surgical Research

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“…Although cardiac output is frequently increased in sepsis, high lactate levels and increased tonometric partial pressure of CO 2 (pCO 2 ) in tissues indicate at least regional tissue dysoxia. This has been termed oxygen extraction deficit in sepsis and has been well documented in different animal models of shock [23-25]. It is still a matter of debate whether it can be explained by pathologic flow heterogeneity due to dysfunctional autoregulatory mechanisms and microcirculatory dysfunction causing hypoxic pockets, or by mitochondrial dysfunction with associated impaired oxidative phosphorylation [4], or by a combination of both.…”

Section: Heterogeneous Microcirculatory Perfusionmentioning

confidence: 99%

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2004

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“…Vallet and colleagues studied endotoxemic dogs with low blood flow, resuscitated with dextran. Gut flow was increased and oxygen transport normalized, but oxygen uptake and mucosal PO 2 and pH remained low, results that were ascribed to flow redistribution from mucosal to serosal layers [13]. Conversely, Revelly and colleagues described flow redistribution from serosa to mucosa induced by endotoxin [23].…”

Section: Discussionmentioning

confidence: 99%

Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study

Dubin

Murias²,

Maskin

et al. 2005

Crit Care

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Introduction Increased intramucosal-arterial carbon dioxide tension (PCO 2 ) difference (∆PCO 2 ) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in ∆PCO 2 . Methods In 19 anesthetized and mechanically ventilated sheep, we measured cardiac output, superior mesenteric blood flow, lactate, gases, hemoglobin and oxygen saturations in arterial, mixed venous and mesenteric venous blood, and ileal intramucosal PCO 2 by saline tonometry. Intestinal oxygen transport and consumption were calculated. After basal measurements, sheep were assigned to the following groups, for 120 min: (1) sham (n = 6), (2) normal blood flow (n = 7) and (3) increased blood flow (n = 6). Escherichia coli lipopolysaccharide (5 µg/kg) was injected in the last two groups. Saline solution was used to maintain blood flood at basal levels in the sham and normal blood flow groups, or to increase it to about 50% of basal in the increased blood flow group. Results In the normal blood flow group, systemic and intestinal oxygen transport and consumption were preserved, but ∆PCO 2 increased (basal versus 120 min endotoxemia, 7 ± 4 versus 19 ± 4 mmHg; P < 0.001) and metabolic acidosis with a high anion gap ensued (arterial pH 7.39 versus 7.35; anion gap 15 ± 3 versus 18 ± 2 mmol/l; P < 0.001 for both). Increased blood flow prevented the elevation in ∆PCO 2 (5 ± 7 versus 9 ± 6 mmHg; P = not significant). However, anion-gap metabolic acidosis was deeper (7.42 versus 7.25; 16 ± 3 versus 22 ± 3 mmol/l; P < 0.001 for both). Conclusions In this model of endotoxemia, intramucosal acidosis was corrected by increased blood flow and so might follow tissue hypoperfusion. In contrast, anion-gap metabolic acidosis was left uncorrected and even worsened with aggressive volume expansion. These results point to different mechanisms generating both alterations.

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Gut and muscle tissue Po2 in endotoxemic dogs during shock and resuscitation

Cited by 28 publications

References 0 publications

Differential Intestinal Microvascular Dysfunction Occurs during Bacteremia

Differential Intestinal Microvascular Dysfunction Occurs during Bacteremia

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Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study

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