Effect of lipopolysaccharide on intestinal intramucosal hydrogen ion concentration in pigs

Fink, Mitchell P.; Cohn, Stephen M.; Lee, Patrick; Rothschild, Heidie R.; Deniz, Yamo F.; Wang, Hailong; Fiddian-Green, Richard G.

doi:10.1097/00003246-198907000-00009

Cited by 129 publications

(34 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Finally, if minor removal of the laser Doppler probe cannot be excluded, previously reported studies have demonstrated that blood flow measurements in the same area of the stomach are likely to be similar (27,28). Gastric intramucosal acidosis appears to be a sensitive index of gastrointestinal hypoxia (15)(16)(17)(18)(19)(20)(21)(22)(23). Weobtained intramucosal Pco, using a tonometric method (15,16).…”

Section: Dobutamine and Dopamine Effects On Gastric Mucosal Perfusionmentioning

confidence: 99%

The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients.

Nevière¹,

Mathieu²,

Chagnon³

et al. 1996

Am J Respir Crit Care Med

212

View full text Add to dashboard Cite

To test the hypothesis whether or not dobutamine or dopamine infusion increases gastric mucosal perfusion, a prospective randomized crossover trial was conducted on 10 septic patients in the intensive care unit of a university hospital. Systemic hemodynamic, oxygen transport, and gastric perfusion assessed by gastric intramucosal pH and laser Doppler flowmetry were measured at baseline and after administration of dobutamine or dopamine (5 micrograms/kg/min). Both increased oxygen transport. In response to dobutamine, gastric mucosal blood flow increased (+32 +/- 14% from baseline; p < 0.05), gastric tonometered PCO2 and gastric arterial PCO2 difference decreased (58 +/- 7 versus 52 +/- 7 mm Hg; p < 0.05; 16.8 +/- 7.0 versus 10.5 +/- 7.2 mm Hg; p < 0.05), and intramucosal pH increased (7.23 +/- 0.05 versus 7.29 +/- 0.06; p < 0.05). In response to dopamine, gastric mucosal blood flow decreased (-28 +/- 8% from baseline; p < 0.05), gastric tonometered PCO2, gastric-arterial PCO2 difference, and calculated intramucosal pH were unchanged (58 +/- 7 versus 61 +/- 9 mm Hg, ns; 16.8 +/- 7.0 versus 18.9 +/- 8.4 mm Hg, ns; 7.24 +/- 0.05 versus 7.21 +/- 0.06, ns). We speculated that despite an oxygen transport increase, dobutamine and dopamine have affected differently gastric mucosal perfusion in septic patients.

show abstract

Section: Dobutamine and Dopamine Effects On Gastric Mucosal Perfusionmentioning

confidence: 99%

The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients.

Nevière¹,

Mathieu²,

Chagnon³

et al. 1996

Am J Respir Crit Care Med

212

View full text Add to dashboard Cite

show abstract

“…First, if gut blood flow is decreased then gut pHi decreases [11]. Second, endotoxic shock decreases pHi [12]. Third, maintenance of gut blood flow during endotoxemia prevents the decrease of pHi [12,13].…”

mentioning

confidence: 99%

“…Second, endotoxic shock decreases pHi [12]. Third, maintenance of gut blood flow during endotoxemia prevents the decrease of pHi [12,13]. However, does this mean that decreased gastric tonometer pHi always indicates gastric tissue hypoxia?…”

mentioning

confidence: 99%

Gastric tonometry: does it work?

Russell

1997

Intensive Care Medicine

124

View full text Add to dashboard Cite

The fundamental goals of diagnosis and resuscitation of critically ill patients are to detect, prevent, and reverse tissue hypoxia. It had been hoped that global assessment and management of oxygen delivery (DO 2 ) and consumption (VO 2 ) could achieve these goals. However, the DO 2 /VO 2 controversy continues [1]. Global assessment of DO 2 and VO 2 is controversial because of mathematical coupling of shared variables used to calculate DO 2 and VO 2 in many studies [2][3][4], because of the inability to confirm the pathologic dependence of VO 2 on DO 2 when they both are determined independently [2][3][4], and because of conflicting results of randomized controlled trials (RCTs) of supranormal oxygen delivery [5][6][7][8]. Furthermore, very recent prospective, RCTs of supranormal oxygen delivery show either no difference [7] or significantly increased mortality [8] in patients randomized to supranormal oxygen delivery.If global assessment and management of DO 2 and VO 2 are not useful, then a logical alternative is to focus on assessment and management of regional oxygenation at the organ level. Gastric tonometry is a method undergoing extensive evaluation as a tool for assessment and management of gastric oxygenation: does it work and is it ready for clinical use? The technique of gastric tonometry was reviewed in detail recently in Intensive Care Medicine [9]. The purposes of this editorial are review briefly aspects of CO 2 physiology relevant to gastric tonometry, to argue that gastric-arterial CO 2 difference is the tonometer variable of choice, and then to consider several important studies of gastric tonometry as a basis for suggesting that a new prospective RCT of gastric tonometry is required to establish its clinical efficacy.There are several cogent reasons to focus on the gut as a sentinel organ to detect occult tissue hypoxia. First, the counter current flow of the microcirculation of the gut increases the risk of gut mucosal hypoxia. Second, the gut has a higher critical DO 2 than the whole body and other vital organs [10]. Third, gut ischemia increases gut permeability, increases translocation of bacteria, and could therefore increase cytokine synthesis and release by hepatic and systemic mononuclear cells.Several lines of evidence suggest that gastric tonometer pHi may be a marker of gut hypoxia. First, if gut blood flow is decreased then gut pHi decreases [11]. Second, endotoxic shock decreases pHi [12]. Third, maintenance of gut blood flow during endotoxemia prevents the decrease of pHi [12,13]. However, does this mean that decreased gastric tonometer pHi always indicates gastric tissue hypoxia?Decreased gastric tonometer pHi may be relatively non-specific as a marker of gastric tissue hypoxia for several reasons. To develop this argument, I will review briefly the physiologic influences on pHi and other proposed measurements and calculations used in gastric tonometry (Table 1).Gastric tonometer logarithm of hydrogen ion concentration (pHi) is calculated using the measurement of CO 2 tension in ...

show abstract

“…23,24 Indeed, active transport of luminal substrates by the small intestine is inhibited during and after a period of low mesenteric blood floW.2117 In addition, sepsis may adversely affect intestinal function by the release of free oxygen radicals, cytokines, or inflammatory mediators (eg, platelet-activating factor, thromboxane A2). 15,17,[28][29][30] At the enterocytic level, ischemia or the action of inflammatory mediators may result in a decrease in energy stores for active transport (adenosine 5'-triphosphate), in the affinity or number of transport proteins, or in utilization or export of absorbed amino acid.…”

Section: Discussionmentioning

confidence: 99%

The Role of the Imino Transporter Protein in Sepsis‐Impaired Intestinal Proline Absorption

Gardiner

Barbul

1993

J Parenter Enteral Nutr

View full text Add to dashboard Cite

Recently, sepsis has been shown to impair intestinal amino acid absorption in addition to gut metabolic and barrier functions. We investigated intestinal proline absorption in a rabbit model of sepsis. Twelve hours after intraperitoneal injection of lipopolysaccharide, proline uptake by everted jejunal sacs prepared from septic animals (480.4 +/- 67.4 nmol per sac per hour) was significantly reduced compared with controls (846.8 +/- 73.5 nmol per sac per hour) (p < .001 by t test). We next investigated whether reduced expression of transporter proteins contributed to the impaired intestinal proline uptake during sepsis. The proline (imino) carrier of rabbit jejunum is covalently bound by fluorescein isothiocyanate (FITC) and/or phenylisothiocyanate with irreversible inhibition of proline uptake. This binding and inhibition is prevented by sodium chloride and L-proline. Single-cell suspensions of rabbit enterocytes were prepared 12 hours after intraperitoneal injection of lipopolysaccharide/saline or saline alone. Enterocytes were incubated for 30 minutes in tris(hydroxymethyl)aminomethane/ethylenediaminetetraacetate (Tris/EDTA) buffer; buffer with 1 mM phenylisothiocyanate; or buffer with 10 mM proline, 100 mM sodium chloride, and 1 mM phenylisothiocyanate. After incubation with 10 microM FITC in Tris/EDTA buffer for 15 minutes, the percent positivity and fluorescent intensity of FITC binding to enterocytes were determined by using flow cytometry. Sepsis significantly reduced the percentage of enterocytes binding FITC and the fluorescent intensity of FITC binding of proline/sodium chloride-pretreated or untreated cells. This suggests that sepsis depresses the expression of imino transporters by rabbit enterocytes, which may explain the reduced intestinal proline absorption.

show abstract

Effect of lipopolysaccharide on intestinal intramucosal hydrogen ion concentration in pigs

Cited by 129 publications

References 0 publications

The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients.

The contrasting effects of dobutamine and dopamine on gastric mucosal perfusion in septic patients.

Gastric tonometry: does it work?

The Role of the Imino Transporter Protein in Sepsis‐Impaired Intestinal Proline Absorption

Contact Info

Product

Resources

About