Intestinal energy metabolism after ischemia-reperfusion: Effects of moderate hypothermia and perfluorocarbons

Vejchapipat, Paisarn; Proctor, E; Ramsay, Alan G.; Petros, Andy; Gadian, David G.; Spitz, Lewis; Pierro, Agostino

doi:10.1053/jpsu.2002.32288

Cited by 28 publications

(16 citation statements)

References 18 publications

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“…Intestinal I/R in our model induces intestinal histologic changes and energy failure, liver energy failure, and lung neutrophil infiltration, 13,14,6,31 and these are thought to contribute to multiple organ failure. In the current study, we have additionally shown, although cardiac phosphoenergetics were maintained after intestinal I/R at normothermia, CPT I activity was impaired by the effects of intestinal I/R.…”

Section: Discussionmentioning

confidence: 85%

“…These suggest that the balance of substrate utilisation was shifted from fatty acid oxidation to either carbohydrate or ketone body utilisation. We have shown previously that moderate hypothermia (body temperature between 30°C and 32°C) has beneficial effects on liver function 6 and gut histology 13 and prevents pulmonary neutrophil infiltration 14 subsequent to intestinal ischaemia-reperfusion injury. Interestingly, moderate hypothermia prevented the inhibition of cardiac CPT I activity after intestinal I/R, together with our previous studies showing the benefits of hypothermia to the gut, liver, and lungs, supporting the potential clinical utility of moderate hypothermia in amelioration of multisystem organ failure caused by intestinal ischaemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 98%

“…We have shown previously that intestinal I/R induces not only by intestinal but also hepatic energy failure and that mortality is closely associated with the depletion of hepatic highenergy phosphate. 6,13 Moderate hypothermia attenuates loss of high-energy phosphate and histologic changes in the gut, 13 prevents hepatic bioenergetic failure, 6 decreases lung neutrophil infiltration, 14 and abolishes mortality in this model. The aims of this study were to characterise cardiac bioenergetic status after intestinal I/R (experiment A), and to evaluate the effects of intestinal I/R and moderate hypothermia on cardiac fatty acid oxidation (experiment B).…”

mentioning

confidence: 87%

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Heart energy metabolism after intestinal ischaemia and reperfusion

Stefanutti

Vejchapipat

Williams

et al. 2004

Journal of Pediatric Surgery

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 87%

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Heart energy metabolism after intestinal ischaemia and reperfusion

Stefanutti

Vejchapipat

Williams

et al. 2004

Journal of Pediatric Surgery

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“…Another study recently showed that mild hypothermia improves the neurologic outcome after cardiac arrest without increasing complications, compared to standard treatment with normothermia [11] . Moreover, several investigations have shown that mild or moderate hypothermia decreases the formation of reactive oxygen species and post-ischemic vascular resistance in the liver [12] , as well as ameliorates the depletion of ATP level in the intestine [13] , liver [14] , and heart [15] after intestinal ischemia reperfusion. It was also shown that mild hypothermia ameliorates damage after transient forebrain ischemia with a high recovery rate of high-energy phosphate metabolism [16] .…”

mentioning

confidence: 99%

Mild Hypothermia Ameliorates Lung Ischemia Reperfusion Injury in an ex vivo Rat Lung Model

Tanaka

Omasa²,

Nakamura³

et al. 2005

Eur Surg Res

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Background: Ischemia reperfusion (I-R) injury of the lung frequently occurs after cardiopulmonary bypass, pulmonary thromboendarterectomy, lung transplantation, and major pulmonary resection with vascular reconstruction. Mild hypothermia ameliorates ischemia reperfusion injury of the brain and the liver. However, the effect of mild hypothermia on I-R injury of the lung has not been investigated. Methods: The lungs of Lewis rats underwent 80 min of ischemia followed by 60 min of reperfusion in an ex vivo perfusion model. The ambient temperature was maintained at either normothermia (38°C, n = 6) or mild hypothermia (35°C, n = 6) during the ischemia and reperfusion. Results: Pulmonary shunt fraction, peak inspiratory pressure, mean pulmonary arterial pressure during reperfusion, and the wet/dry weight ratio of the lung tissue at the end of reperfusion in the mild hypothermia group were significantly (p < 0.05) lower than those in the normothermia group. Total adenine nucleotide, adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate after reperfusion in the mild hypothermia group were significantly (p < 0.05) higher than those in the normothermia group. Conclusion: Mild hypothermia attenuates I-R injury of the lung with maintained levels of intrapulmonary high-energy phosphate compounds after reperfusion, suggesting its beneficial effect on warm lung I-R in clinical settings.

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“…The controlled moderate hypothermia has been proposed as a potentially promising therapy against several conditions including intestinal ischemia-reperfusion [1], hemorrhagic shock [2], stroke [3], and fulminant liver failure associated with encephalopathy [4]. Its mechanisms in ameliorating the severity of these conditions have been reported to be involved in the process of oxidative stress [5], a reduction in leukocyte accumulation [6,14], a modification of transcription factor activation [15], and an association with serum levels of adhesion molecules [7].…”

Section: Discussionmentioning

confidence: 99%

The effects of moderate hypothermia on energy metabolism and serum inflammatory markers during laparotomy

et al. 2005

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The objective of this study was to investigate energy metabolism of the gut and liver as well as serum inflammatory cytokines following exploratory laparotomy at moderate hypothermia. Two groups of rats were studied, (n=6-8/group); laparotomy at normothermia for 120 min and laparotomy at hypothermia (32-33 degrees C) for 120 min. Study 1: Intestinal glucose, succinate, lactate, phosphocreatine, and ATP as well as hepatic glucose, succinate, lactate, and ATP were measured in terms of micromole per gram using magnetic resonance spectroscopy. Study 2: Serum levels of TNF-alpha, IL-1beta, LPS-inducible chemokine (LIX), and sICAM-1 were measured by ELISA. Histology of the gut and liver were interpreted. Data are expressed as mean and SEM. In Study 1, laparotomy at hypothermia caused an increase in intestinal glucose levels (0.78+/-0.03 vs. 1.29+/-0.11, P=0.0012) with a decrease in hepatic lactate levels (0.82+/-0.04 vs. 0.44+/-0.06, P<0.001). There were no differences in the other metabolites between the two groups. In Study 2, there were no differences in serum TNF-alpha, IL-1beta, LIX, or sICAM-1 between the two groups. Histological features of the gut and liver among groups were comparable. In conclusion, the intestine and liver react to hypothermia differently. However, levels of high-energy phosphates in both organs are not affected by hypothermia suggesting adequate energy for the organs. It is unlikely that hypothermia induces either systemic inflammatory response or hypoxic damage to the intestine and liver in this model.

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Intestinal energy metabolism after ischemia-reperfusion: Effects of moderate hypothermia and perfluorocarbons

Cited by 28 publications

References 18 publications

Heart energy metabolism after intestinal ischaemia and reperfusion

Heart energy metabolism after intestinal ischaemia and reperfusion

Mild Hypothermia Ameliorates Lung Ischemia Reperfusion Injury in an ex vivo Rat Lung Model

The effects of moderate hypothermia on energy metabolism and serum inflammatory markers during laparotomy

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