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Dietary Restriction Compromises Resistance to Gut Ischemia-Reperfusion, Despite Reduction in Circulating Leukocyte Activation

Chikara Ueno, MD^*, Kazuhiko Fukatsu, MD, Yoshinori Maeshima, MD^*, Tomoyuki Moriya, MD, Eiji Shinto, MD, Etsuko Hara, MT, Hidetoshi Nagayoshi, MD^*, Hoshio Hiraide, MD and Hidetaka Mochizuki, MD^*

From the ^* Department of Surgery I, National Defense Medical College, Saitama, Japan; Division of Basic Traumatology, National Defense Medical College Research Institute, Saitama, Japan; Department of Surgery I, Chiba University Graduate School of Medicine, Chiba, Japan; and the Department of Pathology II, National Defense Medical College, Saitama, Japan

Correspondence: Kazuhiko Fukatsu, MD, Division of Basic Traumatology, National Defense Medical College Research Institute, 3–2 Namiki, Tokorozawa, Saitama, Japan 359-8513. Electronic mail may be sent to fukatsu{at}ndmc.ac.jp.

Background: Gut ischemia-reperfusion (gut I/R) accompanying severe surgical insults leads to neutrophil-mediated injury and is regarded as a triggering event in early multiple-organ failure. Our previous study demonstrated dietary restriction to down-regulate leukocyte activation. Therefore, we hypothesized dietary restriction might be beneficial in terms of surviving I/R. We also evaluated leukocyte activation and the level of organ glutathione, an antioxidative substance. Methods: Institute of Cancer Research mice received chow, 170 (ad libitum), 119 (MR: mild restriction) or 68 (SR: severe restriction) g/kg per day for 7 days. Exp. 1: The mice (n = 59) underwent 15 or 45 minutes of gut ischemia and survival was observed. Exp. 2: The mice (n = 73) were killed before or 60 or 120 minutes after 15-minute ischemia. Reactive oxygen intermediate (ROI) production by circulating myeloid cells and CD11b expression was determined. Some mice were assessed for nuclear factor B (NFB) activation. Glutathione levels were measured in some of the small intestine and liver samples from each group. Results: Dietary restriction decreased survival. Circulating myeloid cell priming and activation, in terms of ROI production and CD11b expression, were enhanced in the ad libitum group but not in the restricted groups. NFB was activated only in the ad libitum group. Gut and hepatic glutathione levels were lower in the SR than in the ad libitum group. Dietary restriction caused histologic damages in gut, liver, and lung 120 minutes after reperfusion. Conclusions: Dietary restriction blunts leukocyte priming and activation after gut ischemic insult but worsens the outcome by, at least in part, decreasing antioxidative activities. Clinically, nutrition replenishment may be required to improve the outcome of gut hypoperfusion.

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