Protective effect of carbon monoxide inhalation for cold-preserved small intestinal grafts

Nakao, Atsunori; Kimizuka, Kei; Stolz, Donna B.; Neto, João Seda; Kubo, Takashi; Choi, Augustine M.K.; Uchiyama, Takashi; Zuckerbraun, Brian S.; Bauer, Anthony J.; Nalesnik, Michael A.; Otterbein, Leo E.; Geller, David A.; Murase, Noriko

doi:10.1067/msy.2003.238

Cited by 86 publications

(69 citation statements)

References 20 publications

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“…There have been several reports that inhalation of CO can be protective against acute rejection of intestine, lung, and kidney transplants (11,12,23,24). The protective actions of CO inhalation in transplantation are associated with a decrease in inflammation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Vera

Henegar²,

Drummond³

et al. 2005

Journal of the American Society of Nephrology

129

105

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Heme oxygenase (HO) induction has been demonstrated to be beneficial in limiting the extent of cellular damage after ischemia-induced acute renal failure (ARF). Because increased HO activity is associated with the production of carbon monoxide (CO) as well as the potent antioxidant bilirubin, it is unclear which of the two is of greater importance in the protective effects of HO induction. The purpose of this study was to determine the protective role of CO alone in ischemia-induced ARF. Bilateral clamping of the renal pedicle for 40 min was associated with a ninefold increase in the levels of plasma creatinine 24 h after reperfusion as compared with normal plasma creatinine levels; however, administration of CO donor compounds tricarbonyldichlororuthenium(II) dimer, ([Ru(CO) 3 Cl 2 ] 2 , 10 mg/kg) or tricarbonylchloro(glycinato)ruthenium(II) ([Ru(CO) 3 Cl(glycinate)], (CORM-3) 1 h before the onset of ischemia significantly decreased the levels of plasma creatinine 24 h after reperfusion as compared with vehicle-treated mice. Surprising, treatment with the CO donors was associated with an increase in HO activity 24 h after ischemia. For determining whether the protective effects of the CO donors were due to CO or HO-1 induction, experiments were performed in which HO was inhibited before administration of the CO donors. Pretreatment with the HO inhibitor had no effect on the level of plasma creatinine 24 h after reperfusion after treatment with the CO donor compounds. These results suggest that CO itself may be protective and limit renal damage in ischemia induced ARF. 16: 950-958, 2005. J Am Soc Nephrol

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Vera

Henegar²,

Drummond³

et al. 2005

Journal of the American Society of Nephrology

129

105

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“…3). Similarly, scanning electron microscopy shows numerous vacuolization and disorganization of the internal cellular architecture of VECs, indicating the mitochondrial breakdown and irreversible degeneration in VECs induced by I/R [16,70,71] (Fig. 3).…”

Section: Vec Protection and Vasorelaxation By Comentioning

confidence: 99%

“…Since transplant-induced I/R injury involves vigorous inflammatory reactions, the use of CO to ameliorate I/R injury in the transplant setting is a straightforward application. In the series of rodent experiments in our laboratory, recipient CO exposure at a dose of 250 ppm for 1 hr before and 24 hrs after transplantation significantly reduces inflammatory cell infiltration in I/R injury induced in small intestine, kidney, heart, lung and liver grafts with extended cold preservation and following transplantation [15,16,70,71,98]. The levels of mRNA for pro-inflammatory mediators including IL-6, TNFα, IL-1β, inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2 rapidly elevate peaking 1 to 3 hrs after reperfusion after transplantation.…”

Section: Co Has An Anti-inflammatory Effectmentioning

confidence: 99%

“…In the last decade, induction of HO-1 has been shown to be beneficial against pitfalls associated with organ transplantation, including I/R injury [6][7][8][9] and allogenic immune reactions due to histoincompatibility including graft rejection [4,[10][11][12][13] and graft-versushost disease [14]. Likewise, carbon monoxide (CO), one of the byproducts of heme degradation through HO, has a wide range of effectiveness in preventing impairment of the transplanted grafts during I/R injury [15,16], tissue injuries associated with acute rejection [17], and also mouse-to-rat xenograft rejection [18]. This review article summarizes the efforts made in understanding the cytoprotective effects of CO in organ transplantation in order to advance our knowledge of the potential clinical application of CO in the field of transplantation.…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of carbon monoxide in transplantation

Nakao¹

2006

J Cell Mol Med

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During the last decades due to the development of new immunosuppressive agents and improvements in organ preservation methods, surgical techniques, and postoperative care, organ transplantation has become an ultimate therapeutic option for irreversible organ failure. Early graft survival has significantly improved; however, the long-term outcome remains unsatisfactory. Multiple factors, both immunogenic and non-immunogenic etiologies, are involved in the deterioration of the allografts, and the recent use of expanded criteria donors to overcome the organ shortage may also contribute to the graft losses. Carbon monoxide (CO) is commonly viewed as a poison in high concentrations due to its ability to interfere with oxygen delivery. However, CO is endogenously produced in the body as a byproduct of heme degradation by the heme oxygenase (HO) and has recently received notable attention as a gaseous regulatory molecule. In fact, an augmentation of endogenous CO by induction of HO-1 or exogenously added CO is known to have potent cytoprotective effects in various disease models. Several recent reports have demonstrated that CO provides potent cytoprotective effects in the field of organ and cell transplantation. CO is able to prevent ischemia/reperfusion injury, allograft rejection, and xenograft rejection via its anti-inflammatory, anti-apoptotic and anti-proliferation effects, suggesting that CO might be a valuable therapeutic option in the field of transplantation. Based on the recent advancement of our understanding of CO as a new therapeutic molecule, this review attempts to summarize the functional roles as well as biological and molecular mechanisms of CO in transplantation and discusses potential CO application to the clinical transplant setting.

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“…The rats that inhaled CO had improved micro-vascular blood flow, decreased m-RNA for inflammatory mediators such as IL-6, COX-2, iNOS and ICAM-1, and almost no histopathological changes. The CO exposed animals also had improved gastrointestinal transit and no animal deaths after the operation, compared to a survival of 58 % for the nonexposed rats (Nakao et al, 2003). In a model of acute lung injury in mice, CO showed cytoprotective effects and an attenuation of the lung injury, along with prolonged survival during exposure to lethal hyperoxia (Otterbein et al, 2003).…”

Section: Inflammationmentioning

confidence: 87%

Carbon monoxide in biological systems: an experimental and clinical study

Åberg¹

2008

Acta Anaesthesiol Scand

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Protective effect of carbon monoxide inhalation for cold-preserved small intestinal grafts

Cited by 86 publications

References 20 publications

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Protective effect of carbon monoxide in transplantation

Carbon monoxide in biological systems: an experimental and clinical study

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