Increased exhaled carbon monoxide concentration during living donor liver transplantation

Matsusaki, Takashi; Morimatsu, Hiroshi; Takahashi, Toru; Matsumi, Masaki; Sakai, Kenji; Kaku, Ryuji; Sato, Tetsufumi; Yagi, T.; Tanaka, Noriaki; Morita, Kiyoshi

doi:10.3892/ijmm.21.1.75

Cited by 9 publications

(13 citation statements)

References 30 publications

(43 reference statements)

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“…1A). This result was almost the same as that in our previous report (14). Pre-and post-reperfusion HO-1 gene expression levels were 0.04±0.05 and 0.13±0.08, respectively.…”

Section: Resultssupporting

confidence: 81%

“…This increase in exhaled CO levels positively correlated with HO-1 gene expression levels in the grafted liver. Previously, we reported that exhaled CO levels significantly increased in critically ill patients in intensive care units and LDLT recipients after reperfusion (14,19). In this study, we again found an increase in post-reperfusion exhaled CO levels.…”

Section: Discussionsupporting

confidence: 76%

“…Exhaled CO levels were measured using a CO analyzer (Carbolyzer™ mBA-2000, Taiyo Instruments, Inc., Osaka, Japan), as described previously (14). The instrument had a sensitivity of 0.1 ppm CO and was capable of continuous side stream sampling.…”

Section: Methodsmentioning

confidence: 99%

“…We previously demonstrated that exhaled CO levels increased in LDLT recipients after I/R injury, and suggested that exhaled CO levels indicate the extent of oxidative tissue Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation injury in the affected organ (14). However, the origin of exhaled CO remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

et al. 2011

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Abstract. Living donor liver transplantation (LDLT) requires ischemia/reperfusion (I/R), which can cause early graft injury. However, the detailed mechanism of I/R injury remains unknown. Heme oxygenase-1 (HO-1) is a rate-limiting enzyme in heme catabolism and results in the production of iron, carbon monoxide (CO), and biliverdin IXα. Furthermore, in animals, HO-1 has a protective effect against oxidative stress associated with I/R injury. However, in humans, the molecular mechanism and clinical significance of HO-1 remain unclear. We previously demonstrated that exhaled CO levels increase during LDLT, and postulated that this may indicate I/R injury. In this study, we elucidate the origin of increased exhaled CO levels and the role of HO-1 in I/R injury during LDLT. We studied 29 LDLT donors and recipients each. For investigation of HO-1 gene expression by polymerase chain reaction and HO-1 localization by immunohistological staining, liver biopsies from the grafted liver were conducted twice, once before and once after I/R. Exhaled CO levels and HO-1 gene expression levels significantly increased after I/R. In addition, HO-1 levels significantly increased after I/R in Kupffer cells. Furthermore, we found a significant positive correlation between exhaled CO levels and HO-1 gene expression levels.These results indicated that increased heme breakdown in the grafted liver is the source of increased exhaled CO levels. We also found a significant relationship between HO-1 gene expression levels and alanine aminotransferase (ALT) levels; i.e., the higher the HO-1 gene expression levels, the higher the ALT levels. These results suggest that HO-1-mediated heme breakdown is caused by I/R during LDLT, since it is associated with increased exhaled CO levels and liver damage.

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“…1A). This result was almost the same as that in our previous report (14). Pre-and post-reperfusion HO-1 gene expression levels were 0.04±0.05 and 0.13±0.08, respectively.…”

Section: Resultssupporting

confidence: 81%

Section: Discussionsupporting

confidence: 76%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

et al. 2011

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“…One study demonstrated that the increased concentration of COHb in liver transplantation is associated with initial function of the transplanted liver (Ali et al 2007). The extent of damage can be estimated through expired CO levels after reperfusion in liver transplantation (Matsusaki et al 2008). However, there are not yet studies about COHb and MetHb as predictors of hemodynamic change due to CO and NO during living donor liver transplantation (LDLT).…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic Implications of Carbon Monoxide (CO) and Nitrogen Oxide (NO) during Living Donor Liver Transplantation

Lim

Lee

Kim

2017

Tohoku J. Exp. Med.

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Carbon monoxide (CO) and nitrogen oxide (NO) affect vasodilation and cause hemodynamic change. Hemodynamic instability due to liver transplantation may result in poor prognosis of graft. This study investigated the hemodynamic implications of CO and NO levels measured using carboxyhemoglobin (COHb) and methemoglobin (MetHb) during living donor liver transplantation (LDLT). The hemodynamic instability with a pressor dose (norepinephrine equivalent) was estimated 1 hour after graft reperfusion. COHb and MetHb were used as indexes of CO and NO, and were measured using an arterial blood gas analyzer. One hundred and ten recipients who underwent LDLT from May 2011 to July 2013 were selected. Recipients were divided into high (≥ 1.9%) and low (< 1.9%) COHb groups with COHb concentrations at 5 minutes after reperfusion. Recipients were also divided into high (≥ 0.4%) and low (< 0.4%) MetHb groups with MetHb concentrations at 30 minutes after reperfusion. Data are presented as mean ± standard deviation or number (percentage). Model for End-stage Liver Disease (MELD) scores were different for the two COHb groups (low: 13.4 ± 9.0 vs. high: 19.7 ± 10.6, p < 0.001), and pressor doses adjusted by MELD scores were also different between the two COHb groups (low: 0.09 ± 0.01 μg/kg/min vs. high: 0.14 ± 0.01 μg/kg/min, p = 0.029). By contrast, pressor doses and MELD scores were not different between the two MetHb groups. In conclusion, CO rather than NO has hemodynamic implications during LDLT. Therefore, the increase in COHb during LDLT is predictive of hemodynamic instability.

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Medicinal Chemistry and Therapeutic Applications of the GasotransmittersNO,CO, andH₂Sand their Prodrugs

Szabó

2010

Burger's Medicinal Chemistry and Drug Discovery

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Nitric oxide ( NO ), carbon monoxide ( CO ), and hydrogen sulfide ( H 2 S ) are the main endogenous gasotransmitters. These gases are produced by the body by enzymatic reactions and serve physiological regulatory purposes including vasodilatation and anti‐inflammatory effects. Over the past decades, multiple approaches have been identified for the therapeutic exploitation of these three gasotransmitters, based on inhalation of the gases and/or the parenteral or enteral administration of various formulations of these molecules or their prodrugs. Here we overview the medicinal chemistry and the therapeutic applications of NO, CO, and H 2 S and their prodrugs. Inhaled NO is used clinically to selectively dilate the pulmonary vasculature in the therapy of the primary pulmonary hypertension of the newborn. Organic nitrates such as glyceryl trinitrate or nitroglycerin are used in the therapy of acute and chronic angina. Sodium nitroprusside is used to counteract acute hypertensive crisis. Another class of clinical‐stage NO donor drugs is the sydnonimines (molsidomine, linsidomine). Additional classes of NO donors include diazeniumdiolates (NONOates) and S ‐nitrosothiols, with beneficial effects in various preclinical models of disease. With respect to CO, the main therapeutic approaches are CO inhalation (currently in clinical trials for the experimental therapy of delayed graft function associated with kidney transplantation) and carbon monoxide releasing compounds of various classes (in preclinical stage). With respect to H 2 S, a parenteral injectable formulation of the gas is currently is Phase I trials. Several classes of H 2 S donor molecules have also been identified, which are used in preclinical studies.

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Increased exhaled carbon monoxide concentration during living donor liver transplantation

Cited by 9 publications

References 30 publications

Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

Hemodynamic Implications of Carbon Monoxide (CO) and Nitrogen Oxide (NO) during Living Donor Liver Transplantation

Medicinal Chemistry and Therapeutic Applications of the GasotransmittersNO,CO, andH₂Sand their Prodrugs

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Increased exhaled carbon monoxide concentration during living donor liver transplantation

Cited by 9 publications

References 30 publications

Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

Heme breakdown and ischemia/reperfusion injury in grafted liver during living donor liver transplantation

Hemodynamic Implications of Carbon Monoxide (CO) and Nitrogen Oxide (NO) during Living Donor Liver Transplantation

Medicinal Chemistry and Therapeutic Applications of the GasotransmittersNO,CO, andH2Sand their Prodrugs

Contact Info

Product

Resources

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Medicinal Chemistry and Therapeutic Applications of the GasotransmittersNO,CO, andH₂Sand their Prodrugs