Published online Dec 27, 2022. doi: 10.4240/wjgs.v14.i12.1329
Peer-review started: August 25, 2022
First decision: September 2, 2022
Revised: September 11, 2022
Accepted: November 7, 2022
Article in press: November 7, 2022
Published online: December 27, 2022
Processing time: 124 Days and 2 Hours
Mesenteric ischemia introduces unfavorable clinical outcomes particularly when bowel necrosis is diagnosed, and it can happen even after revascularization. However, promising treatment has not been developed to prevent bowel necrosis after revascularization.
Hydrogen gas inhalation has showed tissue preserving effects for several ischemia-reperfusion injuries by reducing reactive oxygen species (ROS) in various animal and clinical studies. In addition, the safety of hydrogen gas was shown by clinical studies that examined the efficacy of hydrogen on myocardial infarction and post-cardiac arrest syndrome. Therefore, hydrogen gas for mesenteric ischemia can be a novel noninvasive treatment.
This study aimed to clarify the favorable effects of hydrogen gas inhalation for mesenteric ischemia and reperfusion. We hypothesized that the degree of tissue damage in the intestines following ischemia and reperfusion would be mitigated by continuous initiation of 3% hydrogen gas.
Rats were allocated to three groups: ischemia (control 1) that underwent 60-min occlusion of mesenteric artery by clamping under laparotomy, reperfusion (control 2) that underwent the ischemia procedure and 60-min release of occlusion, and hydrogen that underwent the ischemia and reperfusion under 0.3% hydrogen gas inhalation at a rate of 0.2 L/min. Then, the tissue damages at the ileum were histologically evaluated, using immunostaining against caspase-3, 8-hydroxy-2'-deoxyguanosine, and leucine-rich repeat-containing G-protein-coupled 5 (LGR5). Several mRNA, including LGR5, were quantitatively measured with RT-PCR.
The reperfusion procedure introduced intestinal tissue destruction, which was mitigated by hydrogen gas inhalation. In addition, the intestinal tissue injury by the reperfusion involved intestinal stem cell that was marked by LGR5, whereas the ischemia without reperfusion did not affect the stem cell. The expression of LGR5 was significantly lower in the reperfusion group than in the ischemia group, whereas the expression of LGR5 was higher in the hydrogen group than in the reperfusion group.
This study reported on the tissue-protective effects of continuous hydrogen gas inhalation in the ischemia and reperfusion injury at the intestine. The target cells of hydrogen might be intestinal stem cells that are injured by excessive ROS caused by reperfusion following ischemia.
Hydrogen may reduce ROS in other tissues in addition to the intestinal mucosa, which should be examined in the future study. Moreover, the mechanisms of the reduction of ROS toxicity by hydrogen should be revealed to validate the hydrogen as a noninvasive novel treatment.