Hydrogen Gas Doesn't Help Intestinal Damage in Pig Study

Authors
Journal
Acute Medicine & Surgery
Year
DOI
10.1002/ams2.70072
Study Type
Pig
Outcome
Neutral
Peer Reviewed
Yes
Country
Japan
Health Condition
Non-occlusive mesenteric ischemia
Body System
Gastrointestinal

TL;DR

In this pig study, hydrogen gas therapy did not significantly reduce intestinal damage caused by severe blood flow restriction.

Key Finding

Hydrogen gas inhalation did not significantly reduce intestinal damage or markers of oxidative stress in pigs with non-occlusive mesenteric ischemia without severe tissue death.

Summary

Researchers tested whether breathing hydrogen gas could help reduce intestinal damage in pigs with a condition called non-occlusive mesenteric ischemia (a type of intestinal blood flow problem that doesn't involve a complete blockage). They induced this condition in eight pigs and gave half of them hydrogen gas to breathe while monitoring intestinal damage over four hours. The hydrogen treatment did not reduce intestinal damage compared to the control group, suggesting that hydrogen gas may not be effective for this particular type of intestinal injury.

Practical Takeaway

This animal study suggests that hydrogen gas therapy may have limited effectiveness for certain types of intestinal ischemia, at least in cases without severe tissue damage. However, this is a single small study in pigs, and results from animal models don't always translate to humans. More research would be needed to understand whether hydrogen therapy might work better for other conditions or more severe forms of intestinal injury.

Abstract

Aim: Hydrogen inhalation therapy, a novel therapy for reducing oxidative stress in post-cardiac arrest syndrome, was beneficial for superior mesenteric artery (SMA) occlusion. We assessed the efficacy and feasibility of hydrogen inhalation therapy in swine models of critically ill conditions leading to non-occlusive mesenteric ischemia (NOMI) without acute surgical intervention. Methods: NOMI was induced in eight 3- to 4-month-old female swine under general anesthesia. We defined the initiation of epinephrine administration via the SMA as T = 0 and the initiation of phlebotomy as T = -30 relative to this point. Hemorrhagic shock was induced by combining phlebotomy (T = -30 to -10), continuous systemic norepinephrine administration (T = -30 to 240), and continuous epinephrine injection through the SMA (T = 0-240). The extent of mesenteric ischemia was assessed through gross observation of the intestinal serosa, biomarkers, intestinal pathology, and computed tomography angiography. Results: Control (n = 4) and hydrogen (n = 4) groups with similar baseline characteristics were included. All animals survived until euthanasia (T = 240). The serosa became dark during local epinephrine administration. At T = 240, lactate levels in the control and hydrogen groups were 7.4 (4.7-11.3) and 5.6 (5.0-6.4) mmol/L, respectively, while median 8-hydroxy-2'-deoxyguanosinelevels were 0.15 (0.14-0.18) and 0.15 (0.13-0.16) ng/mL. The pH, base excess, and potassium levels were similar. No significant differences existed in the ischemic grade of the intestinal tract at any time or site. Conclusion: Although critically ill conditions can trigger NOMI, the model used in this study did not involve transmural necrosis. Under such conditions, hydrogen inhalation therapy did not reduce histological ischemic damage. Keywords: acute abdomen; experimental animal model; hydrogen gas; mesenteric ischemia; oxidative stress.