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Article ; Online: Sulfide catabolism in hibernation and neuroprotection.

Ichinose, Fumito / Hindle, Allyson

2024 Volume 146, Page(s) 19–23

Abstract: The mammalian brain is exquisitely vulnerable to lack of oxygen. However, the mechanism underlying the brain's sensitivity to hypoxia is incompletely understood. In this narrative review, we present a case for sulfide catabolism as a key defense ... ...

Abstract	The mammalian brain is exquisitely vulnerable to lack of oxygen. However, the mechanism underlying the brain's sensitivity to hypoxia is incompletely understood. In this narrative review, we present a case for sulfide catabolism as a key defense mechanism of the brain against acute oxygen shortage. We will examine literature on the role of sulfide in hypoxia/ischemia, deep hibernation, and leigh syndrome patients, and present our recent data that support the neuroprotective effects of sulfide catabolism and persulfide production. When oxygen levels become low, hydrogen sulfide (H
MeSH term(s)	Hibernation/physiology ; Animals ; Humans ; Neuroprotection ; Sulfides/metabolism ; Sulfides/pharmacology ; Hydrogen Sulfide/metabolism ; Brain/metabolism ; Mice ; Sciuridae/metabolism ; Leigh Disease/metabolism ; Quinone Reductases/metabolism
Chemical Substances	Sulfides ; Hydrogen Sulfide (YY9FVM7NSN) ; Quinone Reductases (EC 1.6.99.-)
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2024.03.002
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Article ; Online: Selenium-Based Catalytic Scavengers for Concurrent Scavenging of H

Ni, Xiang / Marutani, Eizo / Shieh, Meg / Lam, Yannie / Ichinose, Fumito / Xian, Ming

Angewandte Chemie (International ed. in English)

2024 Volume 63, Issue 6, Page(s) e202317487

Abstract: Hydrogen sulfide ( ... ...

Abstract	Hydrogen sulfide (H
MeSH term(s)	Reactive Oxygen Species ; Selenium ; Oxidative Stress ; Hydrogen Sulfide ; Gasotransmitters ; Hydrogen Peroxide/pharmacology
Chemical Substances	Reactive Oxygen Species ; Selenium (H6241UJ22B) ; Hydrogen Sulfide (YY9FVM7NSN) ; Gasotransmitters ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2024-01-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.202317487
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Article: Emerging pharmacological tools to control hydrogen sulfide signaling in critical illness.

Marutani, Eizo / Ichinose, Fumito

Intensive care medicine experimental

2020 Volume 8, Issue 1, Page(s) 5

Abstract: Hydrogen sulfide ( ... ...

Abstract	Hydrogen sulfide (H
Language	English
Publishing date	2020-01-31
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2740385-3
ISSN	2197-425X
ISSN	2197-425X
DOI	10.1186/s40635-020-0296-4
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Article ; Online: Role of hemolysis on pulmonary arterial compliance and right ventricular systolic function after cardiopulmonary bypass.

Rezoagli, Emanuele / Redaelli, Simone / Bittner, Edward A / Fumagalli, Roberto / Ichinose, Fumito / Berra, Lorenzo

Nitric oxide : biology and chemistry

2024 Volume 146, Page(s) 24–30

Abstract: Background: Cardiopulmonary bypass (CPB) is associated with intravascular hemolysis which depletes endogenous nitric oxide (NO). The impact of hemolysis on pulmonary arterial compliance (PAC) and right ventricular systolic function has not been explored ...

Abstract	Background: Cardiopulmonary bypass (CPB) is associated with intravascular hemolysis which depletes endogenous nitric oxide (NO). The impact of hemolysis on pulmonary arterial compliance (PAC) and right ventricular systolic function has not been explored yet. We hypothesized that decreased NO availability is associated with worse PAC and right ventricular systolic function after CPB. Methods: This is a secondary analysis of an observational cohort study in patients undergoing cardiac surgery with CPB at Massachusetts General Hospital, USA (2014-2015). We assessed PAC (stroke volume/pulmonary artery pulse pressure ratio), and right ventricular function index (RVFI) (systolic pulmonary arterial pressure/cardiac output), as well as NO consumption at 15 min, 4 h and 12 h after CPB. Patients were stratified by CPB duration. Further, we assessed the association between changes in NO consumption with PAC and RVFI between 15min and 4 h after CPB. Results: PAC was lowest at 15min after CPB and improved over time (n = 50). RVFI was highest -worse right ventricular function- at CPB end and gradually decreased. Changes in hemolysis, PAC and RVFI differed over time by CPB duration. PAC inversely correlated with total pulmonary resistance (TPR). TPR and PAC positively and negatively correlated with RVFI, respectively. NO consumption between 15min and 4 h after CPB correlated with changes in PAC (-0.28 ml/mmHg, 95%CI -0.49 to -0.01, p = 0.012) and RVFI (0.14 mmHgL Conclusion:* PAC and RVFI are worse at CPB end and improve over time. Depletion of endogenous NO may contribute to explain changes in PAC and RVFI after CPB.
MeSH term(s)	Humans ; Cardiopulmonary Bypass ; Male ; Hemolysis ; Female ; Middle Aged ; Ventricular Function, Right/physiology ; Aged ; Pulmonary Artery/physiology ; Pulmonary Artery/physiopathology ; Nitric Oxide/metabolism ; Systole/physiology ; Cohort Studies ; Compliance
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2024.03.003
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Article ; Online: Nitric Oxide in Post-cardiac Arrest Syndrome.

Miyazaki, Yusuke / Ichinose, Fumito

Journal of cardiovascular pharmacology

2020 Volume 75, Issue 6, Page(s) 508–515

Abstract: Sudden cardiac arrest is a leading cause of death worldwide. Although the methods of cardiopulmonary resuscitation have been improved, mortality is still unacceptably high, and many survivors suffer from lasting neurological deficits due to the post- ... ...

Abstract	Sudden cardiac arrest is a leading cause of death worldwide. Although the methods of cardiopulmonary resuscitation have been improved, mortality is still unacceptably high, and many survivors suffer from lasting neurological deficits due to the post-cardiac arrest syndrome (PCAS). Pathophysiologically, generalized vascular endothelial dysfunction accompanied by platelet activation and systemic inflammation has been implicated in the pathogenesis of PCAS. Because endothelial-derived nitric oxide (NO) plays a central role in maintaining vascular homeostasis, the role of NO-dependent signaling has been a focus of the intense investigation. Recent preclinical studies showed that therapeutic interventions that increase vascular NO bioavailability may improve outcomes after cardiac arrest complicated with PCAS. In particular, NO inhalation therapy has been shown to improve neurological outcomes and survival in multiple species. Clinical studies examining the safety and efficacy of inhaled NO in patients sustaining PCAS are warranted.
MeSH term(s)	Administration, Inhalation ; Animals ; Cardiovascular Agents/administration & dosage ; Humans ; Nitric Oxide/administration & dosage ; Nitric Oxide/metabolism ; Nitric Oxide Donors/therapeutic use ; Post-Cardiac Arrest Syndrome/drug therapy ; Post-Cardiac Arrest Syndrome/metabolism ; Post-Cardiac Arrest Syndrome/physiopathology ; Treatment Outcome
Chemical Substances	Cardiovascular Agents ; Nitric Oxide Donors ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2020-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000000765
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Article ; Online: Response by Hayashida and Ichinose to Letter Regarding Article, "Improvement in Outcomes After Cardiac Arrest and Resuscitation by Inhibition of S-Nitrosoglutathione Reductase".

Hayashida, Kei / Ichinose, Fumito

Circulation

2019 Volume 140, Issue 6, Page(s) e192–e193

MeSH term(s)	Aldehyde Oxidoreductases ; Heart Arrest ; Humans ; Oxidoreductases ; Resuscitation
Chemical Substances	Oxidoreductases (EC 1.-) ; Aldehyde Oxidoreductases (EC 1.2.-) ; formaldehyde dehydrogenase, glutathione-independent (EC 1.2.1.46)
Language	English
Publishing date	2019-08-05
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.119.041024
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Article ; Online: Improving outcomes after cardiac arrest using NO inhalation.

Ichinose, Fumito

Trends in cardiovascular medicine

2013 Volume 23, Issue 2, Page(s) 52–58

Abstract: Despite advances in cardiopulmonary resuscitation (CPR) methods including therapeutic hypothermia (TH), long-term neurological outcomes and survival after sudden cardiac arrest (CA) remains to be dismal. While nitric oxide (NO) prevents organ injury ... ...

Abstract	Despite advances in cardiopulmonary resuscitation (CPR) methods including therapeutic hypothermia (TH), long-term neurological outcomes and survival after sudden cardiac arrest (CA) remains to be dismal. While nitric oxide (NO) prevents organ injury induced by ischemia and reperfusion (I/R), systemic vasodilation induced by intravenous NO-donor compounds typically precludes its use in post-CA patients in whom blood pressure is often low and unstable. Although developed as a selective pulmonary vasodilator, inhaled NO has systemic benefits in a variety of pre-clinical and clinical studies without causing potentially harmful systemic vasodilation. Breathing NO after CPR may prevent post-CA brain injury and improve long-term outcomes after CA and CPR.
MeSH term(s)	Administration, Inhalation ; Animals ; Cardiopulmonary Resuscitation ; Heart Arrest/therapy ; Mice ; Nitric Oxide/administration & dosage ; Treatment Outcome
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2013-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1097434-9
ISSN	1873-2615 ; 1050-1738
ISSN (online)	1873-2615
ISSN	1050-1738
DOI	10.1016/j.tcm.2012.08.011
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Zs.A 3419: Show issues

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Article ; Online: Inhaled Pulmonary Vasodilators in Cardiac Surgery Patients: Correct Answer Is "NO".

Ichinose, Fumito / Zapol, Warren M

Anesthesia and analgesia

2017 Volume 125, Issue 2, Page(s) 375–377

MeSH term(s)	Administration, Inhalation ; Cardiac Surgical Procedures ; Humans ; Hypertension, Pulmonary ; Lung ; Nitric Oxide ; Vasodilator Agents
Chemical Substances	Vasodilator Agents ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80032-6
ISSN	1526-7598 ; 0003-2999
ISSN (online)	1526-7598
ISSN	0003-2999
DOI	10.1213/ANE.0000000000002239
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Uk I Zs.78: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 149: Show issues

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Article ; Online: Intranasal administration of polysulfide prevents neurodegeneration in spinal cord and rescues mice from delayed paraplegia after spinal cord ischemia.

Kanemaru, Eiki / Miyazaki, Yusuke / Marutani, Eizo / Ezaka, Mariko / Goto, Shunsaku / Ohshima, Etsuo / Bloch, Donald B / Ichinose, Fumito

Redox biology

2023 Volume 60, Page(s) 102620

Abstract: Background: Delayed paraplegia is a devastating complication of thoracoabdominal aortic surgery. Hydrogen sulfide (H: Methods and results: Spinal cord ischemia was induced in male and female C57BL/6J mice by clamping the aortic arch and the left ... ...

Abstract	Background: Delayed paraplegia is a devastating complication of thoracoabdominal aortic surgery. Hydrogen sulfide (H Methods and results: Spinal cord ischemia was induced in male and female C57BL/6J mice by clamping the aortic arch and the left subclavian artery. Glutathione trisulfide (GSSSG), glutathione (GSH), glutathione disulfide (GSSG), or vehicle alone was administered intranasally at 0, 8, 23, and 32 h after surgery. All mice treated with vehicle alone developed paraplegia within 48 h after surgery. GSSSG, but not GSH or GSSG, prevented paraplegia in 8 of 11 male mice (73%) and 6 of 8 female mice (75%). Intranasal administration of Conclusions: Intranasal administration of polysulfides rescued mice from delayed paraplegia after transient spinal cord ischemia. The neuroprotective effects of GSSSG were associated with increased levels of polysulfides and sulfane sulfur in the lumbar spinal cord. Targeted delivery of sulfane sulfur by polysulfides may prove to be a novel approach to the treatment of neurodegenerative diseases.
MeSH term(s)	Mice ; Male ; Female ; Animals ; Administration, Intranasal ; Glutathione Disulfide ; Mice, Inbred C57BL ; Spinal Cord Ischemia/drug therapy ; Spinal Cord Ischemia/complications ; Sulfur ; Paraplegia/drug therapy ; Paraplegia/etiology ; Paraplegia/prevention & control
Chemical Substances	polysulfide (9080-49-3) ; sulfur-32 ; Glutathione Disulfide (ULW86O013H) ; Sulfur (70FD1KFU70)
Language	English
Publishing date	2023-02-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102620
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Article ; Online: Continuous, but not intermittent, regimens of hypoxia prevent and reverse ataxia in a murine model of Friedreich's ataxia.

Ast, Tslil / Wang, Hong / Marutani, Eizo / Nagashima, Fumiaki / Malhotra, Rajeev / Ichinose, Fumito / Mootha, Vamsi K

Human molecular genetics

2023 Volume 32, Issue 16, Page(s) 2600–2610

Abstract: Friedreich's ataxia (FA) is a devastating, multi-systemic neurodegenerative disease affecting thousands of people worldwide. We previously reported that oxygen is a key environmental variable that can modify FA pathogenesis. In particular, we showed that ...

Abstract	Friedreich's ataxia (FA) is a devastating, multi-systemic neurodegenerative disease affecting thousands of people worldwide. We previously reported that oxygen is a key environmental variable that can modify FA pathogenesis. In particular, we showed that chronic, continuous normobaric hypoxia (11% FIO2) prevents ataxia and neurological disease in a murine model of FA, although it did not improve cardiovascular pathology or lifespan. Here, we report the pre-clinical evaluation of seven 'hypoxia-inspired' regimens in the shFxn mouse model of FA, with the long-term goal of designing a safe, practical and effective regimen for clinical translation. We report three chief results. First, a daily, intermittent hypoxia regimen (16 h 11% O2/8 h 21% O2) conferred no benefit and was in fact harmful, resulting in elevated cardiac stress and accelerated mortality. The detrimental effect of this regimen is likely owing to transient tissue hyperoxia that results when daily exposure to 21% O2 combines with chronic polycythemia, as we could blunt this toxicity by pharmacologically inhibiting polycythemia. Second, we report that more mild regimens of chronic hypoxia (17% O2) confer a modest benefit by delaying the onset of ataxia. Third, excitingly, we show that initiating chronic, continuous 11% O2 breathing once advanced neurological disease has already started can rapidly reverse ataxia. Our studies showcase both the promise and limitations of candidate hypoxia-inspired regimens for FA and underscore the need for additional pre-clinical optimization before future translation into humans.
MeSH term(s)	Humans ; Mice ; Animals ; Friedreich Ataxia/genetics ; Neurodegenerative Diseases ; Disease Models, Animal ; Polycythemia ; Hypoxia ; Oxygen ; Ataxia
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2023-06-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddad091
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