Publication

The role of endogenous H2S production during hibernation and forced hypothermia: towards safe cooling and rewarming in clinical practice

Dugbartey, G. J., 2015, [Groningen]: University of Groningen. 127 p.

Research output: ThesisThesis fully internal (DIV)Academic

APA

Dugbartey, G. J. (2015). The role of endogenous H2S production during hibernation and forced hypothermia: towards safe cooling and rewarming in clinical practice. [Groningen]: University of Groningen.

Author

Dugbartey, George Johnson. / The role of endogenous H2S production during hibernation and forced hypothermia : towards safe cooling and rewarming in clinical practice. [Groningen] : University of Groningen, 2015. 127 p.

Harvard

Dugbartey, GJ 2015, 'The role of endogenous H2S production during hibernation and forced hypothermia: towards safe cooling and rewarming in clinical practice', Doctor of Philosophy, University of Groningen, [Groningen].

Standard

The role of endogenous H2S production during hibernation and forced hypothermia : towards safe cooling and rewarming in clinical practice. / Dugbartey, George Johnson.

[Groningen] : University of Groningen, 2015. 127 p.

Research output: ThesisThesis fully internal (DIV)Academic

Vancouver

Dugbartey GJ. The role of endogenous H2S production during hibernation and forced hypothermia: towards safe cooling and rewarming in clinical practice. [Groningen]: University of Groningen, 2015. 127 p.


BibTeX

@phdthesis{d7d7de5d34d84890aa8b3646d2a02a45,
title = "The role of endogenous H2S production during hibernation and forced hypothermia: towards safe cooling and rewarming in clinical practice",
abstract = "Therapeutic hypothermia as employed during transplantation, surgery or trauma unavoidably leads to organ damage due to ischemia/reperfusion injury (IRI). Interestingly, hibernating mammals have solved this problem, as they manage to periodically lower their metabolism and body temperature during periods referred to as torpor. Torpor periods are regularly intersected by brief periods (‘arousals’), during which these parameters are restored without organ damage. Several adaptive physiological mechanisms in hibernators may underlie this resistance to organ damage during these period of physiological extremes. We recently identified a reversible remodeling of lung tissue in hibernating Syrian hamsters with regulation of the H2S-producing enzyme, cystathionine-β-synthase (CBS) as one of the adaptive mechanisms. Therefore, this PhD aimed at investigating mechanisms that confer resistance to hypothermia/rewarming with a focus on the role of endogenous hydrogen sulfide gas (H2S) and its synthesizing enzymes in the kidney, representing an organ highly susceptible to hypothermic damage. Main findings are that torpid animals show an upregulation of H2S-synthesizing enzymes and increased blood H2S level. Further, pharmacological inhibition of the H2S-synthesizing pathways prevented entrance into torpor and induced renal injury. Together, this suggests that the H2S pathway is essential not only in inducing hibernation but also in protecting the kidney during these temperature extremes. Further, we found that pharmacological induction of H2S formation by dopamine also protected from kidney damage in rats subjected to forced hypothermia/rewarming. Therefore, maintenance or upregulation of endogenous H2S-synthesizing pathways may offer a novel therapeutic approach in preventing renal IRI associated with clinical conditions which require cooling/rewarming.",
author = "Dugbartey, {George Johnson}",
year = "2015",
language = "English",
isbn = "978-90-367-7741-4",
publisher = "University of Groningen",
school = "University of Groningen",

}

RIS

TY - THES

T1 - The role of endogenous H2S production during hibernation and forced hypothermia

T2 - towards safe cooling and rewarming in clinical practice

AU - Dugbartey, George Johnson

PY - 2015

Y1 - 2015

N2 - Therapeutic hypothermia as employed during transplantation, surgery or trauma unavoidably leads to organ damage due to ischemia/reperfusion injury (IRI). Interestingly, hibernating mammals have solved this problem, as they manage to periodically lower their metabolism and body temperature during periods referred to as torpor. Torpor periods are regularly intersected by brief periods (‘arousals’), during which these parameters are restored without organ damage. Several adaptive physiological mechanisms in hibernators may underlie this resistance to organ damage during these period of physiological extremes. We recently identified a reversible remodeling of lung tissue in hibernating Syrian hamsters with regulation of the H2S-producing enzyme, cystathionine-β-synthase (CBS) as one of the adaptive mechanisms. Therefore, this PhD aimed at investigating mechanisms that confer resistance to hypothermia/rewarming with a focus on the role of endogenous hydrogen sulfide gas (H2S) and its synthesizing enzymes in the kidney, representing an organ highly susceptible to hypothermic damage. Main findings are that torpid animals show an upregulation of H2S-synthesizing enzymes and increased blood H2S level. Further, pharmacological inhibition of the H2S-synthesizing pathways prevented entrance into torpor and induced renal injury. Together, this suggests that the H2S pathway is essential not only in inducing hibernation but also in protecting the kidney during these temperature extremes. Further, we found that pharmacological induction of H2S formation by dopamine also protected from kidney damage in rats subjected to forced hypothermia/rewarming. Therefore, maintenance or upregulation of endogenous H2S-synthesizing pathways may offer a novel therapeutic approach in preventing renal IRI associated with clinical conditions which require cooling/rewarming.

AB - Therapeutic hypothermia as employed during transplantation, surgery or trauma unavoidably leads to organ damage due to ischemia/reperfusion injury (IRI). Interestingly, hibernating mammals have solved this problem, as they manage to periodically lower their metabolism and body temperature during periods referred to as torpor. Torpor periods are regularly intersected by brief periods (‘arousals’), during which these parameters are restored without organ damage. Several adaptive physiological mechanisms in hibernators may underlie this resistance to organ damage during these period of physiological extremes. We recently identified a reversible remodeling of lung tissue in hibernating Syrian hamsters with regulation of the H2S-producing enzyme, cystathionine-β-synthase (CBS) as one of the adaptive mechanisms. Therefore, this PhD aimed at investigating mechanisms that confer resistance to hypothermia/rewarming with a focus on the role of endogenous hydrogen sulfide gas (H2S) and its synthesizing enzymes in the kidney, representing an organ highly susceptible to hypothermic damage. Main findings are that torpid animals show an upregulation of H2S-synthesizing enzymes and increased blood H2S level. Further, pharmacological inhibition of the H2S-synthesizing pathways prevented entrance into torpor and induced renal injury. Together, this suggests that the H2S pathway is essential not only in inducing hibernation but also in protecting the kidney during these temperature extremes. Further, we found that pharmacological induction of H2S formation by dopamine also protected from kidney damage in rats subjected to forced hypothermia/rewarming. Therefore, maintenance or upregulation of endogenous H2S-synthesizing pathways may offer a novel therapeutic approach in preventing renal IRI associated with clinical conditions which require cooling/rewarming.

M3 - Thesis fully internal (DIV)

SN - 978-90-367-7741-4

PB - University of Groningen

CY - [Groningen]

ER -

ID: 20598435