Hydrogen sulfide improves resuscitation via non-hibernatory mechanisms in a porcine shock model

Satterly, Steven; Salgar, Shashikumar K.; Hoffer, Zachary S.; Hempel, James; DeHart, Mary; Wingerd, Mark A.; Huang, Ran; Stallings, Jonathan D.; Martin, Matthew J.

doi:10.1016/j.jss.2015.04.001

Cited by 21 publications

(18 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 16 however, creatinine levels were not affected by hydrogen sulfide treatment at the time of animal euthanasia (6 hours) [51]. Clinically, it seems that while targeting free radical may show some benefit, any successful treatment for end organ damage needs to exert pleiotropic effects or will require some type of treatment cocktail.…”

Section: Accepted Manuscriptmentioning

confidence: 96%

“…In HS rats (MAP maintained at 35±5 mmHg) and pigs (MAP maintained at 40 mmHg), kidney expression of these growth factors and their receptors is reduced however; this lack of expression may be due to time of collection or severity of kidney injury [49,51]. Interestingly, in diabetic HS mice VEGF-2 receptor was reduced to a lesser extent than in non-diabetic HS mice [49].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…ROS and NOS facilitate the translocation of the transcription factor nuclear factor κ-B (NF-κB) from the cytoplasm to the nucleus, which elicits the inflammatory cascade. Once in the nucleus, NF-κB initiates expression of iNOS [49,51], tumor necrosis factor α (TNF-α) [58][59][60] and interleukin 6 (IL-6); all elevated in rat kidneys within 2 hours of hemorrhagic shock and…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…NO derived from iNOS propagates the inflammatory response and contributes to enhanced tissue damage. Additionally, endothelial nitric oxide synthase (eNOS) was capable of generating NO in the kidney 6 hours following HS in pigs [51] but not in mice [49]. In contrast, hypoxia from hemorrhage in rats was associated with a 10-fold drop in NO and renal damage and dysfunction [62].NO has also been shown to regulate water permeability via inhibition of vasopressin [63].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…Administration of hydrogen sulfide also neutralized reactive molecules and has been shown to reduce kidney injury scores in a HS + ischemia reperfusion (aortic cross clamp) pig model [51];…”

Section: Accepted Manuscriptmentioning

confidence: 99%

See 4 more Smart Citations

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

Burmeister

Gómez

Dubick

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.

show abstract

Section: Accepted Manuscriptmentioning

confidence: 96%