Table.

Summary of H₂S in Ischemia/Reperfusion Injury

Organ	Experimental Model*	Treatment**	Effects	Ref.
Heart	Langendorff hanging heart model (30 min I/2 hr R)	NaHS (1 (µM) in perfusate 10 min prior to R	20% reduction in infarct size	46
	Perfused rat heart (30 min I/90 min R)	NaHS (1 µM) at onset of R	Significant decrease in myocardial infarct size	50
	Langendorff hanging heart model (30 min I/10 min R)	NaHS (100 µM) in perfusate prior to I	Decreased duration and severity of I/R-induced arrhythmias	37
	Isolated rat cardiac myocytes	NaHS (10–100 µM) with simulated I solution	Increased myocyte viability and shape	37
	Langendorff hanging heart model (40 min I/2 hr R)	PAG-treated (prior to I)	38% increase in myocardial infarct size	41
	in vivo (25 min I/2 hr R)	NaHS (3 mg/kg, r.j.v.) 15 min prior to I	26% reduction in myocardial infarct size	40
	in vivo (30 min I/24 hr R)	Na2S (50 µg/kg, i.c.) at R	72% reduction in infarct size	39
	in vivo (45 min I/24 hr R)	Na2S (100 µg/kg, i.v.) 24 hr before I	46% reduction in infarct; reduction of oxidative stress; decreased anti-apoptotic signaling	47
	in vivo (60 min I/2 hr R)	Na2S (100 µg/kg, i.v.) 10 min before R	2.3-fold reduction in infarct size in porcine model	48
	in vivo (60 min I/2 hr R)	Na2S (2 mg/kg per hr, i.v. infusion) at I	significantly decreased the area of necrosis; higher expression of cell survival proteins; decrease apoptosis	49
Brain	Primary cultures of cortical neurons	NaHS (100 µM) with glutamate	Protects neurons from glutamate toxicity	38
	Cultured hippocampal HT22 cells	NaHS (300 µM) with glutamate	Improved survival of HT22 cells	55
	Cultured brain endothelial cells	NaHS (0.05 and 0.1 mM) with methionine	Attenuated cell death and radical formation	56
	in vivo (24 hr I of MCA)	NaHS (0.18 mmol/kg, i.p.) 10 min prior I	Increased infarct volume 150%	58
	in vivo (90 min I of MCA)	2 days of H2S gas (80 ppm)	Reduced infarct size by 50%	42
	in utero (5 min I/24 hr R of BUA)	NaHS (O.4375 µmol/kg, i.p.)	Protects fetal brains by reinstating the GSH levels decreased by in utero I/R	59
	in vivo (8 min CA followed by CPR)	Na2S (0.55 mg/kg f.v.) 1 min before CPR	Improved neurological function; decreased apoptotic proteins and activation of anti-apoptotic proteins	60
Liver	in vivo (60 min I/5 hr R)	Na2S (1 mg/kg, i.v.) 5 min prior to R	Reduced AST and ALT levels, LPO levels, increase in antioxidant signaling and decrease in anti-apoptotic signaling	43
Kidney	in vivo (45 min I/72 hr R)	PAG (1 ml/kg, i.p.) NaHS (100 µmol/kg) topically on kidney	PAG decreased renal function; NaHS treatment increased renal function	44
	in vivo (45 min I/6 hr R)	--	Ischemia decreased CBS activity and H2S levels	45
Lung	in vivo (45 min I/ 45 min R of PA)	H2S gas (50, 100 µmol/l) 5 min prior to I	Pulmonary protecion; decreased histological injury; increased perfusion flow rate; lowered lung wet/dry ratio; improved lung compliance; lowered MDA levels	62

^*I = Ischemia; R = Reperfusion; CA = Cardiac Arrest; CPR = Cardiopulmonary Resuscitation; MCA = Middle Cerebral Artery; BUA = Bilateral Uteroovarian Artery; PA = Pulmonary Artery; LV = left ventricle;

^**r.j.v. = right jugular vein; i.c. = intracardiac; i.v. = intravenous; i.p. = intraperitoneal; f.v. = femoral venous