Table 1.

Effects of H₂S donors on different experimental settings.

Cell type	Experimental model	Concentration of H2S donors	Effect of H2S or it donors	Refs
	Male Spargue–Dawley rat	NaSh 0.1–1 μM	Cytoprotection against ischemia/reperfusion	[67]
	Langendorff perfusion
PAEC (porcine pulmonary arterial endothelial cell)		ACS6 10 μM NaSH 1–40 μM	Inhibition of O2̇−	[95]
	Male Wistar rat, LAD occlusion	NaSH 3 mg/kg	AAR reduction	[69]
Rat cardiomyocyte		NaSH 100 μM	Delayed cardioprotection against lethal ischemia	[71]
Rat aortic vascular smooth muscle (primary and immortalized)		S-Didofenac 10–100 μM	Decrease cell survival	[96]
	- Miocardial 1/R murine model and mitochondria isolation	− 50 μg/kg	Respiration rate in mitochondria was increase 2.2 fold	[66]
	- Mitochondria isolation from murine heart	−10 μM	Recovery of respiration after 39' of hypoxia
	Male Wistar rat	NaSH 100 μl/kg	Inhibition aspirin-induced leukocyte adherence	[50]
VSMCs	Male SHR rat	5×10−5, 1×104, 5×10−4 mol/L	Decrease blood pressure Inhibition	[54]
			Ang II-induced VSMCs proliferation
	Male Wistar rat
	- Hippocampus	NaSH 50–160 μM	Induction of long term potentiation	[87]
	- Portal vein	EC50 = 160 μM	Induction of relaxation	[28]
	- Thoracic aorta	EC50 > 1 mM
	Isolated pregnant rat uterine strips in vitro	L–Cysteine, NaSH 10−3 M	Decreases in utherine spontaneous contractillity	[52]
	Mice, hepatic 1/R injury	1K11001 (Na2S) 0.3 mg/kg	Attenuation hepatic 1/R injury	[72]

The cell type, the experimental model, the concentration of H₂S, the main effect, and the bibliographic reference number are reported.