H2S in acute lung injury: a therapeutic dead end(?)

Intensive Care Medicine Experimental

Table 2 Lung function in a resuscitated comorbid porcine model of hemorrhagic shock [122]

Timepoint	Group assignment	Horowitz index (mmHg)	PEEP (cmH₂O)
Baseline	Control	400 (338, 448)	0
Baseline	Thiosulfate	351 (328, 427)	0
After shock (start of STS infusion)	Control	376 (322, 431)	0
After shock (start of STS infusion)	Thiosulfate	352 (283, 405)	0
24 h after shock (end of STS infusion)	Control	387 (326, 418)	10 (10, 10)
24 h after shock (end of STS infusion)	Thiosulfate	385 (355, 417)	10 (10, 10)
48 h after shock	Control	230 (195, 270)#	12.5 (12.5, 15)
48 h after shock	Thiosulfate	299 (263, 339)*	11.3 (10, 12.5)
72 h after shock	Control	289 (106, 323)#	15 (12.5, 15)
72 h after shock	Thiosulfate	337 (300, 387)	10 (10, 12.5)*

Atherosclerotic pigs were surgically instrumented and, after a short recovery period, underwent 3 h of hemorrhagic shock (target mean arterial pressure 40 ± 5 mmHg). Seventy-two hours of resuscitation comprised re-transfusion of the shed blood and fluid and catecholamine administration targeted to the pre-shock mean arterial pressure. Further details about the experimental protocol can be found in [122]. STS was administered during the first 24 h of resuscitation after hemorrhagic shock. Effects on lung function were most pronounced at 48 h after hemorrhagic shock. Data shown are median (lower quartile, upper quartile)
*Significant to control group
#Significant to baseline (p < 0.05 in two-way ANOVA)