Table 2.

Summary of in vivo experimental studies investigating the infarct-limiting effect of myocardial cooling during the reperfusion phase, i.e. with cooling started only 5 min before reperfusion or later yielding normothermic ischaemia and hypothermic reperfusion

Species	Ref.	Cooling procedure	Duration of CAO (min)/CAR (h)	Target heart temperature (°C)	Time of coolinga	IS with Cooling vs. Control groups (% decrease)
Rabbit	36	Topical epicardial cooling	30/3	∼33	25 min CAO →15 min CAR	43 ± 4 vs. 44 ± 4 (NS)
Rabbit	25	Total liquid ventilation	30/3	∼32	25 min CAO →30 min CAR	35 ± 4 vs. 38 ± 1 (NS)
Rabbit	37	Surface cooling (water blankets)	30/3	∼37.0	25 min CAO → 180 min CAR	44 ± 2 vs. 59 ± 1 (−25%)
					30 min CAO → 180 min CAR	51 ± 2 vs. 59 ± 1 (NS)
Pig	38	Regional blood cooling through heat exchanger	45/3	∼33	43 min CAO → 120 min CAR	71 ± 8 vs. 68 ± 1 (NS)
Pig	28	Intracoronary cold saline infusion	60/3	∼33	0 min CAR → 30 min CAR	33 ± 2 vs. 45 ± 5 (NS)
Pig	35	Intravenous infusion of cold saline + endovascular cooling	40/∼4.3	∼33	0 min CAR →30 min CAR	80 ± 6 vs. 75 ± 5 (NS)

CAO, coronary artery occlusion; CAR, coronary artery reperfusion; IS, infarct size (expressed as % of area at risk); Ref, reference number.

^aThe time of the application of the cooling strategy and not the actual time at which the target temperature was reached. In several studies, a delay was inevitable between the onset of the cooling protocol and the time of achievement of the target temperature (e.g. with low rate cooling strategy such as surface cooling).