BACKGROUND: Allicin is a sulfur-containing compound extracted from garlic, with antiaggregatory, anti- migratory, anti-oxidant and pulmonary vasodilator actions. We hypothesized that allicin might be beneficial in lung ischemia-reperfusion. METHODS: A non-nothermic rat lung ischemia-reperfusion model was established by clamping left pulmonary artery (PA) for 1 hr, followed by reperfusion for 2 hrs by clamping right PA to reflect solely the function of left lung. Groups were control (n=7), allicin 0.1 mg (n=8) and allicin 0.01 mg (n=4). In the beginning of reperfusion allicin/saline were injected. Pulmonary artery pressures (PAP), pulmonary artery flow (PAF), left atrial pressure (LAP) were monitored. At the end of reperfusion period arterial blood gas (ABG) analysis was done. RESULTS: Six of 7 control and 3 of 8 group 2 animals died before completing the experiment. In group 1 all animals completed the experiment (p=0.015 vs control). PAF was significantly increased after 30, 60 and 120 min of reperfusion in group 1 (p=0.0028, 0.0009, 0.0003 respectively vs control) and after 60 and 120 minutes in group 2 (p=0.0453, 0.018 respectively vs control). Pulmonary vascular resistance was lower at 30 min in allicin 0.01 mg group (p=0.0017 vs control). PAP was increased after 60 and 120 min of reperfusion in group 1 (p=0.016, 0.0029 respectively vs control) and after 120 min in group 2 (p=0.0104 vs control). CONCLUSIONS: This study shows that allicin improves postischemic PAF in this model. Allicin needs further investigation of potential utility and mechanism(s) of action.
BACKGROUND:Allicin is a sulfur-containing compound extracted from garlic, with antiaggregatory, anti- migratory, anti-oxidant and pulmonary vasodilator actions. We hypothesized that allicin might be beneficial in lung ischemia-reperfusion. METHODS: A non-nothermic ratlung ischemia-reperfusion model was established by clamping left pulmonary artery (PA) for 1 hr, followed by reperfusion for 2 hrs by clamping right PA to reflect solely the function of left lung. Groups were control (n=7), allicin 0.1 mg (n=8) and allicin 0.01 mg (n=4). In the beginning of reperfusion allicin/saline were injected. Pulmonary artery pressures (PAP), pulmonary artery flow (PAF), left atrial pressure (LAP) were monitored. At the end of reperfusion period arterial blood gas (ABG) analysis was done. RESULTS: Six of 7 control and 3 of 8 group 2 animals died before completing the experiment. In group 1 all animals completed the experiment (p=0.015 vs control). PAF was significantly increased after 30, 60 and 120 min of reperfusion in group 1 (p=0.0028, 0.0009, 0.0003 respectively vs control) and after 60 and 120 minutes in group 2 (p=0.0453, 0.018 respectively vs control). Pulmonary vascular resistance was lower at 30 min in allicin 0.01 mg group (p=0.0017 vs control). PAP was increased after 60 and 120 min of reperfusion in group 1 (p=0.016, 0.0029 respectively vs control) and after 120 min in group 2 (p=0.0104 vs control). CONCLUSIONS: This study shows that allicin improves postischemic PAF in this model. Allicin needs further investigation of potential utility and mechanism(s) of action.