Y Li1, R A Kloner. 1. Heart Institute Research Hospital of the Good Samaritan, Los Angeles, California 90017.
Abstract
OBJECTIVE: Some reports have suggested that the mechanism of ischaemic "preconditioning" is mediated through prostacyclins. In this study the hypothesis that the cardioprotective effect of preconditioning is due to the synthesis and release of prostaglandin/prostacyclin was tested by assessing whether aspirin, an inhibitor of cyclo-oxygenase, could block or prevent the protective effect of preconditioning. METHODS: In protocol I, three groups of rats were studied. (1) CONTROL: rats received 90 min of coronary occlusion followed by 4.5 h of reperfusion (n = 8). (2) Preconditioning: hearts were preconditioned by three repeated episodes of 3 min of coronary occlusion and 5 min of reperfusion, and then subjected to 90 min of occlusion followed by 4 h of reperfusion (n = 9). (3) Aspirin + preconditioning: aspirin (10 mg.kg-1) was given 10 min prior to the preconditioning. Rats then underwent preconditioning and occlusion/reperfusion as in group 2 (n = 8). In protocol II, two groups were studied. (1) CONTROL: rats received 90 min of occlusion and 4.5 h of reperfusion (n = 6). (2) Aspirin + single occlusion: aspirin (10 mg.kg-1) was given 10 min prior to the 90 min occlusion, and then rats underwent occlusion/reperfusion as in controls (n = 6). Female Sprague-Dawley rats weighing between 235-500 g were used. Planimetry was used to measure area at risk (AR) following blue dye injection and area of necrosis (AN) after tetrazolium staining. RESULTS: Protocol I: all three groups had comparable AR. AN/AR was reduced significantly (p less than 0.05) in both the preconditioning group [29.6(SEM 7.6)%] and the aspirin + preconditioning group [29.6(8.7)%] compared with the control group [59.3(3.4)%]. The incidence of ventricular tachycardia and/or fibrillation was also reduced in both the preconditioning and the aspirin + preconditioning groups. Protocol II: the area at risk, area of necrosis, and the indicence of ventricular arrhythmia were not significantly different between aspirin + 90 min occlusion and control groups. CONCLUSIONS: Preconditioning both with and without aspirin significantly reduced infarct size and the incidence of ventricular tachycardia and/or fibrillation. As the effects of preconditioning were not prevented by aspirin, this suggests that the cardioprotective effects of preconditioning are not mediated by prostanoids in the rat model.
OBJECTIVE: Some reports have suggested that the mechanism of ischaemic "preconditioning" is mediated through prostacyclins. In this study the hypothesis that the cardioprotective effect of preconditioning is due to the synthesis and release of prostaglandin/prostacyclin was tested by assessing whether aspirin, an inhibitor of cyclo-oxygenase, could block or prevent the protective effect of preconditioning. METHODS: In protocol I, three groups of rats were studied. (1) CONTROL: rats received 90 min of coronary occlusion followed by 4.5 h of reperfusion (n = 8). (2) Preconditioning: hearts were preconditioned by three repeated episodes of 3 min of coronary occlusion and 5 min of reperfusion, and then subjected to 90 min of occlusion followed by 4 h of reperfusion (n = 9). (3) Aspirin + preconditioning: aspirin (10 mg.kg-1) was given 10 min prior to the preconditioning. Rats then underwent preconditioning and occlusion/reperfusion as in group 2 (n = 8). In protocol II, two groups were studied. (1) CONTROL: rats received 90 min of occlusion and 4.5 h of reperfusion (n = 6). (2) Aspirin + single occlusion: aspirin (10 mg.kg-1) was given 10 min prior to the 90 min occlusion, and then rats underwent occlusion/reperfusion as in controls (n = 6). Female Sprague-Dawley rats weighing between 235-500 g were used. Planimetry was used to measure area at risk (AR) following blue dye injection and area of necrosis (AN) after tetrazolium staining. RESULTS: Protocol I: all three groups had comparable AR. AN/AR was reduced significantly (p less than 0.05) in both the preconditioning group [29.6(SEM 7.6)%] and the aspirin + preconditioning group [29.6(8.7)%] compared with the control group [59.3(3.4)%]. The incidence of ventricular tachycardia and/or fibrillation was also reduced in both the preconditioning and the aspirin + preconditioning groups. Protocol II: the area at risk, area of necrosis, and the indicence of ventricular arrhythmia were not significantly different between aspirin + 90 min occlusion and control groups. CONCLUSIONS: Preconditioning both with and without aspirin significantly reduced infarct size and the incidence of ventricular tachycardia and/or fibrillation. As the effects of preconditioning were not prevented by aspirin, this suggests that the cardioprotective effects of preconditioning are not mediated by prostanoids in the rat model.
Authors: T Miura; R Ishimoto; J Sakamoto; A Tsuchida; K Suzuki; T Ogawa; K Shimamoto; O Iimura Journal: Basic Res Cardiol Date: 1995 May-Jun Impact factor: 17.165