Y Liu1, J M Downey. 1. Department of Physiology, University of South Alabama, Mobile 36688.
Abstract
OBJECTIVE: Adenosine receptor antagonists and pertussis toxin both block the anti-infarct effect of preconditioning in rabbit heart. Because adenosine receptor blockers were found to have no effect against preconditioning in rat heart, a study was performed to test whether ribosylating G proteins with pertussis toxin would block the protection. METHODS: A branch of the left coronary artery was occluded for 30 min and reperfused for 2 h to produce infarction in open chest rats. Infarct size was assessed by tetrazolium staining. Pertussis toxin was given 48 h before surgery. Preconditioned rats experienced three cycles of 5 min regional ischaemia and 5 min reperfusion before the 30 min occlusion. RESULTS: Four groups of rats were studied. Non-treated control rats had 68.8(SEM 2.2)% infarction of the risk zone and preconditioning reduced this to 32.0(6.5)%. Pertussis toxin completely eliminated the G protein mediated bradycardia caused by intravenous acetylcholine or adenosine infusion. Pertussis toxin treatment had no effect on infarct size in non-preconditioned rats [60.9(4.2)% infarction]. Preconditioning the pertussis toxin treated heart reduced infarction to 21.3(5.6)%, an amount comparable to that seen in non-treated rats. Arrhythmias during the 30 min ischaemia were reduced in preconditioned hearts and this protection was not altered by pertussis toxin treatment. CONCLUSIONS: Preconditioning against either infarction or arrhythmias in the rat does not appear to involve a pertussis toxin sensitive G protein.
OBJECTIVE:Adenosine receptor antagonists and pertussis toxin both block the anti-infarct effect of preconditioning in rabbit heart. Because adenosine receptor blockers were found to have no effect against preconditioning in rat heart, a study was performed to test whether ribosylating G proteins with pertussis toxin would block the protection. METHODS: A branch of the left coronary artery was occluded for 30 min and reperfused for 2 h to produce infarction in open chest rats. Infarct size was assessed by tetrazolium staining. Pertussis toxin was given 48 h before surgery. Preconditioned rats experienced three cycles of 5 min regional ischaemia and 5 min reperfusion before the 30 min occlusion. RESULTS: Four groups of rats were studied. Non-treated control rats had 68.8(SEM 2.2)% infarction of the risk zone and preconditioning reduced this to 32.0(6.5)%. Pertussis toxin completely eliminated the G protein mediated bradycardia caused by intravenous acetylcholine or adenosine infusion. Pertussis toxin treatment had no effect on infarct size in non-preconditioned rats [60.9(4.2)% infarction]. Preconditioning the pertussis toxin treated heart reduced infarction to 21.3(5.6)%, an amount comparable to that seen in non-treated rats. Arrhythmias during the 30 min ischaemia were reduced in preconditioned hearts and this protection was not altered by pertussis toxin treatment. CONCLUSIONS: Preconditioning against either infarction or arrhythmias in the rat does not appear to involve a pertussis toxin sensitive G protein.
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