1 To study the e ect of nicotine on the severity of experimental myocardial ischaemia, Langendor hearts of rabbits (n=7 ± 12 per group) were subjected to 2 h of low-¯ow ischaemia followed by 1 h of reperfusion. 2 Infusion of nicotine (100 ng ml 71 ) caused only minor changes in non-ischaemic conditions but a signi®cant (P50.05) increase in end-diastolic pressure (LVEDP), loss of creatine kinase (CK) and troponin (TnT) as well as increase in noradrenaline (NA) over¯ow in reperfused ischaemic hearts. 3 RT ± PCR was done on total RNA for mRNA expression of the constitutive (COX-1) and inducible cyclooxygenase (COX-2). There was no COX-2 in non-ischaemic hearts but a signi®cant expression in ischaemia (n=5) which was further increased by nicotine. These data were con®rmed at the protein level by Western blotting and additionally shown that COX-1 remained unchanged. 4 There was a marked increase in prostacyclin (PGI 2 ) and a 2 fold increase in NA over¯ow which were both stimulated by nicotine. 5 The aggravating e ects of nicotine on myocardial ischaemia (CK release) as well as the expression of COX-2 mRNA were prevented by pretreatment with the b-blocker pindolol (1 mM). 6 The data demonstrate marked deleterious actions of nicotine in reperfused ischaemic hearts. These actions are probably related to the increase in catecholamine over¯ow, are b-receptor-mediated and involve enhanced gene expression of COX-2.
It is not yet known, whether different Col III/Col I ratios differentially influence diastolic compliance. Our data suggest that inflammatory mechanisms seen in inflammatory cardiomyopathy influence the mRNA abundance of collagen subtypes I and III.
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