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Evidence of histamine induced myocardial ischemia reversal by chlorpheniramine and potentiation by atherosclerosis



Evidence of histamine induced myocardial ischemia reversal by chlorpheniramine and potentiation by atherosclerosis



Cardiovascular Research 19(12): 744-753



The effects of histamine on coronary vasomotor tone and on myocardial blood flow distribution were studied in the anaesthetised rabbit in the absence of histamine H1-receptor blockade and calcium channel blockade. Two groups of rabbits were used, those fed a normal diet and those fed a high cholesterol diet (2%) for 8 to 12 weeks. Continuous recordings of standard limb lead electrocardiograms (ECG) were obtained, and all animals were pretreated with cimetidine, an H2-receptor blocker, to minimise the intervening systemic effects of histamine. In the absence of H1-receptor blockade, histamine produced a marked (40 to 50%) reduction in coronary blood flow without significantly affecting other cardiovascular variables. This effect was seen uniformly across the free wall of the left ventricle, ie endo-epi flow ratios did not significantly change. Concomitant with the coronary vasoconstriction were significant depressions (.gtoreq. 0.1 mV) of the ECG-ST-segment and elevation of cardiac tissue lactate and lactate:pyruvate ratio. These histamine-mediated responses were independently abolished by chlorpheniramine (1.5 mg .cntdot. kg-1 iv) and verapamil (0.5 mg .cntdot. kg-1 iv). Atherosclerosis reduced the average dose of histamine needed to induce these ischaemic changes from 55 .+-. 6 to 34 .+-. 6 .mu.g .cntdot. kg-1 .cntdot. min-1 (p < 0.05). These findings suggest that in the H2-receptor blocked rabbit coronary vascular bed histamine causes tissue ischaemia by an H1-receptor mechanism. The decrement in myocardial blood flow appears to involve activation of plasma membrane calcium channels and is sensitive to atherosclerosis.

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Accession: 005411467

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PMID: 4084932



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